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Use Anti-acetyl-p53 (Lys320) Antibody (Rabbit Polyclonal Antibody) validated in WB to detect acetyl-p53 (Lys320) also known as Antigen NY-CO-13, Phosphoprotein p53, Tumor suppressor p53, p53 antigen.
More>>Use Anti-acetyl-p53 (Lys320) Antibody (Rabbit Polyclonal Antibody) validated in WB to detect acetyl-p53 (Lys320) also known as Antigen NY-CO-13, Phosphoprotein p53, Tumor suppressor p53, p53 antigen. Less<<
Anti-acetyl-p53 (Lys320) Antibody: SDB (Sicherheitsdatenblätter), Analysenzertifikate und Qualitätszertifikate, Dossiers, Broschüren und andere verfügbare Dokumente.
p53 was discovered in 1979 as a cellular protein associating with the transforming protein of SV40 tumor virus. Since then, many different biochemical functions have been attributed to the 53 kD phosphoprotein. Experimental evidence has suggested that p53 acts as a negative regulator of cell growth in normal cells (Finlay, 1989). Thus, the inactivation or mutation of p53 may be an essential step in the development of malignancy (Lane and Benchmol, 1990). Wild-type p53 levels in normal cells and tissues were found to be very low. Mutant p53 polypeptide, however, is often found to be present at high concentrations in mammalian tumors and tumor cell lines. For example, in an immuno-histochemistry study 40% of human breast cancer showed elevated levels of mutant p53 in the cell nucleus. Mutations of the p53 protein have some characteristic features: a) Most of them are missense point mutations giving rise to an altered protein function. b) Many -but not all- mutant p53 proteins exhibit a common mutant structure, which can be recognized by monoclonal antibodies specific for p53 in the mutant conformation.
References
Product Information
Format
Affinity Purified
Control
Recombinant proteins
Presentation
Purified rabbit polyclonal in buffer containing 0.1 M Tris-Glycine (pH 7.4), 150 mM NaCl with 0.05% sodium azide.
Use Anti-acetyl-p53 (Lys320) Antibody (Rabbit Polyclonal Antibody) validated in WB to detect acetyl-p53 (Lys320) also known as Antigen NY-CO-13, Phosphoprotein p53, Tumor suppressor p53, p53 antigen.
Key Applications
Western Blotting
Application Notes
Western Blot Analysis: 5 µg/mL antibody detected p53 on 10 µg of A549 cells treated with UV & TSA lysate.
Western Blot (SNAP ID) Analysis: 5 µg/mL antibody detected p53 on 10 µg of recombinant proteins.
Biological Information
Immunogen
KLH-conjugated linear peptide corresponding to p53 at Lys320.
Epitope
Acetyl Lys 320
Concentration
Please refer to the Certificate of Analysis for the lot-specific concentration.
Host
Rabbit
Specificity
This antibody recognizes p53 acetylated at Lys320.
Species Reactivity
Human
Chimpanzee
Bovine
Species Reactivity Note
Demonstrated to react with human. Predicted to react with chimpanzee and bovine based on 100% sequence homology.
This gene encodes tumor protein p53, which responds to diverse cellular stresses to regulate target genes that induce cell cycle arrest, apoptosis, senescence, DNA repair, or changes in metabolism. p53 protein is expressed at low level in normal cells and at a high level in a variety of transformed cell lines, where it's believed to contribute to transformation and malignancy. p53 is a DNA-binding protein containing transcription activation, DNA-binding, and oligomerization domains. It is postulated to bind 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 this gene occur not only as somatic mutations in human malignancies, but also as germline mutations in some cancer-prone families with Li-Fraumeni syndrome. Multiple p53 variants due to alternative promoters and multiple alternative splicing have been found. These variants encode distinct isoforms, which can regulate p53 transcriptional activity. [provided by RefSeq].
FUNCTION: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. Implicated in Notch signaling cross-over.
Cofactor Binds 1 zinc ion per subunit.
