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3761
Phospho-ASK1 (Ser83) Antibody
Primary Antibodies

Phospho-ASK1 (Ser83) Antibody #3761

Reviews ()
Citations (12)

Supporting Data

REACTIVITY
SENSITIVITY
MW (kDa) 155
SOURCE Rabbit

Application Key:

  • W-Western
  • IP-Immunoprecipitation
  • IHC-Immunohistochemistry
  • ChIP-Chromatin Immunoprecipitation
  • IF-Immunofluorescence
  • F-Flow Cytometry
  • E-P-ELISA-Peptide

Species Cross-Reactivity Key:

  • H-Human
  • M-Mouse
  • R-Rat
  • Hm-Hamster
  • Mk-Monkey
  • Mi-Mink
  • C-Chicken
  • Dm-D. melanogaster
  • X-Xenopus
  • Z-Zebrafish
  • B-Bovine
  • Dg-Dog
  • Pg-Pig
  • Sc-S. cerevisiae
  • Ce-C. elegans
  • Hr-Horse
  • All-All Species Expected

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.

Specificity / Sensitivity

Phospho-ASK1 (Ser83) Antibody detects transfected ASK1 only when phosphorylated at Ser83.

Source / Purification

Polyclonal antibodies are produced by immunizing animals with a synthetic phosphopeptide corresponding to residues around Ser83 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).

ASK1 is a substrate for phosphorylation at Ser83 by Akt, and that this phosphorylation is associated with a decrease in stimulated ASK1 kinase activity (6).

  1. Ichijo, H. et al. (1997) Science 275, 90-94.
  2. Wang, X.S. et al. (1996) J. Biol. Chem. 271, 31607-31611.
  3. Matsuzawa, A. and Ichijo, H. (2001) J. Biochem. (Tokyo) 130, 1-8.
  4. Tobiume, K. et al. (2001) EMBO Rep. 2, 222-228.
  5. Nishitoh, H. et al. (2002) Genes Dev. 16, 1345-1355.
  6. Zhang, L. et al. (1999) Proc. Natl. Acad. Sci. USA 96, 8511-8515.
  7. Tobiume, K. et al. (2002) J. Cell. Physiol. 191, 95-104.
  8. Goldman, E.H. et al. (2004) J. Biol. Chem. in press, .
  9. Kim, A.H. et al. (2001) Mol. Cell. Biol. 21, 893-901.

Pathways & Proteins

Explore pathways + proteins related to this product.

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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