Datasheet

生物学的記述

Specificity	Acetyl-p53 (Lys373) Antibody [J7D9] detects endogenous levels of total p53 protein only when it is Acetylated at Lys373.
Background	Acetyl-p53 (Lys373) refers to the post-translationally modified form of the p53 tumor suppressor protein, a sequence-specific DNA-binding transcription factor belonging to the p53 family that regulates genes involved in cell cycle arrest, DNA repair, senescence, and apoptosis. p53 features an N-terminal transactivation domain (TAD), a central DNA-binding domain containing key residues like K120, and a C-terminal regulatory domain with multiple lysine sites, including K373 (often studied alongside K382), that undergo acetylation by histone acetyltransferases such as p300/CBP, which neutralizes their positive charge to promote an open conformation and enhance DNA binding affinity. Acetylation at K373/K382 stabilizes p53 by reducing ubiquitination and degradation, recruits p300 to promoters like that of p21^Waf1/Cip1, and boosts transcriptional activation of cell cycle inhibitors independent of N-terminal phosphorylation (e.g., Ser15, Ser20, Ser392), thereby inducing p21 expression, G1/S arrest, and tumor suppression while responding to HDAC inhibitors like depsipeptide. This modification fine-tunes p53's pathway choices, favoring growth arrest over apoptosis in certain contexts such as DNA damage or genotoxic stress, with disease relevance in cancer, where its dysregulation promotes proliferation.

Specificity

Acetyl-p53 (Lys373) Antibody [J7D9] detects endogenous levels of total p53 protein only when it is Acetylated at Lys373.

Background

Acetyl-p53 (Lys373) refers to the post-translationally modified form of the p53 tumor suppressor protein, a sequence-specific DNA-binding transcription factor belonging to the p53 family that regulates genes involved in cell cycle arrest, DNA repair, senescence, and apoptosis. p53 features an N-terminal transactivation domain (TAD), a central DNA-binding domain containing key residues like K120, and a C-terminal regulatory domain with multiple lysine sites, including K373 (often studied alongside K382), that undergo acetylation by histone acetyltransferases such as p300/CBP, which neutralizes their positive charge to promote an open conformation and enhance DNA binding affinity. Acetylation at K373/K382 stabilizes p53 by reducing ubiquitination and degradation, recruits p300 to promoters like that of p21^Waf1/Cip1, and boosts transcriptional activation of cell cycle inhibitors independent of N-terminal phosphorylation (e.g., Ser15, Ser20, Ser392), thereby inducing p21 expression, G1/S arrest, and tumor suppression while responding to HDAC inhibitors like depsipeptide. This modification fine-tunes p53's pathway choices, favoring growth arrest over apoptosis in certain contexts such as DNA damage or genotoxic stress, with disease relevance in cancer, where its dysregulation promotes proliferation.

使用情報

Application

WB, IF, FCM

Dilution

WB	IF	FCM
1:5000	1:100 - 1:250	1:120

Reactivity

Human

Source

Rabbit Monoclonal Antibody

MW

43 kDa

Storage Buffer

PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage
(from the date of receipt)

-20°C (avoid freeze-thaw cycles), 2 years

プロトコール

References

https://pubmed.ncbi.nlm.nih.gov/16537920/
https://pubmed.ncbi.nlm.nih.gov/25545885/

Acetyl-p53 (Lys373) Antibody [J7D9]

生物学的記述

使用情報

References

Application Data