Acetyl-p53 (Lys373) Antibody [J7D9]

Catalog No.: F2048

Application: Reactivity: Human

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代表番号: 045-509-1970|電子メール：sales@selleck.co.jp

使用情報

Dilution
WB1:5000 IF1:100 - 1:250 FCM1:120

Application
WB, IF, FCM

Source
Rabbit Monoclonal Antibody

Reactivity
Human

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

Predicted MW Observed MW
43 kDa 53 kDa
^*なぜ予測分子量と実際の分子量が異なるのか？下記の原因により、実際の分子量が予測と異なる：タンパク質の翻訳後修飾（リン酸化/糖鎖付加），スプライシングバリアント，イソフォーム，相対的な電荷，ポリマー。

Datasheet & SDS

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.

Clone
J7D9

Synonym(s)
P53; TP53; Cellular tumor antigen p53; Antigen NY-CO-13; Phosphoprotein p53; Tumor suppressor p53

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.

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.

References
[1] Zhao Y, et al. Mol Cell Biol. 2006 Apr;26(7):2782-90. [2] Reed SM, et al. Cancers (Basel). 2014 Dec 23;7(1):30-69.

PVDFメンブレン孔径参考表

Protein Size (kDa)	PVDF Transfer Membrane Pore Size (μm)
< 10	0.22
10-20	0.22
20-30	0.45
30-45	0.45
45-70	0.45
80-100	0.45
100-140	0.45
> 140	0.45

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Protein Size (kDa)	Separating Gel Percentage
4-40	20%
12-45	15%
10-70	12.5%
15-100	10%
25-100	8%
60-210	5%