Bio-Connect

Apolipoprotein CI

16-16-120301
Athens Bioscience
Protein IDP02654
Product group Proteins / Signaling Molecules
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Overview

  • Supplier
    Athens Bioscience
  • Product Name
    Apolipoprotein CI
  • Delivery Days Customer
    9
  • Applications Supplier
    In Vitro Diagnostic, Cardiovascular, Diabetes, Alzheimer's, Obesity
  • Certification
    Research Use Only
  • Estimated Purity
    ≥95% by SDS-PAGE
  • Protein IDP02654
  • Protein Name
    Apolipoprotein C-I
  • Scientific Description
    Apolipoprotein CI (Apo CI) is a component of triglyceride-rich lipoproteins (VLDL, chylomicrons) and HDL, with normal plasma concentrations of 4–7 mg/100 mL. Synthesized primarily in the liver, Apo CI modulates lipid metabolism by inhibiting cholesteryl ester transfer protein (CETP) and lipoprotein lipase (LPL), while activating lecithin-cholesterol acyltransferase (LCAT). These interactions influence HDL remodeling and VLDL clearance, impacting systemic lipid homeostasis. Elevated Apo CI levels correlate with reduced visceral adiposity and protection against obesity and insulin resistance, likely through impaired lipid storage in adipose tissue. Conversely, the APOC1 H2 allele is linked to late-onset Alzheimer’s disease (LOAD), particularly in carriers of the APOE epsilon4 variant, by altering cerebral lipoprotein metabolism and amyloid-bèta clearance. In diabetes, glycation of Apo CI disrupts its CETP inhibitory function, exacerbating dyslipidemia and cardiovascular risk. Clinically, Apo CI serves as a biomarker for LOAD susceptibility and metabolic syndrome progression. Therapeutic strategies targeting its lipid-modulating properties or mitigating glycation effects hold promise for managing Alzheimer’s, diabetes, and obesity-related disorders.
  • Shelf life instruction
    more then 1 year
  • Source
    Prepared from fresh, non-frozen plasma shown to be non reactive for HBsAg, anti-HCV, anti-HBc, and negative for anti-HIV 1 & 2 by FDA approved tests.
  • Storage Instruction
    -20C
  • UNSPSC
    41116100

References

  • Deng, M. et al., (2018), 'LILRB4 signalling in leukaemia cells mediates T cell suppression and tumour infiltration', Nature, 562: pp 605–609
    Read this paper