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News
December 21, 2023
Exercise-induced Irisin Attenuates Amyloid-β Pathology
Accumulation of amyloid-β (Aβ) peptide aggregates in brain areas is a hallmark of Alzheimer's Disease (AD) neuropathology. Physical exercise attenuates pathology impairments in AD models. However, the molecular mechanisms of neuroprotection by physical exercise in AD remain poorly characterized. Irisin, an exercise-induced hormone secreted from muscles, is cleaved from fibronectin type III domain-containing protein 5 (FNDC5) and has a beneficial role in adipose tissues, bone remodeling, and the brain. A recent study by the lab of Dr. Rudolph Tanzi and Dr. Hoon Choi (Harvard Medical School) describes in the journal Neuron a mechanism by which irisin limits Aβ accumulation in the brain. They showed that irisin decreases Aβ pathology by promoting astrocytic release of the Aβ-degrading enzyme neprilysin (NEP). Irisin binds to its receptor integrin αV/β5 on astrocytes which down-regulates ERK-STAT3 signaling and induces NEP secretion leading to Aβ clearance. These new findings offer new potential for the protein irisin as a therapeutic target for AD treatment and prevention.
AdipoGen Life Sciences provides unique recombinant Irisin/FNDC5 proteins, antibodies and ELISA kits to study Irisin and FNDC5 in vitro and in vivo:
- Fc (LALA-PG)-KIH (human):Irisin (monomeric) (rec.) (Prod. No. AG-40B-0246) (for in vivo studies)
- Irisin (rec.) (HEK293) (monomeric) (Prod. No. AG-40B-0102)
- Irisin (rec.) (CHO) (monomeric) (Prod. No. AG-40B-0136)
- Irisin (rec.) (untagged) (E.coli) (Prod. No. AG-40B-0103)
- FNDC5 (rec) (untagged) (Prod. No. AG-40B-0128)
- FNDC5:Fc (human) (rec) (Prod. No. AG-40B-0153)
- anti-Irisin, pAb (IN102) (Prod. No. AG-25B-0027)
- Irisin Competitive ELISA Kit (Prod. No. AG-45A-0046Y)
LIT: Irisin reduces amyloid-b by inducing the release of neprilysin from astrocytes following downregulation of ERK-STAT3 signaling: E. Kim, et al.; Neuron 11, 3619 (2023)
April 18, 2023
BAFF and APRIL have Opposite Functions in Inflammation during Parturition
The B cell-stimulating molecules, BAFF (B cell activating factor) and APRIL (a proliferation-inducing ligand), are critical factors in the maintenance of the B cell pool and humoral immunity. Both signal through the receptors TACI and BCMA, and BAFF also activates the receptor BAFF-R. BAFF has been shown to play a role during pregnancy with levels of BAFF fluctuating during pregnancy or parturition. BAFF seems to be involved in preterm labor, but how the BAFF axis affects systemic and local immune responses in pregnancy and preterm birth (PTB) remains unknown.
A recent study from the lab of Professor Senad Divanovic (Cincinnati Children’s Hospital Medical Center, Cincinnati) reports in the journal Cell Reports, that the BAFF/APRIL axis is activated in inflammation-induced PTB. Macrophages produce BAFF at the maternal-fetal interface and BAFF enhances inflammatory responsiveness and increases susceptibility to PTB. APRIL has the opposite function in PTB decreasing inflammation. Therefore, the new roles of BAFF or APRIL in parturition open new therapeutic possibilities for mitigating the risk of inflammation-induced PTB.
In this study they used the APRIL and BAFF blocking antibodies available from AdipoGen Life Sciences:
- anti-APRIL (mouse), mAb (rec.) (blocking) (Apry-1-1) (preservative free) (Prod. No. AG-27B-0001PF)
- anti-BAFF (mouse), mAb (blocking) (Sandy-2) (preservative free) (Prod. No. AG-20B-0063PF)
AdipoGen Life Sciences provides many unique reagents to study APRIL and BAFF in vitro and in vivo:
- anti-April (mouse), mAb (blocking) (Centotto-1) (preservative free) (Prod. No. AG-20B-0083PF)
- anti-APRIL (human), mAb (blocking) (Mahya-1) (preservative free) (Prod. No. AG-20B-0078PF)
- APRIL (human) (multimeric) (rec.) (Prod. No. AG-40B-0017)
- APRIL (mouse) (multimeric) (rec.) (Prod. No. AG-40B-0089)
- BAFF, Soluble (human) (60-mer) (rec.) (highly active) (Prod. No. AG-40B-0112)
- BCMA (mouse):Fc (human) (rec.) (Prod. No. AG-40B-0076)
- APRIL (human) ELISA Kit (Prod. No. AG-45B-0012)
- BAFF, Soluble (human) ELISA Kit (hypersensitive) (Prod. No. AG-45B-0001)
LIT:
BAFF and APRIL counterregulate susceptibility to inflammation-induced preterm birth: R.J. Doll, et al.; Cell Reports 42, 112352 (2023)
February 22, 2023
Periostin Deficiency Reduces PD-1+ Tumor-associated Macrophages
Periostin is a 90kDa matricellular protein that binds to integrin and is involved in many fundamental biological processes such as cell proliferation, cell invasion and angiogenesis, and in many aspects of allergic inflammation and cancer. Changes in periostin expression are commonly detected in various cancers (including colorectal cancer (CRC), breast cancer, leukemia, and hepatocellular carcinoma) and contribute to tumorigenesis, cancer progression and metastasis. Periostin has been shown to be secreted by cancer-associated fibroblasts (CAF) in a model of CRC leading to programmed death receptor 1 (PD-1) expression on tumor-associated macrophages (TAMs), but the exact role of Periostin in CRC has still to be characterized.
A recent study from the labs of Prof. G. Ouyang and T. Wu (Xiamen Universiy, China) reports in the journal Cell Reports the mechanism of action of Periostin in CRC. Periostin deficiency in tumor microenvironment (TME) significantly decreases the infiltration of PD-1+ TAMs (pro-tumoral) in colorectal cancer tissues of mice leading to suppression of tumor growth. Periostin functions via induction of the expression of PD-1 on TAMs by integrin-lLK-nuclear factor κB (NF-κB) signaling. The PD-1+ TAMs then produce lL-6 and lFN-γ to induce the expression of PD-L1 on colorectal tumor cells, inhibiting the immune response to cancer cells and leading to tumor growth. In this study, inhibition of both periostin and PD-1 sígnificantly suppresses CRC progression. These findings suggest that the combined blockade of periostin and PD-1 could improve immune therapy efficacy in CRC in human.
AdipoGen Life Sciences provides the key Periostin monoclonal antibody Stiny-1 used in this study:
- anti-Periostin, mAb (Stiny-1) (Prod. No. AG-20B-0033)
Other reagents available in the Periostin and PD-1 field:
- anti-Periostin, mAb (blocking) (OC-20) (preservative free) (Prod. No. AG-20B-6000PF)
- Periostin (mouse) (rec.) (Prod. No. AG-40B-0081)
- Periostin (human) (rec.) (Prod. No. AG-40B-0104)
- Periostin (human) ELISA Kit (Prod. No. AG-45B-0004)
- Periostin (mouse) ELISA Kit (Prod. No. AG-45B-0005)
- anti-PD-1 (m), mAb (blocking) (1H10) (preservative free) (Prod. No. AG-20B-0075PF)
- PD-1 (human) ELISA Kit (Prod. No. AG-45B-0015)
LIT: Periostin deficiency reduces PD-1+ tumor-associated macrophage infiltration and enhances anti-PD-1 efficacy in colorectal cancer: T. Wei, et al.; Cell Reports 42, 112090 (2023)
November 22, 2022
FMRP Regulates Tumor Growth by Activating T Regulatory Cells via Interleukin-33
Interleukin-33 (IL-33) is an IL-1 family member and the ligand for the suppression of tumorigenicity 2 (ST2) receptor, with crucial roles in tissue homeostasis and repair, type 2 immunity, allergic and non-allergic inflammation, viral infection, and cancer. Fragile X mental retardation protein (FMRP), which regulates protein translation and mRNA stability, is expressed at high levels in neuronal synapses and is also involved in tumor progression, in particular stimulating invasion and metastasis in certain tumor types, but its role has still to be clarified.
