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CREB-H (D10D8) Rabbit mAb #8700

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Inquiry Info. # 8700

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    Product Specifications

    REACTIVITY H M R Mk
    SENSITIVITY Endogenous
    MW (kDa) 75
    Source/Isotype Rabbit IgG
    Application Key:
    • WB-Western Blotting 
    • IP-Immunoprecipitation 
    Species Cross-Reactivity Key:
    • H-Human 
    • M-Mouse 
    • R-Rat 
    • Mk-Monkey 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000
    Immunoprecipitation 1:50

    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

    CREB-H (D10D8) Rabbit mAb recognizes endogenous levels of total and cleaved CREB-H proteins.

    Species Reactivity:

    Human, Mouse, Rat, Monkey

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Leu93 of human CREB-H protein.

    Background

    CREB-H belongs to the bZIP transmembrane transcription factor family that activates transcription by binding to cAMP responsive elements (1,2). CREB-H interacts with ATF-6 and binds to conserved elements in the APR genes to synergistically activate transcription (2-4). Evidence suggests that CREB-H is activated by cleavage upon ER stress, inflammatory stimuli (2-5), and metabolic stress (5,6). Known chemical activators of ER stress, such as tunicamycin and thapsigargin, have been shown to induce cleavage of the full-length 75 kDa from of CREB-H, releasing the 50 kDa N-terminal fragment, which translocates to the nucleus (1-4). Upon ER stress, the transmembrane domain of CREB-H is cleaved by Golgi proteases, which allows subsequent translocation to the nucleus. Liberated nuclear CREB-H plays a crucial role in the acute systemic inflammatory response by activating transcription of genes that encode serum amyloid P-component (SAP) and C-reactive protein (CRP) (2,3). Recent studies suggest that activated CREB-H functions as a crucial metabolic regulator of hepatic lipogenesis, fatty acid (FA) oxidation, and lipolysis (5,6). Metabolic stress inducers, such as saturated fatty acids, insulin, and atherogenic high-fat diets have been shown to activate CREB-H in the liver (5-7).

    Alternate Names

    cAMP responsive element binding protein 3 like 3; cAMP responsive element binding protein 3-like 3; cAMP-responsive element-binding protein 3-like protein 3; cAMP-responsive element-binding protein, hepatic-specific; CR3L3; CREB-H; CREB/ATF family transcription factor; CREB3L3; CREBH; Cyclic AMP-responsive element-binding protein 3-like protein 3; HYST1481; MGC126553; MGC126557; Processed cyclic AMP-responsive element-binding protein 3-like protein 3; Transcription factor CREB-H

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