AdipoGen Life Sciences

Isthmin-1 (human) ELISA Kit

CHF 540.00
In stock
AG-45B-0032-KI0196 wellsCHF 540.00
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Product Details
Synonyms C20orf82; ISM1; ISM
Product Type Kit
Properties
Application Set Quantitative ELISA
Specificity

Detects human Isthmin-1 in plasma and cell culture supernatant. It detects also mouse Isthmin-1 (very conserved).

Crossreactivity Human
Mouse
Quantity

1 x 96 wells

Sensitivity 0.4 ng/ml
Range 0.625 to 40ng/ml
Sample Type Cell Culture Supernatant
Plasma
Assay Type Sandwich
Detection Type Colorimetric
Other Product Data

UniProt link B1AKI9: Isthmin-1 (human)

Accession Number B1AKI9
Shipping and Handling
Shipping BLUE ICE
Short Term Storage +4°C
Long Term Storage +4°C
Handling Advice After standard reconstitution, prepare aliquots and store at -20°C.
Avoid freeze/thaw cycles.
Plate and reagents should reach room temperature before use.
Use/Stability 12 months after the day of manufacturing. See expiry date on ELISA Kit box.
Documents
Manual Download PDF
MSDS Inquire
Product Specification Sheet
Datasheet Download PDF
Description

Isthmin-1 (ISM1) was first identified as a gene expressed in the Xenopus midbrain-hindbrain organizer called the isthmus, with a proposed role during early brain development. Isthmin-1 encodes a predicted ~50kDa 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. Mature adipocytes secrete isthmin-1 and trigger 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.

Isthmin-1 levels positively correlate with obesity in human plasma and are also associated with T cell depletion markers (PD-1, LAG-3, TIM-3 or CTLA-4), suggesting its use as a biomarker during immunotherapy.

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