A recent study from the lab of Prof. Dr. Douglas Hanahan (ISREC and Oncology Department (CHUV), Lausanne, Switzerland) reports in the journal Science that FMRP hyper-expressing cancer cells produce interleukin-33 (IL-33), as well as the tumor-secreted protein S (PROS1) ligand and exosomes. IL-33 secreted from cancer cells overexpressing FMRP modulates Tregs cells, which limit the recruitment and expansion of CD8 and CD4 T cells with the help of PROS1 and exosomes that activate immune-suppressive (M2) macrophage cells. FMRP acts as a regulator of a network of genes (IL-33, PROS1) and cells (Treg, M2 macrophages and potentially additional classes of myeloid cells) in the tumor microenvironment that helps cancer cells to evade immune destruction.
AdipoGen Life Sciences provides many unique reagents to study mouse and human IL-33 in vitro and in vivo:
- IL-33 (human) (rec.) (untagged) (Prod. No. AG-40B-0038)
- IL-33 (oxidation resistant) (human) (rec.) (untagged) (Prod. No. AG-40B-0160) UNIQUE
- IL-33 (mouse) (rec.) (untagged) (Prod. No. AG-40B-0041)
- IL-33 (human), mAb (IL33305B) (Prod. No. AG-20A-0041)
- IL-33 (mouse), mAb (rec.) (blocking) (Bondy-1-1) (Prod. No. AG-27B-0013) UNIQUE
- HpARI (Alarmin Release Inhibitor) (rec.) (His) (Prod. No. AG-40B-0178) UNIQUE
- HpARI (CCP1/2) (rec.) (His) (Prod. No. AG-40B-0201) UNIQUE
- ST2 (human):Fc (human) (rec.) (Prod. No. AG-40A-0059)
- anti-ST2 (human), pAb (Prod. No. AG-25A-0058)
- anti-ST2 (human), mAb (ST33868) (Prod. No. AG-20A-0044)
LIT: Aberrant hyperexpression of the RNA binding protein FMRP in tumors mediates immune evasion: Q. Zeng, et al.; Science 378, 746 (2022)
August 03, 2022
The Innate Sensor ZBP1 is inhibited by ADAR1
ADAR1 (RNA-editing enzyme adenosine deaminase acting on RNA 1) contains a Zα domain that recognizes and disrupts the duplex structure of endogenous immunostimulatory double-stranded Z-RNA. Interaction of ADAR1 with Z-RNA is required to prevent activation of pathogenic Interferon (IFN) responses and mutations of the Zα domain of ADAR1 cause severe autoinflammatory diseases associated with chronic activation of type I interferon (IFN) responses, including Aicardi–Goutières syndrome and bilateral striatal necrosis. It remains unclear how the interaction of ADAR1 with Z-RNA prevents IFN-dependent pathologies.
Four studies published recently in the journals Cell Reports and Nature (see References 1 to 4) identify the IFN-induced protein ZBP1, the only other protein in mammals known to harbor Zα domains binding to Z-dsRNA, as a key effector of autoinflammatory pathology induced by mutations of the Z-DNA-binding domain of ADAR1. ADAR1 co-immunoprecipitates with Z-DNA-binding protein 1 (ZBP1) via RNA ligands and inhibits ZBP1. Mutations of ADAR1 or ADAR1-deficient cells disrupt this binding, leading to activation of ZBP1 that triggers cell death and transcriptional responses through the kinases RIPK1 and RIPK3, and the protease caspase 8, but also cause tissue damage and inflammation. These findings indicate that ADAR1 is a negative regulator of sterile ZBP1 activation.
In all four publications, the protein ZBP1 is studied and detected using the Gold Standard antibody from AdipoGen Life Sciences:
- anti-ZBP1, mAb (Zippy-1) (Prod. No. AG-20B-0010)
Also available from AdipoGen Life Sciences in this research field:
- anti-Caspase-1 (p20) (mouse), mAb (Casper-1) (Prod. No. AG-20B-0042)
- anti-Caspase-1 (p20) (human), mAB (Bally-1) (Prod. No. AG-20B-0048)
- PANoptosome Human Antibodies Starter Set (Prod. No. AG-44B-0012)
- PANoptosome Mouse Antibodies Starter Set (Prod. No. AG-44B-0013)
- anti-Caspase-8 (mouse), mAb (3B10) (Prod. No. AG-20T-0138)
LIT: ADAR1 restricts ZBP1-mediated immune response and PANoptosis to promote tumorigenesis: R. Karki, et al.; Cell Reports 19, 37 (2021) | ADAR1 mutation causes ZBP1-dependent immunopathology: N.W. Hubbard, et al.; Nature 607, 769 (2022) | ADAR1 averts fatal type I interferon induction by ZBP1: H. Jiao, et al.; Nature 607, 776 (2022) | ADAR1 prevents autoinflammation by suppressing spontaneous ZBP1 activation: R. De Reuver, et al.; Nature 607, 784 (2022)
June 1, 2022
Interleukin-37 declines with Aging in Healthy Humans
IL-37 is a unique member of the IL-1 family of cytokines, which functions as a natural suppressor of inflammatory and immune responses. The IL-37 levels increase to modulate inflammation in several pathophysiological states, including obesity, insulin resistance, and the metabolic syndrome, as well as in aging. Increased baseline inflammation is a feature of aging organisms and tissues and the role of IL-37 in the context of human physiological aging has not been studied.
In a recent study, the lab of Prof. Douglas R. Seals (University of Colorado Boulder, USA) reports in the journal GeroScience an investigation on the role of IL-37 in the context of human physiological aging and compared the levels of IL-37 in young, middle-aged and older adults using the IL-37 (human) ELISA Kit from Adipogen Life Sciences. The IL-37 (human) ELISA Kit has first been validated and its accuracy, reproducibility and specificity confirmed in an independent setting. In this study they observe that circulating concentrations of IL-37 are lower in older compared with younger adults, despite chronic low-grade elevations in pro-inflammatory cytokines in older adults. This suggests that older adults do not mount an appropriate plasma IL-37 response to combat age-related increases in circulating pro-inflammatory markers.
This study provides evidence that IL-37 concentrations decline in older age and are related to selective markers of healthspan in healthy humans and suggests a possible role of IL-37 in biological aging in humans.
AdipoGen Life Sciences provides unique reagents to study human IL-37 in vitro and in vivo:
- IL-37 (human) ELISA Kit (Prod. No. AG-45A-0041YEK)
- IL-37 (human) (rec.) (His) (Prod. No. AG-40A-0174Y)
- IL-37 (aa46-218) (human) (rec.) (His) (Prod. No. AG-40A-0190)
- anti-IL-37 (human), pAb (Prod. No. AG-25A-0111)
LIT: Circulating interleukin‑37 declines with aging in healthy humans: relations to healthspan indicators and IL37 gene SNPs: V.E. Brunt, et al.; GeroScience (2022)
December 22, 2021
Isthmin-1 (Ism1) is a New Insulin-like Adipokine
Understanding energy balance regulation in metabolic disorders needs a better knowledge of the molecular basis for glucose and lipid regulation in normal physiology and pathophysiology.
In a recent study, the lab of Prof. Katrin J. Svensson (Stanford University, USA) reports in the journal Cell Metabolism the protein Isthmin-1 (Ism1), an adipokine secreted by mature adipocytes, triggers a signaling cascade similar to that of insulin, sharing the glucoregulatory function, but unlike insulin, Ism1 counteracts lipid accumulation in the liver by switching hepatocytes from a lipogenic to a protein synthesis state. Ism1 increases adipocyte glucose uptake by a GLUT4-dependent mechanism. Ism1 signaling is dependent on PI3K and shares downstream phosphorylation targets with insulin signaling. Isthmin-1 does not act through the insulin receptor or insulin-like growth factor receptors, but most likely via a not identified yet, receptor tyrosine kinase. This new study suggests that isthmin-1 is a promising candidate for the treatment of diabetes and fatty liver diseases.
AdipoGen Life Sciences provides unique proteins to study mouse and human Isthmin-1 in vitro and in vivo:
- Isthmin-1 (human) (rec.) (His) (Prod. No. AG-40B-0214)
- Isthmin-1 (mouse) (rec.) (His) (Prod. No. AG-40B-0215)
LIT: Isthmin-1 is an adipokine that promotes glucose uptake and improves glucose tolerance and hepatic steatosis: Z. Jiang, et al.; Cell Metab. 33, 1836 (2021)
December 06, 2021
Interleukin-33 is involved in the Resolution of Inflammation
Interleukin-33 (IL-33), an IL-1 family member and the ligand for the suppression of tumorigenicity 2 (ST2) receptor, acts as an alarmin cytokine that triggers inflammation response in multiple organs. The cells called Alternatively Activated Macrophages (AAMs) dominate during later stages of infectious and sterile inflammation and facilitate the clearance of dying cells, foster the resolution of inflammation and initiate tissue repair. The molecular mechanisms involved in the differentiation of macrophages with an AAM-related signature remain incompletely understood.
