Render Target: STATIC
Render Timestamp: 2024-11-07T10:57:21.670Z
Commit: 3c1f305a63297e594ac8d7bb5424007d592d68be
XML generation date: 2024-08-01 15:25:26.214
Product last modified at: 2024-08-20T12:15:15.035Z
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PDP - Template Name: Polyclonal Antibody
PDP - Template ID: *******59c6464

C/EBPalpha (p42) Antibody #2843

Filter:
  • WB

    Supporting Data

    REACTIVITY H
    SENSITIVITY Endogenous
    MW (kDa) 45
    SOURCE Rabbit
    Application Key:
    • WB-Western Blotting 
    Species Cross-Reactivity Key:
    • H-Human 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000

    Storage

    Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA and 50% glycerol. Store at –20°C. Do not aliquot the antibody.

    Protocol

    Specificity / Sensitivity

    C/EBPalpha (p42) Antibody detects endogenous levels of total p42 C/EBPalpha protein but not p30 C/EBPalpha.

    Species Reactivity:

    Human

    The antigen sequence used to produce this antibody shares 100% sequence homology with the species listed here, but reactivity has not been tested or confirmed to work by CST. Use of this product with these species is not covered under our Product Performance Guarantee.

    Species predicted to react based on 100% sequence homology:

    Mouse, Rat

    Source / Purification

    Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to the amino-terminal sequence of human C/EBPalpha. Antibodies are purified by protein A and peptide affinity chromatography.

    Background

    CCAAT/enhancer-binding proteins (C/EBPs) are a family of transcription factors that are critical for cellular differentiation, terminal function, and inflammatory response (1). Six members of the family have been characterized (C/EBPα, β, δ, γ, ε, and ζ) and are distributed in a variety of tissues (1). Translation from alternative start codons results in two isoforms of C/EBPα (p42 and p30), which are both strong transcriptional activators (2). It has been reported that insulin and insulin-like growth factor-I stimulate the dephosphorylation of C/EBPα, which may play a key role in insulin-induced repression of GLUT4 transcription (3). Phosphorylation of C/EBPα at Thr222, Thr226, and Ser230 by GSK-3 seems to be required for adipogenesis (4).
    For Research Use Only. Not For Use In Diagnostic Procedures.
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