Category: Proteins & Peptides

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  • Brand: AdipoGen
  • Brand: Invent
  • Brand: SignalChem Diagnostics
Reference: AG-35B-0001

Enhances the biological activity of TRAIL, Soluble (human) (rec.) (AG-40B-0003) and FasL, Soluble (human) (rec.) (AG-40B-0001).

Reference: AG-35B-0008

Fc (mouse) IgG2b Control (rec.) (Prod. No. AG-35B-0008) serves as a negative control in experiments with anti-APRIL (mouse), mAb (rec.) (Blocking) (APRY-1-1) (Prod. No. AG-27B-0001) or anti-Angiopoietin-2, mAb (rec.) (blocking) (Angy-2-1) (Prod. No. AG-27B-0016).

Reference: AG-35B-0009

Fc (human) IgG2 Control (rec.) (AG-35B-0009) serves as a negative control in experiments with monoclonal antibodies (recombinant) (AG-27B-XXXX) containing a Fc (human) IgG2.

Reference: AG-37B-0001

Blocking Peptide for anti-Asc, pAb (AL177) https://adipogen.com/catalogsearch/result/?q=al177 . This vial contains 100µg peptide in 100µl sterile water. The Asc Antibody (AL177) Blocking Peptide can be used in conjunction with several variants of the anti-Asc pAb (AL177) (Prod. No. AG-25B-0006) to block protein-antibody complex formation.

Reference: AG-40A-0008

GITRL (Glucocorticoid-induced TNF receptor ligand) is expressed on dendritic cells (DC), monocytes, macrophages, B cells, activated T cells, endothelial cells, osteoclasts and various healthy non-lymphoid tissues (e.g. testis). GITRL is constitutively expressed and released as soluble form by solid tumors and various hematopoietic malignancies. GITRL causes differentiation of osteoclasts, activation of macrophages, but also alteration of carcinoma and leukemia cells and influences apoptosis. Binding to GITR is important in regulating T cell proliferation and TCR-mediated apoptosis. GITRL is implicated in development of autoimmune diseases and in the immune response against infectious pathogens and tumors.

Reference: AG-40A-0010Y

The adipocytokine resistin which belongs to a family of cysteine-rich C-terminal proteins known as resistin-like molecules (RELM; RELM-alpha/FIZZ 1 and RELM-beta/FIZZ 2) of FIZZ (found in inflammatory zone) are thought to be involved in inflammatory processes. Previous studies in mice showed that resistin impairs glucose tolerance and insulin action. In addition, resistin also inhibits adipogenesis in murine 3T3-L1 cells. Therefore resistin has also been proposed as an adipocyte-secreted factor thought to link obesity and T2DM.

Reference: AG-40A-0011

The adipocytokine resistin which belongs to a family of cysteine-rich C-terminal proteins known as resistin-like molecules (RELM; RELM-alpha/FIZZ 1 and RELM-beta/FIZZ 2) of FIZZ (found in inflammatory zone) are thought to be involved in inflammatory processes. Previous studies in mice showed that resistin impairs glucose tolerance and insulin action. In addition, resistin also inhibits adipogenesis in murine 3T3-L1 cells. Therefore resistin has also been proposed as an adipocyte-secreted factor thought to link obesity and T2DM.

Reference: AG-40A-0017

Nicotinamide phosphoribosyltransferase (Nampt; pre-B cell colony-enhancing factor; PBEF; Visfatin) is an adipokine that is localized to the bloodstream and has various functions, including the promotion of vascular smooth muscle cell maturation and inhibition of neutrophil apoptosis. It activates insulin receptor and has insulin-mimetic effects, lowering blood glucose and improving insulin sensitivity. The protein is highly expressed in visceral fat and serum levels of the protein correlate with obesity. Recently NAMPT extracellular (eNAMPT) has been shown to be secreted from macrophages in muscles and to triggers a proliferative signal of muscle stem cell (MusC) by binding to CCR5 located at the surface receptor of MusC.

Reference: AG-40A-0018

Nicotinamide phosphoribosyltransferase (Nampt; pre-B cell colony-enhancing factor; PBEF; Visfatin) is an 52kDa adipokine secreted by adipose tissue and involved in the biosynthesis of nicotinamide adenine dinucleotide (NAD+). Two forms of Nampt exist, an intracellular form (iNampt) and an extracellular form (eNampt). While the function of iNampt as an essential and rate-limiting NAD+ biosynthetic enzyme is well established, the physiological role of eNampt is still a matter of debate. Nampt has various functions, including the promotion of vascular smooth muscle cell maturation and inhibition of neutrophil apoptosis. It activates insulin receptor and has insulin-mimetic effects, lowering blood glucose and improving insulin sensitivity. The protein is highly expressed in visceral fat and serum levels of the protein correlate with obesity.

Reference: AG-40A-0018AA

Nicotinamide phosphoribosyltransferase (Nampt; pre-B cell colony-enhancing factor; PBEF; Visfatin) is an 52kDa adipokine secreted by adipose tissue and involved in the biosynthesis of nicotinamide adenine dinucleotide (NAD+). Two forms of Nampt exist, an intracellular form (iNampt) and an extracellular form (eNampt). While the function of iNampt as an essential and rate-limiting NAD+ biosynthetic enzyme is well established, the physiological role of eNampt is still a matter of debate. Nampt has various functions, including the promotion of vascular smooth muscle cell maturation and inhibition of neutrophil apoptosis. It activates insulin receptor and has insulin-mimetic effects, lowering blood glucose and improving insulin sensitivity. The protein is highly expressed in visceral fat and serum levels of the protein correlate with obesity. Recently NAMPT extracellular (eNAMPT) has been shown to be secreted from macrophages in muscles and to triggers a proliferative signal of muscle stem cell (MusC) by binding to CCR5 located at the surface receptor of MusC.