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48-602MAG
Buffer Detection Kit for Magnetic Beads
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Detect acetyl-p53 (Lys373) with Anti-acetyl-p53 Antibody (Lys373, Lys382) (Rabbit Polyclonal Antibody), that has been shown to work in WB.
More>>Detect acetyl-p53 (Lys373) with Anti-acetyl-p53 Antibody (Lys373, Lys382) (Rabbit Polyclonal Antibody), that has been shown to work in WB. Less<<
Anti-acetyl-p53 (Lys373 Antibody, Lys382): SDB (Sicherheitsdatenblätter), Analysenzertifikate und Qualitätszertifikate, Dossiers, Broschüren und andere verfügbare Dokumente.
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.
Detect acetyl-p53 (Lys373) with Anti-acetyl-p53 Antibody (Lys373, Lys382) (Rabbit Polyclonal Antibody), that has been shown to work in WB.
Key Applications
Western Blotting
Application Notes
Western Blot (on recombinant protein only)
Biological Information
Immunogen
peptide of human p53 corresponding to amino acids 368-389 with a duplication of amino acids 376 and 377 (HLKSKACKGQSTSTSRHKACKLMFKTC) where ACK denotes acetyl-lysine
Concentration
Please refer to lot specific datasheet.
Host
Rabbit
Specificity
Recognizes p53 acetylated in vitro by recombinant p300, and for peptide containing acetyl-lysine 373 but not for the peptide containing acetyl-lysine 320.
Tumor protein p53, a nuclear protein, plays an essential role in the regulation of cell cycle, specifically in the transition from G0 to G1. It is found in very low levels in normal cells, however, in a variety of transformed cell lines, it is expressed in high amounts, and believed to contribute to transformation and malignancy. p53 is a DNA-binding protein containing DNA-binding, oligomerization and transcription activation domains. It is postulated to bind as a tetramer to a p53-binding site and activate expression of downstream genes that inhibit growth and/or invasion, and thus function as a tumor suppressor. Mutants of p53 that frequently occur in a number of different human cancers fail to bind the consensus DNA binding site, and hence cause the loss of tumor suppressor activity. Alterations of the TP53 gene occur not only as somatic mutations in human malignancies, but also as germline mutations in some cancer-prone families with Li-Fraumeni syndrome.
FUNCTION: SwissProt: P04637 # Acts as a tumor suppressor in many tumor types; induces growth arrest or apoptosis depending on the physiological circumstances and cell type. Involved in cell cycle regulation as a trans-activator that acts to negatively regulate cell division by controlling a set of genes required for this process. One of the activated genes is an inhibitor of cyclin-dependent kinases. Apoptosis induction seems to be mediated either by stimulation of BAX and FAS antigen expression, or by repression of Bcl-2 expression. COFACTOR: Binds 1 zinc ion per subunit. SIZE: 393 amino acids; 43653 Da SUBUNIT: Interacts with AXIN1. Probably part of a complex consisting of TP53, HIPK2 and AXIN1 (By similarity). Binds DNA as a homotetramer. Interacts with histone acetyltransferases EP300 and methyltransferases HRMT1L2 and CARM1, and recruits them to promoters. In vitro, the interaction of TP53 with cancer- associated/HPV (E6) viral proteins leads to ubiquitination and degradation of TP53 giving a possible model for cell growth regulation. This complex formation requires an additional factor, E6-AP, which stably associates with TP53 in the presence of E6. C- terminus interacts with TAF1, when TAF1 is part of the TFIID complex. Interacts with ING4 and this interaction may be indirect. Found in a complex with CABLES1 and TP73. Interacts with HIPK1, HIPK2, and P53DINP1. Interacts with WWOX. May interacts with HCV core protein. Interacts with USP7 and SYVN1. Interacts with HSP90AB1 (By similarity). Interacts with BANP. SUBCELLULAR LOCATION: Cytoplasm. Nucleus. Endoplasmic reticulum. Note=Interaction with BANP promotes nuclear localization. DOMAIN: SwissProt: P04637 The nuclear export signal acts as a transcriptional repression domain. PTM: Acetylated. Acetylation of Lys-382 by CREBBP enhances transcriptional activity. Deacetylation of Lys-382 by SIRT1 impairs its ability to induce proapoptotic program and modulate cell