Render Target: STATIC
Render Timestamp: 2024-12-09T12:04:42.783Z
Commit: 224419269841c11382c4555dbee545259bf6c379
XML generation date: 2024-08-01 15:23:32.687
Product last modified at: 2024-10-17T12:45:34.041Z
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PDP - Template Name: Polyclonal Antibody
PDP - Template ID: *******59c6464

ASK1 Antibody #3762

Filter:
  • WB

    Supporting Data

    REACTIVITY H
    SENSITIVITY Endogenous
    MW (kDa) 155
    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

    ASK1 Antibody detects endogenous ASK1 protein independent of its phosphorylation state.

    Species Reactivity:

    Human

    Source / Purification

    Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues surrounding amino acid residue 280 of human ASK1. Antibodies are purified by protein A and peptide affinity chromatography.

    Background

    Apoptosis signal-regulating kinase 1 (ASK1), a MAP kinase kinase kinase, plays essential roles in stress-induced apoptosis (1,2). ASK1 is activated in response to a variety of stress-related stimuli through distinct mechanisms and activates MKK4 and MKK3, which in turn activate JNK and p38 (3). Overexpression of ASK1 activates JNK and p38 and induces apoptosis in several cell types through signals involving the mitochondrial cell death pathway. Embryonic fibroblasts or primary neurons derived from ASK1-/- mice are resistant to stress-induced JNK and p38 activation as well as cell death (4,5). Phosphorylation at Ser967 is essential for ASK1 association with 14-3-3 proteins and suppression of cell death (6). Oxidative stress induces dephosphorylation of Ser967 and phosphorylation of Thr845 in the activation loop of ASK1, both of which are correlated with ASK1 activity and ASK1-dependent apoptosis (7,8). Akt phosphorylates ASK1 at Ser83, which attenuates ASK1 activity and promotes cell survival (9).
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