A recent study from the lab of Prof. Gerhard Krönke (Universitatsklinikum Erlangen, Germany) reports in the journal Immunity that IL-33 induces differentiation of AAM macrophages by metabolic reprogramming that resulted in increased production of the mitochondria-derived metabolite itaconate. Itaconate activates the transcription factor GATA3, which orchestrates differentiation of macrophages (AAMs) and promoted the resolution of inflammation and initiation of repair in response to tissue injury. These data show that IL-33, although initially serving as a pro-inflammatory ‘‘alarmin,’’ also supports a central role during the resolution of injury-induced inflammation and the consecutive process of tissue repair by controlling macrophage plasticity.
AdipoGen Life Sciences provides many unique reagents to study mouse and human IL-33 in vitro and in vivo:
- IL-33 (human) (rec.) (untagged) (Prod. No. AG-40B-0038)
- IL-33 (oxidation resistant) (human) (rec.) (untagged) (Prod. No. AG-40B-0160) UNIQUE
- IL-33 (mouse) (rec.) (untagged) (Prod. No. AG-40B-0041)
- IL-33 (human), mAb (IL33305B) (Prod. No. AG-20A-0041)
- IL-33 (mouse), mAb (rec.) (blocking) (Bondy-1-1) (Prod. No. AG-27B-0013) UNIQUE
- HpARI (Alarmin Release Inhibitor) (rec.) (His) (Prod. No. AG-40B-0178) UNIQUE
- HpARI (CCP1/2) (rec.) (His) (Prod. No. AG-40B-0201) UNIQUE
- ST2 (human):Fc (human) (rec.) (Prod. No. AG-40A-0059)
- anti-ST2 (human), pAb (Prod. No. AG-25A-0058)
- anti-ST2 (human), mAb (ST33868) (Prod. No. AG-20A-0044)
LIT: IL-33-induced metabolic reprogramming controls the differentiation of alternatively activated macrophages and the resolution of inflammation: M. Faas, et al.; Immunity 54, 2531 (2021)
August 30, 2021
APRIL Limits Atherosclerosis by Binding to Heparan Sulfate Proteoglycans
A proliferation-inducing ligand (APRIL) is a TNF superfamily member cytokine produced by myeloid cells and stromal cells. APRIL is involved in antibody class switching and plasma cell survival through its binding to two receptors, TACI (transmembrane activator and CAML interactor) and BCMA (B cell maturation antigen), respectively. Patients with coronary artery disease have increased APRIL levels in plasma, but its role in atherosclerosis remains unclear.
A recent study from the lab of Prof. Christoph J. Binder (Medical University of Vienna, Austria) reports in the journal Nature that APRIL confers atheroprotection by binding to heparan sulfate chains of heparan-sulfate proteoglycan 2 (HSPG2), which limits the retention of low-density lipoproteins, accumulation of macrophages and formation of necrotic cores. In this study, they use AdipoGen’s specific anti-APRIL (mouse) antibody (Apry-1-1) that promotes the binding of APRIL to HSPGs to reduce experimental atherosclerosis. They also observe that serum levels of a specific form of human APRIL that binds to HSPGs (termed non-canonical APRIL), are associated with long-term cardiovascular mortality in patients with atherosclerosis.
In this study they used many APRIL-related reagents for in vitro and in vivo studies, available from AdipoGen Life Sciences:
- anti-APRIL (mouse), mAb (rec.) (blocking) (Apry-1-1) (preservative free) (Prod. No. AG-27B-0001PF)
- anti-April (mouse), mAb (blocking) (Centotto-1) (preservative free) (Prod. No. AG-20B-0083PF)
- anti-APRIL (human), mAb (blocking) (Mahya-1) (preservative free) (Prod. No. AG-20B-0078PF)
- APRIL (human) (multimeric) (rec.) (Prod. No. AG-40B-0017)
- APRIL (mouse) (multimeric) (rec.) (Prod. No. AG-40B-0089)
- BAFF, Soluble (human) (60-mer) (rec.) (highly active) (Prod. No. AG-40B-0112)
- BCMA (mouse):Fc (human) (rec.) (Prod. No. AG-40B-0076)
- APRIL (human) ELISA Kit (Prod. No. AG-45B-0012)
LIT: APRIL limits atherosclerosis by binding to heparan sulfate proteoglycans: D. Tsiantoulas, et al.; Nature 597, 92 (2021)
July 12, 2021
Viral Inhibition of Translation Drives Caspase-3/GSDME-dependent Pyroptosis
The initiation of innate immunity in metazoans is predominantly attributed to the activation of pattern recognition receptors (PRRs). But these receptors may not differentiate between pathogenic and non-pathogenic microbial encounters. For this reason, cells use additional intracellular sensors called guard proteins to sense pathogenic host-microbe interactions. Guard proteins do not interact directly with microbial factors but are activated by disruption of key host pathways during infection leading to cell death. The role of guard proteins during infectious contexts is still not well characterized.
A recent study from the lab of Prof. Jonathan C. Kagan (Harvard Medical School, US) reports in the journal Immunity that inhibition of protein synthesis during viral infection (VSV and HSV-1) is sensed by the host cell as defense mechanism and initiates pyroptosis in human keratinocytes. They show in this study that the BCL-2 family members MCL-1 and BCL-xL are guard proteins whose activities monitor translational activity. During viral infection, inhibition of translation reduces the levels of MCL-1 and BCL-xL leading to mitochondrial damage, caspase-3-dependent cleavage of Gasdermin E (but not Gasdermin D), release of interleukin-1α and finally pyroptotic cell death. This new study highlights the role of the Gasdermin E in virus infected cells and adds a new role of BCL-2 family members as guard proteins and mediators of pyroptosis.
AdipoGen Life Sciences provides standard reagents in the innate immune response field:
- Gasdermin E (human) ELISA Kit (Prod. No. AG-45B-0024) (detects the soluble C-terminal part of human Gasdermin E)
- anti-Caspase-1 (p20) (mouse), mAb (Casper-1) (Prod. No. AG-20B-0042)
- anti-Caspase-1 (p20) (human), mAB (Bally-1) (Prod. No. AG-20B-0048)
- anti-NLRP3/NALP3, mAb (Cryo-2) (Prod. No. AG-20B-0014)
- anti-Asc, pAb (AL177) (Prod. No. AG-25B-0006)
- anti-Gasdermin D (mouse), pAb (IN110) (Prod. No. AG-25B-0036)
- anti-Caspase-4 /11 (p20), mAb (Flamy-1) (Prod. No. AG-20B-0060)
- MCC950 . sodium salt [NLRP3 Inhibitor] (Prod. No. AG-CR1-3615)
- Monosodium urate (ready-to-use) [NLRP3 Activator] (Prod. No. AG-CR1-3951)
LIT: Virus-mediated inactivation of anti-apoptotic Bcl-2 family members promotes Gasdermin-E-dependent pyroptosis in barrier epithelial cells: M.H. Orzalli, et al.; Immunity 54, 1 (2021)
March 25, 2021
Extracellular Nampt (eNampt) secreted from macrophages promotes muscle regeneration
Nicotinamide phosphoribosyltransferase (Nampt) is a regulator of the intracellular nicotinamide adenine dinucleotide (NAD) and thus regulates the activity of NAD-dependent enzymes. Its secreted form (eNampt) is pro-mitogenic for a number of tissues and can alter the expression of myogenic regulatory factors in myoblasts motility.
A recent study from the lab of Prof. Peter Curie (Monash University, Australia) reports in the journal Nature that in zebrafish, macrophage cells, known to modulate the innate immune response, also induces proliferation of muscle stem cells and muscle repair upon injury. They show that a specific subset of macrophages transiently moves within the muscle injury, establishing a niche for muscle stem cell proliferation by secreting eNampt. eNampt is required for muscle regeneration, acting through the C-C motif chemokine receptor type 5 (CCR5). After muscle stem cell proliferation, macrophages and daughter myoblasts migrated away from each other. In the same study, a similar mechanism is observed in mammalian cells. The addition of human recombinant Nampt (hrNampt) protein to C2C12 mouse cells also results in significant dose-dependent increases in myoblast proliferation; hrNampt binds to both human CCR5 and mouse CCR5. This study reveals a new surprising role of the innate immune system in muscle regeneration.
