06-916
Anti-acetyl-p53 (Lys373) Antibody
serum, Upstate®
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About This Item
Código UNSPSC:
12352203
eCl@ss:
32160702
NACRES:
NA.41
Produtos recomendados
fonte biológica
rabbit
Nível de qualidade
forma do anticorpo
serum
tipo de produto de anticorpo
primary antibodies
clone
polyclonal
reatividade de espécies
human
fabricante/nome comercial
Upstate®
técnica(s)
immunoprecipitation (IP): suitable
western blot: suitable
Isotipo
IgG
nº de adesão NCBI
nº de adesão UniProt
Condições de expedição
wet ice
modificação pós-traducional do alvo
acetylation (Lys373)
Informações sobre genes
human ... TP53(7157)
Descrição geral
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.
Especificidade
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.
Imunogênio
peptide corresponding to amino acids 367-379 of human p53 (SHLKSKACKGQSTSR, where ACK denotes acetyl-lysine).
Aplicação
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.
Qualidade
routinely evaluated by immunoblot on GST-p53 acetylated by recombinant p300, HAT domain (Catalog #14-418) in an in vitro acetyl transferase assay
Descrição-alvo
53 kDa
Ligação
Replaces: 04-1137
forma física
Protein A Purified immunoglobulin in 0.1M Tris-glycine, pH 7.4, 0.15M NaCl, 0.02% sodium azide, 0.1mg/ml BSA
Outras notas
Concentration: Please refer to the Certificate of Analysis for the lot-specific concentration.
Informações legais
UPSTATE is a registered trademark of Merck KGaA, Darmstadt, Germany
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Código de classe de armazenamento
10 - Combustible liquids
Classe de risco de água (WGK)
WGK 1
Certificados de análise (COA)
Busque Certificados de análise (COA) digitando o Número do Lote do produto. Os números de lote e remessa podem ser encontrados no rótulo de um produto após a palavra “Lot” ou “Batch”.
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Encontre a documentação dos produtos que você adquiriu recentemente na biblioteca de documentos.
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
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
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
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
Deacetylation of p53 after nerve growth factor treatment in PC12 cells as a post-translational modification mechanism of neurotrophin-induced tumor suppressor activation.
Vaghefi, H; Neet, KE
Oncogene null
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