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Merck
CN

06-916

Anti-acetyl-p53 (Lys373) Antibody

serum, Upstate®

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关于此项目

UNSPSC Code:
12352203
NACRES:
NA.41
eCl@ss:
32160702
Clone:
polyclonal
Species reactivity:
human
Application:
IP, WB
Citations:
24
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biological source

rabbit

antibody form

serum

antibody product type

primary antibodies

clone

polyclonal

species reactivity

human

manufacturer/tradename

Upstate®

technique(s)

immunoprecipitation (IP): suitable, western blot: suitable

isotype

IgG

NCBI accession no.

UniProt accession no.

shipped in

wet ice

target post-translational modification

acetylation (Lys373)

Quality Level

Gene Information

human ... TP53(7157)

General description

p53 is a DNA-binding, oligomerization domain and transcription activation domain-containing tumor suppressor that upregulates growth arrest and apoptosis-related genes in response to stress signals, thereby influencing programmed cell death, cell differentiation and cell cycle control mechanisms. p53 localizes to the nucleus yet can be chaperoned to the cytoplasm by the negative regulator MDM2, an E3 ubiquitin ligase that is upregulated in the presence of active p53, where MDM2 polyubiquitinates p53 for proteasome targeting. p53 can assemble into tetramers in the absence of DNA, fluctuates between latent and active (DNA-binding) conformations, and is differentially activated through posttranslational modifications including phosphorylation and acetylation. Mutations in the DNA-binding domain (DBD) (amino acids 110-286) of p53 can compromise energetically favorable association with cis elements and are implicated in several human cancers.
53 kDa

Immunogen

peptide corresponding to amino acids 367-379 of human p53 (SHLKSKACKGQSTSR, where ACK denotes acetyl-lysine).

Application

Anti-acetyl-p53 (Lys373) Antibody is a Rabbit Polyclonal Antibody for detection of acetyl-p53 (Lys373) also known as Antigen NY-CO-13, Phosphoprotein p53, Tumor suppressor p53, p53 antigen & has been tested in IP & WB.

Biochem/physiol Actions

Recognizes p53 acetylated in vitro by recombinant p300, and for peptide containing acetyl-lysine 373 but not for the peptide containing acetyl-lysine 320; modest cross-reactivity for p53 acetylated in vitro by recombinant PCAF.

Physical form

Protein A Purified immunoglobulin in 0.1M Tris-glycine, pH 7.4, 0.15M NaCl, 0.02% sodium azide, 0.1mg/ml BSA

Analysis Note

routinely evaluated by immunoblot on GST-p53 acetylated by recombinant p300, HAT domain (Catalog #14-418) in an in vitro acetyl transferase assay

Other Notes

Concentration: Please refer to the Certificate of Analysis for the lot-specific concentration.
Replaces: 04-1137

Legal Information

UPSTATE is a registered trademark of Merck KGaA, Darmstadt, Germany

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存储类别

10 - Combustible liquids

wgk

WGK 1


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Green tea polyphenols increase p53 transcriptional activity and acetylation by suppressing class I histone deacetylases.
Thakur, VS; Gupta, K; Gupta, S
International journal of oncology null
Xiaowen Ge et al.
Frontiers in oncology, 11, 751904-751904 (2021-12-28)
Drug resistance remains a serious challenge to rituximab therapy in B-NHL (B cell non-Hodgkin's lymphoma). CDC (complement-dependent cytotoxicity) has been proposed as a major antitumor mechanism of rituximab, and direct abrogation of CD59 function partially restores rituximab sensitivity with high
A p53-CBP/p300 transcription module is required for GAP-43 expression, axon outgrowth, and regeneration.
Tedeschi, A; Nguyen, T; Puttagunta, R; Gaub, P; Di Giovanni, S
Cell Death and Differentiation null
Hwei-Ling Cheng et al.
Proceedings of the National Academy of Sciences of the United States of America, 100(19), 10794-10799 (2003-09-10)
SIRT1 is a mammalian homolog of the Saccharomyces cerevisiae chromatin silencing factor Sir2. Dominant-negative and overexpression studies have implicated a role for SIRT1 in deacetylating the p53 tumor suppressor protein to dampen apoptotic and cellular senescence pathways. To elucidate SIRT1
The histone acetyltransferase p300 promotes intrinsic axonal regeneration.
Gaub, P; Joshi, Y; Wuttke, A; Naumann, U; Schnichels, S; Heiduschka, P; Di Giovanni, S
Brain null

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