AdipoGen Life Sciences is an expert company in Inflammation and Immune Response, providing many active and validated reagents to study mouse and human eNAMPTin vitro and in vivo:
- anti-Nampt (Visfatin/PBEF), mAb (OMNI379) (Prod. No. AG-20A-0034)
- Nampt (Visfatin/PBEF) (human) (rec.) (Prod. No. AG-40A-0031Y)
- Nampt (Visfatin/PBEF) (mouse) (rec.) (Prod. No. AG-40A-0056Y)
- Nampt (Visfatin/PBEF) (rat) (rec.) (Prod. No. AG-40A-0058)
- Nampt (mouse) (rec.) (enzymatically active) (Prod. No. AG-40B-0179)
- Nampt (Visfatin/PBEF) (human) ELISA Kit (Prod. No. AG-45A-0006YEK) THE STANDARD
- Nampt (Visfatin/PBEF) (mouse/rat) Dual ELISA Kit (Prod. No. AG-45A-0007YEK) THE STANDARD
- STF-31 (Nampt Inhibitor) (Prod. No. AG-CR1-3693)
- CHS-828 (Nampt Inhibitor) (Prod. No. AG-CR1-0064)
- FK-866 (Nampt Inhibitor) (Prod. No. AG-CR1-0011)
LIT: Macrophages provide a transient muscle stem cell niche via NAMPT secretion: D. Ratnayake, et al.; Nature 591, 281 (2021)
February 23, 2021
Interleukin-33 induces Intestinal Serotonin (5-HT) to promote Gut Motility
Interleukin-33 (IL-33), an IL-1 family member and the ligand for the suppression of tumorigenicity 2 (ST2) receptor, acts as an alarmin cytokine in multiple organs including the gut, where it is important for intestinal development and inflammation. IL-33 induces instantaneous peristaltic movement, facilitating parasite clearance in a manner independent of type 2 immunity by a still unknown mechanism.
A recent study from the lab of Dr. Chuan Wu (NIH, Bethesda) reports in the journal Immunity that IL-33 stimulates serotonin (5-hydroxytryptamine, 5-HT) release by mouse enterochromaffin (EC) cells to promote gut motility. Mechanistically, IL-33-ST2 signaling selectively activates TRPA1 channels in EC cell via PLC-γ1 to promote Ca2+ influx and 5-HT release. 5-HT stimulates intrinsic enteric neurons that regulate intestinal peristalsis. Similar effects of IL-33 on HT release are also observed in human EC cells. IL-33 regulates, via 5-HT, intestinal homeostasis and host defense. This study will help to elucidate the role of IL-33 and 5-HT in neurological and immunological intestinal disorders that exhibit dysregulation of the serotonergic system.
AdipoGen Life Sciences provides many unique reagents to study mouse and human IL-33 in vitro and in vivo:
- IL-33 (human) (rec.) (untagged) (Prod. No. AG-40B-0038)
- IL-33 (oxidation resistant) (human) (rec.) (untagged) (Prod. No. AG-40B-0160) UNIQUE
- IL-33 (mouse) (rec.) (untagged) (Prod. No. AG-40B-0041)
- IL-33 (human), mAb (IL33305B) (Prod. No. AG-20A-0041)
- IL-33 (mouse), mAb (rec.) (blocking) (Bondy-1-1) (Prod. No. AG-27B-0013) UNIQUE
- HpARI (Alarmin Release Inhibitor) (rec.) (His) (Prod. No. AG-40B-0178) UNIQUE
- HpARI (CCP1/2) (rec.) (His) (Prod. No. AG-40B-0201) UNIQUE
- ST2 (human):Fc (human) (rec.) (Prod. No. AG-40A-0059)
- anti-ST2 (human), pAb (Prod. No. AG-25A-0058)
- anti-ST2 (human), mAb (ST33868) (Prod. No. AG-20A-0044)
LIT: Interleukin-33 Promotes Serotonin Release from Enterochromaffin Cells for Intestinal Homeostasis: Z.Chen, et al.; Immunity 54, 151 (2021)
January 22, 2021
NINJ1 as a new Player in the Cell Death-related Plasma Membrane Rupture (PMR)
Upon inflammasomes activation, cleavage of the pore forming protein Gasdermin D promotes a potent inflammatory mode of lytic cell death, called pyroptosis leading to IL-1α and IL-1β secretion followed by uncharacterized plasma membrane rupture (PMR).
A recent study from the lab of Dr. Vishva M. Dixit (Genentech Inc., South San Francisco) describes in the journal Nature a new protein, called nerve injury-induced protein 1 (NINJ1), playing an essential role in the induction of PMR. NINJ1 is expressed widely, including in myeloid cells and the central nervous system. It is crucial for PMR, but dispensable for Gasdermin D pore formation and IL-1β release. NINJ1 is also involved in necrosis and apoptotic PMR. NINJ1 reportedly functions as a cell-cell adhesion molecule and the new function in PMR works through different domains. PMR needs oligomerization of NINJ1 induced by a yet still unclear mechanism. NINJ1 mediates PMR and Danger Associated Molecular Pattern (DAMP), key events in the propagation of inflammation.
AdipoGen Life Sciences provides the apoptosis inducer (MegaFasL; MultimericFasL) used in this study:
- FasL (human) (multimeric) (rec.) (Prod. No. AG-40B-0130)
Other reagents in the inflammasome field are also available from AdipoGen Life Sciences:
- anti-Caspase-1 (p20) (mouse), mAb (Casper-1) (Prod. No. AG-20B-0042)
- anti-Caspase-1 (p20) (human), mAB (Bally-1) (Prod. No. AG-20B-0048)
- anti-NLRP3/NALP3, mAb (Cryo-2) (Prod. No. AG-20B-0014)
- anti-Asc, pAb (AL177) (Prod. No. AG-25B-0006)
- anti-Gasdermin D (mouse), pAb (IN110) (Prod. No. AG-25B-0036)
- anti-Caspase-4 /11 (p20), mAb (Flamy-1) (Prod. No. AG-20B-0060)
- MCC950 . sodium salt [NLRP3 Inhibitor] (Prod. No. AG-CR1-3615)
- Monosodium urate (ready-to-use) [NLRP3 Activator] (Prod. No. AG-CR1-3951)
LIT: NINJ1 mediates plasma membrane rupture during lytic cell death: N. Kayagaki, et al.; Nature (Epub ahead of print) (2021)
November 16, 2020
BAFF trimer, not BAFF 60-mer, is the only form of BAFF existing in adult serum and CSF
The B cell-stimulating molecules, BAFF (B cell activating factor also known as BLyS or TALL1) and APRIL (a proliferation-inducing ligand), are critical factors in the maintenance of the B cell pool and humoral immunity. Soluble BAFF exists either as trimer (BAFF 3-mer), or as an ordered assembly of 20 trimers (BAFF 60-mer). BAFF 3-mer and BAFF 60-mer both signal through the receptor BAFF-R, but TACI (and BCMA) only responds to BAFF 60-mer and not to BAFF 3-mer. Which forms of BAFF are present in human is unclear.
A recent study published in Frontiers in Cell and Developmental Biology by the lab of Prof. Pascal Schneider (Department of Biochemistry, University of Lausanne, Switzerland) shows, with the help of sensitive tools developed for the characterization of BAFF 60-mer in biologic fluids, the exclusive presence of BAFF 3-mer in adult human serum and cerebrospinal fluid (CSF) samples. A high molecular weight form of BAFF with some but not all properties of BAFF 60-mer is detected only in cord blood. In addition, a BAFF 60-mer inhibitory activity able to dissociate recombinant 60-mer into 3-mer is present in adult human sera.
Many reagents to study BAFF in vitro and in vivo used in this study are provided by AdipoGen Life Sciences:
- BAFF, Soluble (human) (60-mer) (rec.) (highly active) (Prod. No. AG-40B-0112)
- Fc (human):BAFF (human) (rec.) (Prod. No. AG-40B-0120)
- BCMA (human):Fc (human) (rec.) (Prod. No. AG-40B-0080)
- anti-BAFF (human), mAb (2.81) (Prod. No. AG-20B-0018)
- BAFF, Soluble (human) ELISA Kit (hypersensitive) (Prod. No. AG-45B-0001)
Other reagents in this field can be found on: https://adipogen.com/autoimmune-diseases-biomarker
LIT: BAFF 60-mer, and differential BAFF 60-mer dissociating activities in human serum, cord blood and cerebrospinal fluid: M. Eslami, et al.; Front. Cell Dev. Biol. 8, 577662 (2020)
September 28, 2020
Gasdermin D Succination by Fumarate inactivates and blocks Pyroptosis
Inflammasomes are large multimolecular complexes involved in innate immunity that upon activation lead to cleavage of the pore forming protein Gasdermin D to promote inflammatory cell death, called pyroptosis.
