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Bad (Ser-26), Phosphospecific Antibody

Applications

  • WB

Reactivity

  • Mouse
  • Rat
Overview
Catalog # bs-70357r-100ul
Product Name Bad (Ser-26), Phosphospecific Antibody
Applications WB
Specificity The antibody detects a 23 kDa* doublet corresponding to the apparent molecular mass of phosphorylated Bad on SDS-PAGE immunoblots of mouse J774A.1 treated with calyculin A. This reactivity is not observed after lambda phosphatase treatment. This peptide sequence is highly conserved in rat Bad, but is not found in human Bad.
Reactivity Mouse, Rat
Specifications
Conjugation Unconjugated
Host Rabbit
Source Phospho-Bad (Ser-26) synthetic peptide (coupled to KLH) corresponding to amino acid residues surrounding serine 26 in mouse Bad.
Modification Site Ser-26
Clonality Polyclonal
Isotype IgG
Purification Antigen Affinity purification
Storage Buffer PBS + 1 mg/ml BSA, 0.05% NaN3 and 50% glycerol
Storage Condition Storage at -20°C is recommended, as aliquots may be taken without freeze/thawing due to presence of 50% glycerol. Stable for at least 1 year at -20°C.
Target
Swiss Prot Q61337
Synonyms Bcl2 antagonist of cell death, BAD; Bcl-2-binding component 6, Bbc6, Bcl-xL/Bcl-2-associated death promoter
Background Bad is a member of the BCL-2 family of regulators involved in programmed cell death. This protein positively regulates cell apoptosis by forming heterodimers with BCL-xL and BCL-2, and reversing their death repressor activity. Proapoptotic activity of this protein is regulated through its phosphorylation. Protein kinases AKT IKK, and MAP kinases, as well as protein phosphatase calcineurin are found to be involved in the regulation of this Bad activity. Phosphorylation of Bad occurs on one or more of Ser-26, Ser-112, Ser-136, and Ser-155 in response to survival stimuli, which blocks its pro-apoptotic activity. Phosphorylation on Ser-136 or Ser-112 promotes heterodimerization with 14-3-3 proteins. This interaction then facilitates the phosphorylation at Ser-155, a site within the BH3 motif, leading to the release of Bcl-xL and the promotion of cell survival. Ser-26 is phosphorylated by IKK leading to phosphorylation of C-terminal serine sites and disruption of binding to Bcl-xL. This inactivation of Bad inhibits TNFα-induced apoptosis independent of NF-κB activity.
Application Dilution
WB 1:300-5000