Render Target: STATIC
Render Timestamp: 2024-12-02T11:09:21.908Z
Commit: cd2fae6ca3f811b1ddb1df24ac291ed56d5d501b
XML generation date: 2024-09-30 01:59:28.274
Product last modified at: 2024-11-20T13:00:41.385Z
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PDP - Template Name: Monoclonal Antibody
PDP - Template ID: *******c5e4b77
R Recombinant
Recombinant: Superior lot-to-lot consistency, continuous supply, and animal-free manufacturing.

SREBP-1 (E9F4O) Rabbit mAb #95879

Filter:
  • WB
  • ChIP

    Supporting Data

    REACTIVITY H
    SENSITIVITY Endogenous
    MW (kDa) 60-70, 125
    Source/Isotype Rabbit IgG
    Application Key:
    • WB-Western Blotting 
    • ChIP-Chromatin Immunoprecipitation 
    Species Cross-Reactivity Key:
    • H-Human 

    Product Information

    Product Usage Information

    For optimal ChIP results, use 2.5 μL of antibody and 10 μg of chromatin (approximately 4 × 106 cells) per IP. This antibody has been validated using SimpleChIP® Enzymatic Chromatin IP Kits.
    Application Dilution
    Western Blotting 1:1000
    Chromatin IP 1:200

    Storage

    Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/mL BSA, 50% glycerol, and less than 0.02% sodium azide. Store at –20°C. Do not aliquot the antibody.

    Protocol

    Specificity / Sensitivity

    SREBP-1 (E9F4O) Rabbit mAb recognizes endogenous levels of total SREBP-1 protein. This antibody does not cross-react with SREBP-2 protein.

    Species Reactivity:

    Human

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Gly45 of human SREBP-1 protein.

    Background

    Sterol regulatory element–binding proteins (SREBPs) are basic helix-loop-helix–leucine zipper (bHLH-Zip) transcription factors. Inactive precursor forms of SREBPs are bound to endoplasmic reticulum (ER) membranes. When cells are starved for sterols, SREBPs move from the ER to the Golgi apparatus with the help of SREBP cleavage activating protein (SCAP). In the Golgi apparatus, precursor SREBPs are then sequentially cleaved by two proteases, site-1 protease (S1P) and site-2 protease (S2P). The released N-terminal domain that contains the bHLH-Zip region enters the nucleus and binds to sterol response elements (SREs) in the promoters of a variety of genes responsible for the synthesis of cholesterol, fatty acids, and other lipids, activating their expressions (1,2). Studies show that SREBP-1-dependent fatty acid homeostasis has a critical role in promoting the pro-tumor phenotype of M2-like tumor-associated macrophages (TAMs), and inhibition of SREBP-1 enhances the efficacy of immune checkpoint blockade (3). In addition, suppression of cholesterol biosynthesis by statins stimulates SREBP-1 activation and, therefore, induces TGF-β signaling, promoting the epithelial-to-mesenchymal transition in pancreatic ductal adenocarcinoma (4).
    For Research Use Only. Not For Use In Diagnostic Procedures.
    Cell Signaling Technology is a trademark of Cell Signaling Technology, Inc.
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