Rat Mutant type p53 ELISA Kit | Mt-p53 elisa kit

Rat Mutant type p53 ELISA Kit

Cat. Num. AAA722842

• Gene Names: Tp53; p53; Trp53
• Reactivity: Rat
• Synonyms: Mutant type p53; Rat Mutant type p53 ELISA Kit; Mt-p53 elisa kit

• Reactivity: Rat

• Samples: Serum, plasma, Cell Culture Supernatants, body fluid and tissue homogenate
• Preparation and Storage: Store all reagents at 2-8 degree C.

NCBI and Uniprot Product Information

• NCBI GI #: 11528486
• NCBI GeneID: 24842
• Molecular Weight: 43,451 Da
• NCBI Official Full Name: mutant p53
• NCBI Official Synonym Full Names: tumor protein p53
• NCBI Official Symbol: Tp53
• NCBI Official Synonym Symbols: p53; Trp53
• NCBI Protein Information: cellular tumor antigen p53; tumor suppressor p53; transformation related protein 53; tumor protein p53 (Li-Fraumeni syndrome)
• UniProt Protein Name: Cellular tumor antigen p53
• UniProt Gene Name: Tp53
• UniProt Synonym Gene Names: P53
• UniProt Entry Name: P53_RAT

NCBI Description

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 is 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. Alternatively spliced transcript variants have been found for this gene, but the biological validity of the variants has not been determined. p53 pseudogenes have been found on chromosomes 9 and 18. [provided by RefSeq, Jul 2008]

Uniprot Description

p53: a transcription factor and major tumor suppressor that plays a major role in regulating cellular responses to DNA damage and other genomic aberrations. Activation of p53 can lead to either cell cycle arrest and DNA repair or apoptosis. More than 50 percent of human tumors contain a mutation or deletion of the TP53 gene. p53 is modified post-translationally at multiple sites. DNA damage induces phosphorylation of p53 at S15, S20 and S37, reducing its interaction with the oncoprotein MDM2. MDM2 inhibits p53 accumulation by targeting it for ubiquitination and proteasomal degradation. Phosphorylated by many kinases including Chk2 and Chk1 at S20, enhancing its tetramerization, stability and activity. The phosphorylation by CAK at S392 is increased in human tumors and has been reported to influence the growth suppressor function, DNA binding and transcriptional activation of p53. Phosphorylation of p53 at S46 regulates the ability of p53 to induce apoptosis. The acetylation of p53 appears to play a positive role in the accumulation of p53 during the stress response. Following DNA damage, p53 becomes acetylated at K382, enhancing its binding to DNA. Deacetylation of p53 can occur through interaction with SIRT1, a deacetylase that may be involved in cellular aging and the DNA damage response. p53 regulates the transcription of a set of genes encoding endosomal proteins that regulate endosomal functions. These include STEAP3 and CHMP4C, which enhance exosome production, and CAV1 and CHMP4C, which produce a more rapid endosomal clearance of the EGFR from the plasma membrane. DNA damage regulates a p53-mediated secretory pathway, increasing the secretion of some proteins such as Hsp90, SERPINE1, SERPINB5, NKEF-A, and CyPA, and inhibiting the secretion of others including CTSL and IGFBP-2. Two alternatively spliced human isoforms have been reported. Isoform 2 is expressed in quiescent lymphocytes. Seems to be non-functional. May be produced at very low levels due to a premature stop codon in the mRNA, leading to nonsense-mediated mRNA decay.

Protein type: Transcription factor; Activator; Motility/polarity/chemotaxis; Tumor suppressor; DNA-binding; Nuclear receptor co-regulator

Cellular Component: transcription factor TFIID complex; PML body; nuclear matrix; protein complex; mitochondrion; endoplasmic reticulum; replication fork; cytosol; nucleoplasm; nuclear body; transcription factor complex; mitochondrial matrix; nuclear chromatin; cytoplasm; nucleolus; intracellular; chromatin; nucleus

Molecular Function: protein C-terminus binding; identical protein binding; protease binding; protein phosphatase 2A binding; p53 binding; protein N-terminus binding; receptor tyrosine kinase binding; transcription factor binding; protein phosphatase binding; protein kinase binding; histone acetyltransferase binding; protein binding; enzyme binding; copper ion binding; histone deacetylase regulator activity; DNA binding; protein heterodimerization activity; sequence-specific DNA binding; chaperone binding; ubiquitin protein ligase binding; double-stranded DNA binding; damaged DNA binding; chromatin binding; transcription factor activity; ATP binding

Biological Process: central nervous system development; positive regulation of apoptosis; regulation of cell cycle; positive regulation of leukocyte migration; positive regulation of transcription, DNA-dependent; multicellular organismal development; T cell differentiation in the thymus; gastrulation; determination of adult life span; DNA damage response, signal transduction by p53 class mediator resulting in cell cycle arrest; response to organic cyclic substance; response to caffeine; regulation of apoptosis; response to antibiotic; cellular response to glucose starvation; protein localization; negative regulation of neuroblast proliferation; transforming growth factor beta receptor signaling pathway; response to vitamin B3; regulation of neuron apoptosis; cerebellum development; negative regulation of mitotic cell cycle; protein complex assembly; cell cycle arrest; ER overload response; response to X-ray; response to UV; response to drug; somitogenesis; release of cytochrome c from mitochondria; chromatin assembly; cell aging; positive regulation of cell cycle; response to organic nitrogen; response to amino acid stimulus; circadian behavior; rRNA transcription; regulation of transcription from RNA polymerase II promoter; positive regulation of peptidyl-tyrosine phosphorylation; negative regulation of fibroblast proliferation; negative regulation of DNA replication; regulation of intracellular pH; embryonic organ development; positive regulation of transcription from RNA polymerase II promoter; response to oxidative stress; negative regulation of transcription, DNA-dependent; regulation of tissue remodeling; negative regulation of apoptosis; transcription from RNA polymerase II promoter; G1 DNA damage checkpoint; response to metal ion; wound healing; DNA damage response, signal transduction by p53 class mediator; negative regulation of smooth muscle cell proliferation; apoptosis; negative regulation of transcription from RNA polymerase II promoter; chromosome organization and biogenesis; response to salt stress; entrainment of circadian clock by photoperiod; embryonic development ending in birth or egg hatching; negative regulation of cell proliferation; positive regulation of protein oligomerization; positive regulation of histone deacetylation; DNA damage response, signal transduction by p53 class mediator resulting in transcription of p21 class mediator; regulation of transcription, DNA-dependent; T cell proliferation during immune response; regulation of catalytic activity; positive regulation of neuron apoptosis; double-strand break repair; response to gamma radiation; DNA damage response, signal transduction by p53 class mediator resulting in induction of apoptosis; protein tetramerization; aging; negative regulation of proteolysis; mitochondrial DNA repair; response to inorganic substance; response to retinoic acid; in utero embryonic development; multicellular organism growth; B cell lineage commitment; response to UV-B; regulation of cell proliferation; T cell lineage commitment; neuron apoptosis; response to hyperoxia; protein import into nucleus, translocation; nucleotide-excision repair; response to cytokine stimulus; Ras protein signal transduction; DNA strand renaturation; negative regulation of cell growth; negative regulation of transforming growth factor beta receptor signaling pathway; response to DNA damage stimulus