Recently, the lab of Prof. Katherine A. Fitzgerald (University of Massachusetts Medical School, US) describes in the journal Science that a metabolite of aerobic glycolysis (Krebs’ cycle), fumarate, affects inflammatory responses by inhibiting cleavage of Gasdermin D and consequently pyroptotic cell death. Endogenous fumarate or dimethyl fumarate (DMF) delivered to cells, succinates a critical cysteine of Gasdermin D (GSDMD) to prevent its interaction with caspases, its oligomerization to form membrane pore and its capacity to induce cell death. Interestingly Gasdermin E, a Gasdermin D analog, is also inhibited by fumarate. This study explains the efficacy and the mechanism of action of dimethyl fumarate (called Tecfidera and approved by U.S. Food and Drug Administration) for the treatment of multiple sclerosis (MS).
AdipoGen Life Sciences provides the standard Caspase-1 antibodies used in this study:
- anti-Caspase-1 (p20) (mouse), mAb (Casper-1) (Prod. No. AG-20B-0042)
- anti-Caspase-1 (p20) (human), mAB (Bally-1) (Prod. No. AG-20B-0048)
Other reagents in the inflammasome field are also available from AdipoGen Life Sciences:
- Dimethyl fumarate (Prod. No. AG-CR1-3701)
- Succinate [Succinic acid] (Prod. No. AG-CN2-0521)
- anti-NLRP3/NALP3, mAb (Cryo-2) (Prod. No. AG-20B-0014)
- anti-Asc, pAb (AL177) (Prod. No. AG-25B-0006)
- anti-Gasdermin D (mouse), pAb (IN110) (Prod. No. AG-25B-0036)
- anti-Caspase-4 /11 (p20), mAb (Flamy-1) (Prod. No. AG-20B-0060)
- MCC950 . sodium salt [NLRP3 Inhibitor] (Prod. No. AG-CR1-3615)
- Monosodium urate (ready-to-use) [NLRP3 Activator] (Prod. No. AG-CR1-3951)
LIT: Succination inactivates gasdermin D and blocks pyroptosis: F. Humphries, et al.; Science 369, 1633 (2020)
September 22, 2020
Concanamycin A Enables Immune System to Kill HIV Infected Cells
Recently, the lab of Prof. Kathleen L. Collins (University of Michigan) has discovered an unexpected potential weapon against HIV protein. They describe in a new study a class of drugs that can help the immune system eliminate hard-to-kill cells infected with HIV. HIV can hide inside the human genome, lying dormant and ready to emerge at any time. HIV therefore establishes a persistent infection for which there is no cure, necessitating the development of new approaches to enhance the clearance of HIV-infected cells. HIV encodes Nef, which down-regulates MHC-I expression in infected cells to impair immune-mediated clearance by cytotoxic T lymphocytes. The plecomacrolide family of natural products has been identified as potent inhibitors of Nef, and concanamycin A (a lysosome inactivator) restored MHC-I and enhanced the clearance of HIV-infected primary cells by cytotoxic T lymphocytes. Concanamycin A counteracted Nef from diverse clades of HIV targeting multiple allotypes of MHC-I, indicating the potential for broad therapeutic utility.
AdipoGen Life Sciences is a manufacturer of high purity plecomacrolide antibiotics. All products are available in BULK quantities.
Concanamycin A (Prod. No. BVT-0237)
Concanamycin B (Prod. No. BVT-0253)
Concanamycin C (Prod. No. BVT-0254)
Bafilomycin A1 (Prod. No. BVT-0252)
Bafilomycin B1 (Prod. No. BVT-0004)
Bafilomycin C1 (Prod. No. BVT-0068)
LIT: Concanamycin A counteracts HIV-1 Nef to enhance immune clearance of infected primary cells by cytotoxic T lymphocytes: M.M. Painter, et al.; PNAS (2020)
September 08, 2020
Hyperforin counteracts Cytokine Storm in COVID-19
Pandemic coronavirus disease 2019 (COVID‐19), caused by SARS‐CoV‐2 virus, mainly affects adult or aging individuals with fever, dry cough and dyspnea of variable severity. In ~20% of patients, a widespread alveolar‐interstitial pneumonia develops with acute respiratory distress syndrome. With progression of the disease, when immune response or antiviral therapy fail to get rid of the virus, an excess release of pro‐inflammatory cytokines takes place (e.g., TNF‐α, IL‐1β, IL‐6, IFN‐γ, CXCL10, MCP‐1), the so called “cytokine storm,” eliciting extensive vasculitis, hyper‐coagulability and multi‐organ damage that, together with associated respiratory failure, represent the most common cause of death. Recently, the lab of Prof. Marta Menagazzi (University Verona) suggested that the Hypericum perforatum (St. John's Wort, SJW) extract and its main polyphenol component Hyperforin can, based on their anti-inflammatory activity of and their simultaneous blockade of multiple signaling pathways, such as IFN‐γ/IL‐1β/TNF‐α, JAK/STAT, NF‐κB and MAPK counteract cytokine storm during COVID-19.
AdipoGen Life Sciences is a manufacturer of high purity Hyperforin (Prod. No. AG-CN2-0008). For an overview on other COVID-19 research reagents please visit https://adipogen.com/covid-19/.
LIT: Can Hypericum perforatum (SJW) prevent cytokine storm in COVID‐19 patients? P. Masiello, et al.; Phytother Res. 34, 1471 (2020)
April 14, 2020
NEW Panel of COVID-19 Research Products
AdipopGen Life Sciences launched its first panel of unique COVID-19 Research Products produced in our own facilities in Switzerland. Our landing page provides scientific insights and an overview on the product range related to SARS-CoV-2/COVID-19 research, featuring a unique ACE2 blocking antibody.
For more information visit https://adipogen.com/covid-19/
March 06, 2020
Glutamine Links Obesity to Inflammation
Obesity is defined as a chronic low-grade inflammation of the white adipose tissue and this inflammation is responsible for different obesity-linked pathologies and the onset of insulin resistance. The causative factors of white adipose tissue (WAT) inflammation during obesity remain unclear. A recent study published in Cell Metabolism by the lab of Prof. Mikael Ryden (Karolinska Institute, Sweden) now reports that the levels of glutamine in human white adipose tissue (WAT) are linked with obesity-associated inflammation. They observed that glutamine released from WAT is decreased during obesity and linked to larger fat cell size. This reduction of glutamine is due to reduction of glutamine synthetase (GLUL) and low GLUL expression is associated with pro-inflammatory pathways in human WAT. Interestingly, addition of glutamine in obese mice attenuates adipose tissue inflammation. Reduced glutamine levels during obesity shift the balance from glutaminolysis toward glycolysis, leading to nuclear O-GlcNAcylation, which activates inflammation. Glutamine is therefore a new player in inflammation in addition to its roles in cell proliferation and cancer.
AdipoGen Life Sciences provides multiple reagents in the immunometabolism and obesity field for in vitro and in vivo studies:
- L-Glutamine [H-Gln-OH] (Prod. No. AG-CR1-3534)
- Glutamine Synthetase (human) ELISA Kit (Prod. No. YIF-LF-EK0185)
- anti-Glutamine Synthetase, mAb (8G9) (Prod. No. YIF-LF-MA0095)
- anti-Glutamine Synthetase, mAb (27D10) (Prod. No.YIF-LF-MA0096)
LIT: Glutamine Links Obesity to Inflammation in Human White Adipose Tissue: P. Petrus, et al.; Cell Metab. 31, 375 (2020)
January 20, 2020
VISTA is a checkpoint regulator for naïve T cell quiescence and peripheral tolerance
VISTA (V-domain immunoglobulin suppressor of T cell activation) is a new negative checkpoint regulator homologous to PD-L1. VISTA potently suppresses T cell activation by binding to the receptor P-selectin glycoprotein ligand-1 (PSGL-1) at acidic pH. VISTA is the only negative checkpoint regulator expressed on naïve T cells where its precise function is not clear. A recent study published in Science by the labs of Prof. Randolph J. Noelle and Dr. Chao Cheng (School of Medicine at Dartmouth, Lebanon and Baylor College of Medicine, Houston, respectively) shows that VISTA expressed on naïve T cells acts as a brake for preventing a “homeostatic” conversion of naïve to effector T cells in response to self-antigen recognition. Blockade of the VISTA protein disrupts the major quiescent naïve T cell subset leading to increased frequencies of effector T cells and development of autoimmunity, while VISTA activation suppresses T cell immune responses by enhancing cell death of tolerogenic T cells. VISTA is the first immune checkpoint protein whose function is to enforce quiescence in naïve T lymphocytes in the absence of inflammation.
