Bax (fosfo Thr167) Antilichaam

Accelerates programmed cell death by binding to, and antagonizing the apoptosis repressor BCL2 or its adenovirus homolog E1B 19k protein. Under stress conditions, undergoes a conformation change that causes translocation to the mitochondrion membrane, leading to the release of cytochrome c that then triggers apoptosis. Promotes activation of CASP3, and thereby apoptosis.

581

Q07812

NP_620116.1

Human, Mouse, Rat

Bax (phospho Thr167) antibody was raised against a peptide sequence around phosphorylation site of threonine167 (P-G-T (p) -P-T) derived from Human Bax.

Unconjugated

Primary Antibodies

Phospho-Specific

Antibodies were purified by affinity-chromatography using epitope-specific peptide.

1 mg/mL

Antibody supplied in phosphate buffered saline (without Mg2+ and Ca2+), pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol.

Phospho-Specific

Blue Ice

Store antibody at -20˚ C for up to one year.

21 kDa

IgG

The antibody detects endogenous levels of Bax only when phosphorylated at threonine 167.

BAX

BCL2-associated X protein

Homo sapiens

Francesca Andriani. J Natl Cancer Inst, Sep 2001; 93: 1314 - 1324.

H Martinez-Valdez. J. Exp. Med., Mar 1996; 183: 971.

Joslyn K. Brunelle. J. Biol. Chem., Feb 2004; 279: 4305 - 4312.

BAXA, Apoptosis regulator BAX, membrane isoform alpha, Bcl2-associated X protein

IF

388166

Liquid