Bio-Connect

anti-Isthmin-1, mAb (rec.) (Giusepi-1-4)

AG-27B-0022
AdipoGen Life Sciences
ApplicationsWestern Blot, ELISA
Product group Antibodies
ReactivityHuman, Mouse
TargetISM1
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Overview

  • Supplier
    AdipoGen Life Sciences
  • Product Name
    anti-Isthmin-1, mAb (rec.) (Giusepi-1-4)
  • Delivery Days Customer
    10
  • Antibody Specificity
    Recognizes human and mouse Isthmin-1.
  • Applications
    Western Blot, ELISA
  • Certification
    Research Use Only
  • Clonality
    Monoclonal
  • Clone ID
    Giusepi-1-4
  • Concentration
    1 mg/ml
  • Estimated Purity
    >95%
  • Gene ID140862
  • Target name
    ISM1
  • Target description
    isthmin 1
  • Target synonyms
    bA149I18.1; C20orf82; dJ1077I2.1; ISM; Isthmin; isthmin 1 homolog; isthmin 1, angiogenesis inhibitor; isthmin-1
  • Host
    Mouse
  • Isotype
    IgG2b
  • Protein IDB1AKI9
  • Protein Name
    Isthmin-1
  • Scientific Description
    Isthmin-1 (ISM1) was first identified as a gene expressed in the Xenopus midbrain hind brain organizer called isthmus, with a proposed role during early brain development. Isthmin-1 encodes a predicted ~50-kDa protein containing a signal peptide, a thrombospondin domain and an adhesion-associated domain. Isthmin-1 is important for embryonic and postnatal development. Growing evidence has shown that aberrant expression of Isthmin-1 can also affect the biological behavior of cancer. The Ism1 gene is conserved in mice and humans. A recent study showed that Isthmin-1 is an adipokine that induces glucose uptake in human and mouse adipocytes. Isthmin-1 is secreted by mature adipocytes and triggers a signaling cascade similar to that of insulin, regulating glucose uptake while suppressing lipid accumulation. Recombinant Isthmin-1 or overexpression of Isthmin-1 causes a robust increase in GLUT4-dependent glucose uptake in cultured primary murine and immortalized human adipocytes as well as in primary human muscle cells and prevents insulin resistance and hepatic steatosis in a diet-induced obesity mouse model. Ablation of Isthmin-1 causes glucose intolerance and impaired insulin-stimulated adipocyte glucose uptake. Isthmin-1 suppresses de novo lipogenesis and increases protein synthesis in hepatocytes whereas Isthmin-1 knockdown in adipocytes reduces glucose uptake and insulin-dependent phosphorylation of protein kinase AKT at serine residue 473 (p-AKTSer473). Isthmin-1 signaling is dependent on PI3K and shares downstream phosphorylation targets with insulin signaling, such as p-AKTSer473, p-AKTThr308, p-ERK1/2Thr202/Tyr204 and p-S6Ser235/236. Isthmin-1 does not seem to act through the insulin receptor or the insulin-like growth factor 1 receptor; it is most likely to signal through another, yet-to-be-identified, receptor tyrosine kinase. - Recombinant Antibody. Recognizes human and mouse Isthmin-1. Isotype: Mouse IgG2blambda. Immunogen: Recombinant human Isthmin-1. Applications: ELISA, WB. Liquid. In PBS and 0.02% Proclin-300. Isthmin-1 (ISM1) was first identified as a gene expressed in the Xenopus midbrain hind brain organizer called isthmus, with a proposed role during early brain development. Isthmin-1 encodes a predicted ~50-kDa protein containing a signal peptide, a thrombospondin domain and an adhesion-associated domain. Isthmin-1 is important for embryonic and postnatal development. Growing evidence has shown that aberrant expression of Isthmin-1 can also affect the biological behavior of cancer. The Ism1 gene is conserved in mice and humans. A recent study showed that Isthmin-1 is an adipokine that induces glucose uptake in human and mouse adipocytes. Isthmin-1 is secreted by mature adipocytes and triggers a signaling cascade similar to that of insulin, regulating glucose uptake while suppressing lipid accumulation. Recombinant Isthmin-1 or overexpression of Isthmin-1 causes a robust increase in GLUT4-dependent glucose uptake in cultured primary murine and immortalized human adipocytes as well as in primary human muscle cells and prevents insulin resistance and hepatic steatosis in a diet-induced obesity mouse model. Ablation of Isthmin-1 causes glucose intolerance and impaired insulin-stimulated adipocyte glucose uptake. Isthmin-1 suppresses de novo lipogenesis and increases protein synthesis in hepatocytes whereas Isthmin-1 knockdown in adipocytes reduces glucose uptake and insulin-dependent phosphorylation of protein kinase AKT at serine residue 473 (p-AKTSer473). Isthmin-1 signaling is dependent on PI3K and shares downstream phosphorylation targets with insulin signaling, such as p-AKTSer473, p-AKTThr308, p-ERK1/2Thr202/Tyr204 and p-S6Ser235/236. Isthmin-1 does not seem to act through the insulin receptor or the insulin-like growth factor 1 receptor; it is most likely to signal through another, yet-to-be-identified, receptor tyrosine kinase.
  • Reactivity
    Human, Mouse
  • Storage Instruction
    -20°C,2°C to 8°C
  • UNSPSC
    12352203