senescence. & Phosphorylation on Ser residues mediates transcriptional activation. Phosphorylated by HIPK1 (By similarity). Phosphorylated on Thr-18 by VRK1, which may prevent the interaction with MDM2. Phosphorylated on Thr-55 by TAF1, which promotes MDM2-mediated degradation. Phosphorylated on Ser-46 by HIPK2 upon UV irradiation. Phosphorylation on Ser-46 is required for acetylation by CREBBP. Phosphorylated on Ser-392 following UV but not gamma irradiation. Phosphorylated upon DNA damage, probably by ATM or ATR. Phosphorylated on Ser-15 upon ultraviolet irradiation; which is enhanced by interaction with BANP. & Dephosphorylated by PP2A. SV40 small T antigen inhibits the dephosphorylation by the AC form of PP2A. & May be O-glycosylated in the C-terminal basic region. Studied in EB-1 cell line. & Ubiquitinated by SYVN1, which leads to proteasomal degradation. DISEASE: SwissProt: P04637 # TP53 is found in increased amounts in a wide variety of transformed cells. TP53 is frequently mutated or inactivated in about 60% of cancers. & Defects in TP53 are involved in esophageal squamous cell carcinoma (ESCC) [MIM:133239]. ESCC is a tumor of the esophagus. & Defects in TP53 are a cause of Li-Fraumeni syndrome (LFS) [MIM:151623]. LFS is an autosomal dominant familial cancer syndrome that in its classic form is defined by the existence of both a proband with a sarcoma and two other first-degree relatives with a cancer by age 45 years. In these families the affected relatives develop a diverse set of malignancies at unusually early ages. The spectrum of cancers in LFS includes breast carcinomas, soft-tissue sarcomas, brain tumors, osteosarcoma, leukemia and adreno-cortical carcinoma. Other possible component tumors of LFS are melanoma, gonadal cell tumors and carcinomas of the lung, pancreas and prostate. & Defects in TP53 may be associated with nasopharyngeal carcinoma [MIM:161550]; also known as nasopharyngeal cancer. & Defects in TP53 are found in Barrett metaplasia; also known as Barrett esophagus. It is a condition in which the normally stratified squamous epithelium of the lower esophagus is replaced by a metaplastic columnar epithelium. The condition develops as a complication in approximately 10% of patients with chronic gastroesophageal reflux disease and predisposes to the development of esophageal adenocarcinoma. & Defects in TP53 are involved in head and neck squamous cell carcinomas (HNSCC) [MIM:275355]. & Defects in TP53 are involved in oral squamous cell carcinoma (OSCC). Cigarette smoke is a prime mutagenic agent in cancer of the aerodigestive tract. & Defects in TP53 are a cause of lung cancer [MIM:211980]. & Defects in TP53 are a cause of choroid plexus papilloma [MIM:260500]. Choroid plexus papilloma is a slow-growing benign tumor of the choroid plexus that often invades the leptomeninges. In children it is usually in a lateral ventricle but in adults it is more often in the fourth ventricle. Hydrocephalus is common, either from obstruction or from tumor secretion of cerebrospinal fluid. If it undergoes malignant transformation it is called a choroid plexus carcinoma. Primary choroid plexus tumors are rare and usually occur in early childhood. & Defects in TP53 are a cause of one form of hereditary adrenocortical carcinoma (ADCC) [MIM:202300]. ADCC is a rare childhood tumor, representing about 0.4% of childhood tumors, with a high incidence of associated tumors. ADCC occurs with increased frequency in patients with the Beckwith-Wiedemann syndrome [MIM:130650] and is a component tumor in Li-Fraumeni syndrome [MIM:151623]. SIMILARITY: Belongs to the p53 family.
Molecular Weight
53 kDa
Physicochemical Information
Dimensions
Materials Information
Toxicological Information
Safety Information according to GHS
Safety Information
Product Usage Statements
Quality Assurance
routinely evaluated by an in vitro acetyl transferase assay on recombinant p300, HAT domain (Catalog #14-418)
Usage Statement
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
Storage and Shipping Information
Storage Conditions
Maintain for 2 years at -20°C from date of shipment. Aliquot to avoid repeated freezing and thawing. For maximum recovery of product, centrifuge the original vial after thawing and prior to removing the cap.