AdipoGen Life Sciences provides active proteins to study VISTA and PSGL-1 in vitro and in vivo:
- PSGL-1 (human):Fc (human) (rec.) (Prod. No. AG-40B-0190)
- VISTA (human):COMP (mouse) (rec.) (His) (Prod. No. AG-40B-0183)
- VISTA (mouse):COMP (mouse) (rec.) (His) (Prod. No. AG-40B-0181)
- VISTA [B7-H5] (human):Fc (human) (rec.) (Prod. No. AG-40B-0163)
- VISTA [B7-H5] (mouse):Fc (human) (rec.) (Prod. No. AG-40B-0164)
- VISTA [B7-H5] (human) (rec.) (His) (Prod. No. AG-40B-0177)
LIT: VISTA is a checkpoint regulator for naïve T cell quiescence and peripheral tolerance: M.A. ElTanbouly, et al.; Science 367, 264 (eaay0524) (2020)
November 07, 2019
VISTA is an acidic pH-selective Ligand for PSGL-1
VISTA (V-domain immunoglobulin suppressor of T cell Activation) is type I Ig membrane protein homologous to PD-L1. VISTA is mainly expressed on hematopoietic tissues (spleen, thymus and bone marrow) and on myeloid cells. VISTA is a new negative checkpoint regulator that potently suppresses T cell activation. A recent study published in Nature by the lab of Dr. Alan J. Korman (Bristol-Myers Squibb) shows a new function of the protein P-selectin glycoprotein ligand-1 (PSGL-1) as a new receptor for the immune checkpoint VISTA. Multimer VISTA binds PSGL-1 expressed on leukocytes at acidic pH, but not at the physiological pH 7. VISTA - PSGL-1 interaction shows that immune response can be regulated by acidic environments found in tumors.
AdipoGen Life Sciences provides active proteins to study VISTA and PSGL-1 in vitro and in vivo:
- PSGL-1 (human):Fc (human) (rec.) (Prod. No. AG-40B-0190)
- VISTA (human):COMP (mouse) (rec.) (His) (Prod. No. AG-40B-0183)
- VISTA (mouse):COMP (mouse) (rec.) (His) (Prod. No. AG-40B-0181)
- VISTA [B7-H5] (human):Fc (human) (rec.) (Prod. No. AG-40B-0163)
- VISTA [B7-H5] (mouse):Fc (human) (rec.) (Prod. No. AG-40B-0164)
- VISTA [B7-H5] (human) (rec.) (His) (Prod. No. AG-40B-0177)
LIT: VISTA is an acidic pH-selective ligand for PSGL-1: R.J. Johnston, et al.;Nature 574, 565 (2019)
October 29, 2019
Protective Role of Irisin in chronic Inflammatory Bowel Diseases (IBD)
Irisin is a protein cleaved from fibronectin type III domain-containing protein 5 (FNDC5) and has a beneficial role in adipose tissues, in brain and in bone remodelling. Chronic inflammation of the gut, such as inflammatory bowel disease (IBD), leads to osteoporosis and increased fractures. A recent study published in Scientific Reports by the lab of Prof. Susan Bloomfield (Texas A&M University) showed that injection of recombinant Irisin in a rat model of IBD mitigates inflammatory bone changes. Exogenous treatment with the recombinant Irisin protein from Adipogen Life Sciences (AG-40B-0103) improves bone formation rate and decreases the inflammatory status of bone. Irisin represents therefore a potential anti-inflammatory treatment against chronic diseases, such as IBD.
AdipoGen Life Sciences provides the best-in-class recombinant Irisin/FNDC5 proteins, antibody and ELISA kit to study Irisin and FNDC5 in vitro and in vivo:
- Irisin (rec.) (CHO) (Prod. No. AG-40B-0136)
- Irisin:Fc (human) (rec) (Prod. No. AG-40B-0115) (for in vivo studies)
- Irisin (rec.) (untagged) (E.coli) (Prod. No. AG-40B-0103)
- FNDC5 (rec) (untagged) (Prod. No. AG-40B-0128)
- FNDC5:Fc (human) (rec) (Prod. No. AG-40B-0153)
- anti-Irisin, pAb (IN102) (Prod. No. AG-25B-0027)
- Irisin Competitive ELISA Kit (Prod. No. AG-45A-0046Y)
LIT: DSS-induced colitis produces inflammation-induced bone loss while irisin treatment mitigates the inflammatory state in both gut and bone: C.E. Metzger, et al.; Sci. Rep. 9, 15144 (2019)
September 19, 2019
Protective role for IL-36 cytokines in obesity and metabolic disease
Interleukin-36α, β and γ (IL-36α, β and γ), members of the interleukin-1 (IL-1) family, are pro-inflammatory cytokines mainly involved in skin inflammatory diseases, but also in the inflammation of lung or gut. Recently, the lab of Prof. Patrick T. Walsh (Trinity College Dublin, Ireland) describes in Nature Communication a new protective role of the IL-36 family of cytokines in obesity and metabolic diseases. They observed that IL-36γ is increased in serum of obese patients with diabetes, indicating that elevated IL-36 cytokines may play a protective role in reducing blood sugar levels. IL-36 cytokines function by changing the composition of the intestinal microbiome towards a more metabolically healthy state. IL-36 cytokines enhance mucus-secretion from goblet cells in the colon, which promote the outgrowth of the commensal bacterial strain Akkermansia muciniphila, known to play an important protective role against obesity and metabolic dysfunction.
AdipoGen Life Sciences provides a Sensitive and Specific ELISA Kit to measure IL-36γ in serum/plasma:
- IL-36γ (human) ELISA Kit (Prod. No. AG-45B-0008)
AdipoGen Life Sciences is a Leader in the IL-36 Research field, providing a broad range of high quality ELISA Kits, Proteins and Antibodies:
- IL-36α/IL-36γ (human) Tandem ELISA Kit (Prod. No. AG-45B-4502)
- IL-36α (human) ELISA Kit (Prod. No. AG-45B-0013)
- IL-36β (human) Matched Pair Detection Set (Prod. No. AG-46B-0009)
- IL-36Ra (aa 3-156) (mouse) (rec.) (untagged) (Prod. No. AG-40B-0096)
- IL-36α (aa 8-160) (mouse) (rec.) (untagged) (Prod. No. AG-40B-0098)
- IL-36β (aa 31-183) (mouse) (rec.) (untagged) (Prod. No. AG-40B-0099)
- IL-36γ (aa 13-164) (mouse) (rec.) (untagged) (Prod. No. AG-40B-0100)
... and many other IL-36-related Antibodies and Proteins!
LIT: Interleukin-36 cytokines alter the intestinal microbiome and can protect against obesity and metabolic dysfunction: F. Giannoudaki, et al.; Nat. Commun. 10, 4003 (2019)
September 12, 2019
Stress granules inhibit NLRP3 inflammasome activation by sequestering the helicase DDX3X
Inflammasomes are large multimolecular complexes involved in innate immune response and driving cell fate towards cell death, called pyroptosis. Stress granules are aggregates formed during cellular stress with pro-survival role composed of proteins and mRNA molecules. Recently, the lab of Prof. Thirumala-Devi Kanneganti (St. Jude Children's Research Hospital, Memphis) describes a new role of the stress granules in inhibiting the inflammasome. The stress granule protein DDX3X interacts with NLRP3 to activate the inflammasome. Assembly of stress granules leads to the sequestration of DDX3X, and thereby the inhibition of NLRP3 inflammasome activation. With this dual function, DDX3X regulates a live-or-die cell-fate decisions under stress conditions.
