06-916
Anti-acetyl-p53 (Lys373) Antibody
serum, Upstate®
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About This Item
Code UNSPSC :
12352203
eCl@ss :
32160702
Nomenclature NACRES :
NA.41
Produits recommandés
Source biologique
rabbit
Niveau de qualité
Forme d'anticorps
serum
Type de produit anticorps
primary antibodies
Clone
polyclonal
Espèces réactives
human
Fabricant/nom de marque
Upstate®
Technique(s)
immunoprecipitation (IP): suitable
western blot: suitable
Isotype
IgG
Numéro d'accès NCBI
Numéro d'accès UniProt
Conditions d'expédition
wet ice
Modification post-traductionnelle de la cible
acetylation (Lys373)
Informations sur le gène
human ... TP53(7157)
Description générale
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.
Spécificité
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.
Immunogène
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.
Qualité
routinely evaluated by immunoblot on GST-p53 acetylated by recombinant p300, HAT domain (Catalog #14-418) in an in vitro acetyl transferase assay
Description de la cible
53 kDa
Liaison
Replaces: 04-1137
Forme physique
Protein A Purified immunoglobulin in 0.1M Tris-glycine, pH 7.4, 0.15M NaCl, 0.02% sodium azide, 0.1mg/ml BSA
Autres remarques
Concentration: Please refer to the Certificate of Analysis for the lot-specific concentration.
Informations légales
UPSTATE is a registered trademark of Merck KGaA, Darmstadt, Germany
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Code de la classe de stockage
10 - Combustible liquids
Classe de danger pour l'eau (WGK)
WGK 1
Certificats d'analyse (COA)
Recherchez un Certificats d'analyse (COA) en saisissant le numéro de lot du produit. Les numéros de lot figurent sur l'étiquette du produit après les mots "Lot" ou "Batch".
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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
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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