SUBUNIT STRUCTURE: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. Interacts (via C-terminus) with TAF1; when TAF1 is part of the TFIID complex. Interacts with ING4; this interaction may be indirect. Found in a complex with CABLES1 and TP73. Interacts with HIPK1, HIPK2, and P53DINP1. Interacts with WWOX. May interact with HCV core protein. Interacts with USP7 and SYVN1. Interacts with HSP90AB1. Interacts with CHD8; leading to recruit histone H1 and prevent transactivation activity By similarity. Interacts with ARMC10, BANP, CDKN2AIP and E4F1. Interacts with YWHAZ; the interaction enhances TP53 transcriptional activity. Phosphorylation of YWHAZ on 'Ser-58' inhibits this interaction. Interacts (via DNA-binding domain) with MAML1 (via N-terminus). Interacts with MKRN1. Directly interacts with FBXO42; leading to ubiquination and degradation of TP53. Interacts (phosphorylated at Ser-15 by ATM) with the phosphatase PP2A-PPP2R5C holoenzyme; regulates stress-induced TP53-dependent inhibition of cell proliferation. Interacts with PPP2R.
DOMAIN: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. Phosphorylation at Ser-9 by HIPK4 increases repression activity on BIRC5 promoter. 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-PPP2R5C holoenzyme at Thr-55. 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. Ubiquitinated by MKRN1 at Lys-291 and Lys-292, which leads to proteasomal degradation. Monomethylated at Lys-372 by SETD7, leading to stabilization and increased transcriptional activation. Monomethylated at Lys-370 by SMYD2, leading to decreased DNA-binding activity and subsequent transcriptional regulation activity. Lys-372 monomethylation prevents interaction with SMYD2 and subsequent monomethylation at Lys-370
Sumoylated by SUMO1. Demethylation of di-methylated Lys-370 by KDM1/LSD1 prevents interaction with TP53BP1 and represses TP53-mediated transcriptional activation.
INVOLVEMENT IN DISEASE: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 a proband affected by a sarcoma before 45 years with a first degree relative affected by any tumor before 45 years and another first degree relative with any tumor before 45 years or a sarcoma at any age. Other clinical definitions for LFS have been proposed (Ref.107 and Ref.110) and called Li-Fraumeni like syndrome (LFL). In these families affected relatives develop a diverse set of malignancies at unusually early ages. Four types of cancers account for 80% of tumors occurring in TP53 germline mutation carriers: breast cancers, soft tissue and bone sarcomas, brain tumors (astrocytomas) and adrenocortical carcinomas. Less frequent tumors include choroid plexus carcinoma or papilloma before the age of 15, rhabdomyosarcoma before the age of 5, leukemia, Wilms tumor, malignant phyllodes tumor, colorectal and gastric cancers.
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]; also known as squamous cell carcinoma of the head and neck.
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].
SEQUENCE SIMILARITIES: Belongs to the p53 family.
Molecular Weight
~ 53 kDa observed. Western Blot of A549 cells treated with UV & TSA show bands at ~48 kDa and ~14 kDa which are likely breakdown products of p53 reported for UV treated cells. (Sadji-Ouatas, 2002)
Physicochemical Information
Dimensions
Materials Information
Toxicological Information
Safety Information according to GHS
Safety Information
Product Usage Statements
Quality Assurance
Evaluated by Western Blotting using A549 cells treated with UV & TSA. Western Blotting Analysis: 5 µg/mL of a representative lot of this antibody detected p53 on 10 µg of A549 cells treated with UV & TSA lysate.
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.
Since inactivation of tumor suppressor p53 functions is one of the most common features of human cancer cells, restoring p53 expression and activity is an important focus in cancer therapy. Here we report identification of photoreceptor-specific nuclear receptor (PNR)/NR2E3 as a positive regulator of p53 in a high-throughput genetic screen. In HeLa cells, PNR stimulated p53-responsive promoters in a p53-dependent fashion and induced apoptosis in several cell types. PNR also increased p53 protein stability and specific activity as a transcriptional activator. Our studies of the underlying mechanisms showed that PNR forms complexes with p53 and the acetyltransferase p300, stimulates p53 acetylation, and increases the expression of a subset of p53 target genes. Furthermore, PNR significantly boosted actinomycin D-stimulated p53 acetylation. The unique mechanisms by which PNR stimulates p53 acetylation and functions define this orphan nuclear receptor as a potentially valuable target and tool in p53-associated cancer therapy and offer new insights into the roles of PNR mutation in retinal diseases.
Millipore’s p53 antibodies demonstrate specificity against tumor antigen p53. See below for antibodies, kits, proteins and more for p53 research, based on the expertise of Upstate & Chemicon. Weitere Informationen >>