AdipoGen Life Sciences provides the key standard inflammasome antibodies used in this study:
- anti-Caspase-1 (p20) (mouse), mAb (Casper-1) (Prod. No. AG-20B-0042)
- anti-NLRP3/NALP3, mAb (Cryo-2) (Prod. No. AG-20B-0014)
- anti-Asc, pAb (AL177) (Prod. No. AG-25B-0006)
Other reagents in the inflammasome field are also available from AdipoGen Life Sciences:
- anti-Caspase-4 /11 (p20), mAb (Flamy-1) (Prod. No. AG-20B-0060)
- anti-NLRP6/NALP6 (human), mAb (Clint-1) (Prod. No. AG-20B-0046)
- MCC950 . sodium salt [NLRP3 Inhibitor] (Prod. No. AG-CR1-3615)
- Monosodium urate (ready-to-use) [NLRP3 Activator] (Prod. No. AG-CR1-3951)
LIT: DDX3X acts as a live-or-die checkpoint in stressed cells by regulating NLRP3 inflammasome: P. Samir, et al.; Nature (Epub ahed of print) (2019)
August 09, 2019
The Inflammasome regulates Hematopoiesis through Cleavage of the Factor GATA1
Inflammasomes are large multimolecular complexes involved in innate immune and inflammatory responses. A recent study published by the lab of Prof. Victoriano Mulero (Universidad de Murcia, Spain) describes a new function of the inflammasome as a regulator of the balance between erythroid and myeloid differentiation during hematopoiesis. Activation of the inflammasome and caspase-1 results in the cleavage of the master erythroid transcription factor GATA1, with a decrease in erythrocyte differentiation and in the increase of myeloid cell differentiation.
AdipoGen Life Sciences provides key standard inflammasome research reagents, including Antibodies and Small Molecules. Numerous scientific publications document the quality of our products.
- anti-Caspase-1 (p20) (mouse), mAb (Casper-1) (Prod. No. AG-20B-0042)
- anti-Caspase-1 (p20) (human), mAb (Bally-1) (Prod. No. AG-20B-0048)
- anti-NLRP3/NALP3, mAb (Cryo-2) (Prod. No. AG-20B-0014)
- anti-Asc, pAb (AL177) (Prod. No. AG-25B-0006)
- anti-Caspase-4 /11 (p20), mAb (Flamy-1) (Prod. No. AG-20B-0060)
- anti-NLRP6/NALP6 (human), mAb (Clint-1) (Prod. No. AG-20B-0046)
- MCC950 . sodium salt [NLRP3 Inhibitor] (Prod. No. AG-CR1-3615)
- Monosodium urate (ready-to-use) [NLRP3 Activator] (Prod. No. AG-CR1-3951)
LIT: Inflammasome regulates hematopoiesis through cleavage of the master erythroid transcription factor GATA1: S.D. Tyrkalska, et al.; Immunity 51, 50 (2019)
July 05, 2019
OLFR734 Mediates Glucose Metabolism as a Receptor of Asprosin
Asprosin is a fasting-induced hormone that increases plasma glucose levels in the liver. It also stimulates appetite in the hypothalamus by activating the cAMP signaling pathway via an unknown G protein-coupled receptor (GPCR). In a recent study, the lab of Yiguo Wang (Tsinghua University, 100084 Beijing, China) identifies the multipass G protein-coupled receptor olfactory receptor OLFR734, as the Asprosin receptor in liver. The Asprosin-OLFR734 axis plays a key role in hepatic glucose homeostasis during fasting and in obesity.
AdipoGen Life Sciences provides a recombinant protein, monoclonal antibodies and a detection set to study Asprosin.
- Asprosin (human) (rec.) (His) (Prod. No. AG-40B-0174T)
- anti-Asprosin, mAb (Birdy-1) (Prod. No. AG-20B-0073)
- anti-Asprosin (human), mAb (Birdy-2) (Prod. No. AG-20B-0074)
- Asprosin (human) Matched Pair Detection Set (Prod. No. AG-46B-0011)
LIT: OLFR734 Mediates Glucose Metabolism as a Receptor of Asprosin: E. Li, et al.; Cell Metabolism 30, 1 (2019)
June 20, 2019
Extracellular Vesicles Containing eNAMPT Extend Lifespan
A recent study published in Cell Metabolism by the lab of Shin-Ichiro Ima (Washington University School of Medicine) shows that the circulating levels of extracellular nicotinamide phosphoribosyltransferase (eNAMPT), a key NAD+ biosynthetic enzyme in mammals, decline with age in mice and humans. When overexpressed eNAMPT increases NAD+ levels in multiple tissues, enhances their function and extends lifespan of mice. The majority of eNAMPT found in serum/plasma circulates in extracellular vesicles (EVs) and it is a necessity for eNAMPT to be in EVs to act on target cells. Detection of eNAMPT in this study is performed by western blotting using Adipogen Life Sciences’ monoclonal antibody anti-Nampt (Visfatin/PBEF), mAb (OMNI379) (Prod. No. AG-20A-0034).
AdipoGen Life Sciences provides best reagents to study NAMPT in vitro and in vivo in human or mouse:
- Nampt (Visfatin/PBEF) (human) (rec.) (Prod. No. AG-40A-0031Y)
- Nampt (Visfatin/PBEF) (mouse) (rec.) (Prod. No. AG-40A-0056Y)
- Nampt (Visfatin/PBEF) (rat) (rec.) (Prod. No. AG-40A-0058)
- Nampt (Visfatin/PBEF) (human) ELISA Kit (Prod. No. AG-45A-0006Y)
- Nampt (Visfatin/PBEF) (mouse/rat) Dual ELISA Kit (Prod. No. AG-45A-0007Y)
LIT: Extracellular Vesicle-Contained eNAMPT Delays Aging and Extends Lifespan in Mice: M. Yoshida, et al.; Cell Metabol. (ePub ahead of print) (2019)
March 03, 2019
Fibrinogen-like Protein 1 (FGL1) - A Major Ligand of LAG-3
LAG-3 is a coinhibitory immune checkpoint receptor that inhibits T cell response by binding to MHC-II. In a recent study published in Cell, the lab of Prof Lieping Chen (Yale University, US) identifies Fibrinogen-like protein 1 (FGL1), a molecule secreted by the liver and pancreas, as a major ligand for LAG-3 in both human and mouse. FGL1 binding to LAG-3 inhibits T cell response. FGL1 is upregulated in human cancers and high plasma FGL1 is associated with poor clinical outcomes in patients treated with anti-PD1 therapy.
AdipoGen Life Sciences provides a panel of reagents to study this new protein FGL1:
- Fc (human):FGL1 (human) (rec.) (Prod. No. AG-40B-0184)
- Fc (human):FGL1 (mouse) (rec.) (Prod. No. AG-40B-0185)
- LAG-3 (human):Fc (human) (rec.) (Prod. No. AG-40B-0031)
- LAG-3 (mouse):Fc (mouse) (rec.) (Prod. No. AG-40B-0039)
- anti-LAG-3 (human), mAb (AG-IHC103) (Prod. No. AG-20B-6023)
- anti-LAG-3, mAb (blocking) (11E3) (Prod. No. AG-20B-0011)
- anti-LAG-3 (human), mAb (blocking) (17B4) (Prod. No. AG-20B-0012)
LIT: Fibrinogen-like Protein 1 Is a Major Immune Inhibitory Ligand of LAG-3: J. Wang, et al.; Cell 176, 334 (2019)
February 15, 2019
Protective Role of Irisin in Alzheimer’s Disease
Irisin is a protein cleaved from fibronectin type III domain-containing protein 5 (FNDC5) and has a beneficial role in adipose tissues, bone and brain. A recent study published in Nature Medicine by the labs of O. Arancio, S.Ferreira & F.G. de Felice (Rio de Janeiro, Brazil, New York, US and Kingston, Canada, respectively) showed that FNDC5/Irisin levels are reduced in Alzheimer’s Disease (AD) cerebrospinal fluid in human and mouse and that beneficial effects of exercise on synaptic plasticity and memory in AD models are mediated by FNDC5/Irisin. Addition of AdipoGen Life Sciences' recombinant Irisin (Prod. No. AG-40B-0136) in a mice model of AD was neuroprotective and rescued Amyloid-β oligomer-induced memory impairment.
AdipoGen Life Sciences provides the best recombinant Irisin/FNDC5 proteins, antibody and ELISA kit to study Irisin and FNDC5 in vitro and in vivo:
- Irisin (rec.) (CHO) (Prod. No. AG-40B-0136)
- Irisin:Fc (human) (rec) (Prod. No. AG-40B-0115) (for in vivo studies)
- Irisin (rec.) (untagged) (E.coli) (Prod. No. AG-40B-0103)
- FNDC5 (rec) (untagged) (Prod. No. AG-40B-0128)
- FNDC5:Fc (human) (rec) (Prod. No. AG-40B-0153)
- anti-Irisin, pAb (IN102) (Prod. No. AG-25B-0027)
- Irisin Competitive ELISA Kit (Prod. No. AG-45A-0046Y)
LIT: Exercise-linked FNDC5/irisin rescues synaptic plasticity and memory defects in Alzheimer’s models: M.V. Lourenko, et al.; Nat. Med. 25, 165 (2019)
January 14, 2019
Manganese (Mn2+) as a New Activator of the NLRP3 Inflammasome in the Brain
Inflammasomes are implicated in physiological and pathological inflammation including neurodegenerative disorders such Parkinson or Alzheimer diseases. Divalent manganese (Mn2+) activates chronic inflammation leading to increase of neurotoxicity. Recently, the lab of A.G. Kanthasamy (Iowa State University, US) showed that Mn2+ activates the inflammasome protein NLRP3 through mitochondrial dysfunction in microglial cells, consequently promoting neuroinflammation. Interestingly, it was observed in the same study that Mn2+ stimulates the release of the adaptor protein ASC in exosomes that can propagate inflammasome activation in neighboring cells.
Following standard inflammasome antibodies from AdipoGen Life Sciences are used in this study in western blot and immunocytochemistry applications:
- anti-Caspase-1 (p20) (mouse), mAb (Casper-1) (Prod. No. AG-20B-0042)
- anti-NLRP3/NALP3, mAb (Cryo-2) (Prod. No. AG-20B-0014)
- anti-Asc, pAb (AL177) (Prod. No. AG-25B-0006)
LIT: Manganese activates NLRP3 inflammasome signaling and propagates exosomal release of ASC in microglial cells: S. Sarkar, et al.; Science Signal. 12, 563 (2019)
December 21, 2018
Irisin - New Receptor Found
Irisin, a protein cleaved from fibronectin type III domain-containing protein 5 (FNDC5), has a beneficial role in adipose tissues, brain and bone. In a recent study, the lab of Bruce Spiegelman (Dana-Farber Cancer Institute, Boston) identified the Irisin receptor on bone and fat cells. Irisin mediates its effect via a subset of αV integrin receptors on osteocytes and adipose cells to produce sclerostin, a local modulator of bone remodeling.
AdipoGen Life Sciences provides the best panel of recombinant Irisin proteins (tagged and untagged), antibody and ELISA Kit for in vitro and in vivo studies:
- Irisin (rec.) (untagged) (E.coli) (Prod. No. AG-40B-0103)
- Irisin:Fc (human) (rec) (Prod. No. AG-40B-0115)
- Irisin (rec.) (CHO) (Prod. No. AG-40B-0136)
- Irisin, pAb (IN102) (Prod. No. AG-25B-0027)
- Irisin Competitive ELISA Kit (Prod. No. AG-45A-0046Y)
LIT: Irisin mediates effects on bone and fat via αV integrin receptors: H. Kim, et al.; Cell 175, p1756 (2018)
December 12, 2018
TNF-α - New Function as Potent Growth Factor for Primary Hepatocytes
Supply of cells for regenerative therapies is dependent on the capacity to stably expand healthy primary cells in vitro. However, most adult primary cell types are refractory to in vitro expansion.
A recent study from the lab of Roel Nusse at Standford University shows a key role of the inflammatory cytokine TNF-α in the establishment of long-term 3D mouse organoid cultures from hepatocytes that are able to successfully engraft and repopulate damaged mouse livers. By using a medium for hepatocytes expansion containing the GSK3 inhibitor CHIR99021 (Wnt activator), Growth factor (GF) and Hepatocyte Growth Factor (HGF), they observed that addition of TNF-α (100ng/ml) promotes long-term culture of primary mouse hepatocytes.
AdipoGen Life Sciences manufactures a panel of highly active TNF-α (human) and (mouse) recombinant proteins:
- TNF-α, Soluble (human) (rec.) (Prod. No. AG-40B-0006)
- TNF-α (human) (multimeric) (rec.) (Prod. No. AG-40B-0019)
- TNF-α (mouse) (multimeric) (rec.) (Prod. No. AG-40B-0021)
LIT: Inflammatory cytokine TNFα promotes the long-term expansion of primary hepatocytes in 3D culture: W.C. Peng, et al.; Cell 175, 1607 (2018)
November 16, 2018
LAG-3 - A Selective Immune Checkpoint
LAG-3 is an immune checkpoint receptor that inhibits T cell response and cytokines secretion. Similar to CD4, LAG-3 binds to major histocompatibility complex-II (MHC-II) on antigen presenting cells (APCs). A new study from the lab of Taku Okazaki (Tokushima University, Japan) reveals how LAG-3 inhibits the activation of T cell response: it does not recognize MHC class II universally as previously thought, but instead recognizes selectively MHC class II proteins presenting only stably bound peptides. In addition, the same study shows that LAG does not compete CD4 for MHC-II interaction, but it blocks T cells by transducing inhibitory signals via its intracellular region. This recent study gives a new view on LAG-3 that might function more selectively than previously thought and probably acts to maintain immune tolerance to dominant autoantigens.
AdipoGen Life Sciences provides the best standard reagents to study LAG-3 in vitro and in vivo:
- LAG-3 (human):Fc (human) (rec.) (Prod. No. AG-40B-0031)
- LAG-3 (mouse):Fc (mouse) (rec.) (Prod. No. AG-40B-0039)
- anti-LAG-3 (human), mAb (blocking) (11E3) (Prod. No. AG-20B-0011)
- anti-LAG-3 (human), mAb (blocking) (17B4) (Prod. No. AG-20B-0012)
LIT: LAG-3 inhibits the activation of CD4+ T cells that recognize stable pMHCII through its conformation-dependent recognition of pMHCII: T. Maruhashi, et al.; Nat. Immunol. 19, 1415 (2018)
October 25, 2018
Arzanol - A NEW Brain Glycogen Phosphorylase (bGP) Agonist
Arzanol is a prenylated heterodimeric phloroglucinyl α-pyrone, isolated from Helichrysum italicum L., a plant of perfumery relevance and used in herbal medicine. This anti-inflammatory compound has a broad polypharmacological profile, shows antioxidant activity in vitro and in vivo, inhibits NF-κB activation as well as HIV-1 replication in T cells, and inhibits critical enzymes of the inflammatory cascade (PGES-1, 5-LOX and COX-1), consequently modulating the release of pro-inflammatory mediators (interleukins, TNFα, and PGE2).
In a recent study, F. del Gaudio, et al. showed by using MS-based chemical proteomics, that arzanol is a high affinity agonist of brain glycogen phosphorylase (bGP). Arzanol directly interacts with bGP, competing for the same allosteric binding site on bGP like AMP (but with higher affinity), inducing similar conformational changes and promoting the transition to the active form, consequently leading to increased bGP enzyme activity. GPs are key enzymes in glycogen metabolism, promoting the rate-limiting step of its mobilization. In brain, glycogen acts as an emergency glucose storage to protect neurons against hypoglycemia and hypoxic stress, being critical for high cognitive processes such as learning and memory consolidation. Since reduced glycogen breakdown is associated with impaired cognitive functions and neuro-degeneration, the activation of glycogen breakdown might be a new therapeutic strategy.
AdipoGen Life Sciences produces high purity Arzanol (Prod. No. AG-CN2-0500).
LIT: Chemoproteomic fishing identifies arzanol as a positive modulator of brain glycogen phosphorylase: F. del Gaudio, et al.; Chem. Commun. 54, 12863 (2018)
February 24, 2018
BAFF and APRIL Inhibitors to study Mice Autoimmunity
The TNF superfamily ligands, BAFF and APRIL, are involved in the pathogenesis of a number of autoimmune diseases by regulating plasma cell survival. AdipoGen Life Sciences provides unique antibodies to study autoimmune diseases in mice by blockade of mouse BAFF or APRIL, such as anti-BAFF (mouse), mAb (blocking) (Sandy-2) or anti-APRIL (mouse), mAb (rec.) (blocking) (Apry-1-1).
In a recent study, Haselmayer et al., tested several inhibitors of BAFF or APRIL in a model of mouse autoimmune disease (SLE) to confirm that inhibition of mouse BAFF and APRIL by the receptor TACI-Fc is more efficient than inhibition of BAFF alone or APRIL alone on long-lived plasma cell survival. To block mouse APRIL in this study, anti-APRIL (mouse), mAb (rec.) (blocking) (Apry-1-1) (Prod. No. AG-27B-0001PF) from AdipoGen Life Sciences was injected in C57BL/6 mice.
LIT: A mouse model of systemic lupus erythematosus responds better to soluble TACI than to soluble BAFFR, correlating with depletion of plasma cells: P. Haselmayer, et al.; Eur. J. Immunol. 47, 1075 (2017)