antibody

Rabbit anti-human Cellular tumor antigen p53 polyclonal Antibody, FITC conjugate

MBS1498334

0.05 mg

160 USD

polyclonal

rabbit

FITC

ELISA, enzyme immunoassay

Antibody

Rabbit anti-human Cellular tumor antigen p53 polyclonal Antibody, FITC conjugate

[Cellular tumor antigen p53]

[Antigen NY-CO-13; Phosphoprotein p53; Tumor suppressor p53; TP53; P53]

[cellular tumor antigen p53 isoform a; Cellular tumor antigen p53; cellular tumor antigen p53; tumor protein p53; Antigen NY-CO-13; Phosphoprotein p53; Tumor suppressor p53]

[TP53; TP53; P53; BCC7; LFS1; TRP53; P53]

P53_HUMAN

Polyclonal

IgG

Rabbit

Human

393

>95%, Protein G Purified

Liquid

Upon receipt, store at -20 degree C or -80 degree C. Avoid repeated freeze.

ELISA (EIA)

Storage Buffer: Preservative: 0.03% Proclin 300. Constituents: 50% Glycerol, 0.01M PBS, PH 7.4. Conjugate: FITC

Immunogen: Recombinant human Cellular tumor antigen p53 protein(2-393AA). Species: Homo sapiens (Human). Research Area: Cell Biology. Santa Cruz Alternative: Potential replacement for Santa Cruz Biotechnology antibody catalog# sc-1314 / sc-1311-R / sc-6243

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. In cooperation with mitochondrial PPIF is involved in activating oxidative stress-induced necrosis; the function is largely independent of transcription. Induces the transcription of long intergenic non-coding RNA p21 (lincRNA-p21) and lincRNA-Mkln1. LincRNA-p21 participates in TP53-dependent transcriptional repression leading to apoptosis and seem to have to effect on cell-cycle regulation. Implicated in Notch signaling cross-over. Prevents CDK7 kinase activity when associated to CAK complex in response to DNA damage, thus stopping cell cycle progression. Isoform 2 enhances the transactivation activity of isoform 1 from some but not all TP53-inducible promoters. Isoform 4 suppresses transactivation activity and impairs growth suppression mediated by isoform 1. Isoform 7 inhibits isoform 1-mediatedapoptosis.

120407068

NP_000537.3

NM_000546.5

P04637

AMPK Signaling Pathway (198868); Activation Of BH3-only Proteins Pathway (1270270); Activation Of NOXA And Translocation To Mitochondria Pathway (1270272); Activation Of PUMA And Translocation To Mitochondria Pathway (1270273); Alzheimers Disease Pathway (672448); Amyotrophic Lateral Sclerosis (ALS) Pathway (920975); Amyotrophic Lateral Sclerosis (ALS) Pathway (83099); Amyotrophic Lateral Sclerosis (ALS) Pathway (511); Apoptosis Pathway (198797); Apoptosis Pathway (83060)

This gene encodes a tumor suppressor protein containing transcriptional activation, DNA binding, and oligomerization domains. The encoded protein responds to diverse cellular stresses to regulate expression of target genes, thereby inducing cell cycle arrest, apoptosis, senescence, DNA repair, or changes in metabolism. Mutations in this gene are associated with a variety of human cancers, including hereditary cancers such as Li-Fraumeni syndrome. Alternative splicing of this gene and the use of alternate promoters result in multiple transcript variants and isoforms. Additional isoforms have also been shown to result from the use of alternate translation initiation codons (PMIDs: 12032546, 20937277). [provided by RefSeq, Feb 2013]

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: DNA-binding; Transcription factor; Tumor suppressor; Activator; Motility/polarity/chemotaxis; Nuclear receptor co-regulator. Chromosomal Location of Human Ortholog: 17p13.1. Cellular Component: cytoplasm; cytosol; endoplasmic reticulum; mitochondrial matrix; mitochondrion; nuclear body; nuclear chromatin; nuclear matrix; nucleolus; nucleoplasm; nucleus; PML body; protein complex; replication fork; transcription factor TFIID complex. Molecular Function: ATP binding; chaperone binding; chromatin binding; copper ion binding; damaged DNA binding; DNA binding; double-stranded DNA binding; enzyme binding; histone acetyltransferase binding; histone deacetylase regulator activity; identical protein binding; p53 binding; protease binding; protein binding; protein heterodimerization activity; protein kinase binding; protein N-terminus binding; protein phosphatase 2A binding; protein phosphatase binding; protein self-association; receptor tyrosine kinase binding; sequence-specific DNA binding; transcription factor activity; transcription factor binding; ubiquitin protein ligase binding; zinc ion binding. Biological Process: apoptosis; B cell lineage commitment; base-excision repair; blood coagulation; cell aging; cell cycle arrest; cell differentiation; cell proliferation; cellular response to glucose starvation; cerebellum development; chromatin assembly; chromosome breakage; circadian behavior; determination of adult life span; DNA damage response, signal transduction by p53 class mediator; DNA damage response, signal transduction by p53 class mediator resulting in cell cycle arrest; DNA damage response, signal transduction by p53 class mediator resulting in induction of apoptosis; DNA damage response, signal transduction by p53 class mediator resulting in transcription of p21 class mediator; DNA repair; DNA strand renaturation; double-strand break repair; embryonic organ development; entrainment of circadian clock by photoperiod; ER overload response; G1 DNA damage checkpoint; gastrulation; gene expression; in utero embryonic development; mitochondrial DNA repair; multicellular organism growth; multicellular organismal development; negative regulation of apoptosis; negative regulation of cell growth; negative regulation of cell proliferation; negative regulation of fibroblast proliferation; negative regulation of helicase activity; negative regulation of neuroblast proliferation; negative regulation of proteolysis; negative regulation of telomerase activity; negative regulation of transcription from RNA polymerase II promoter; negative regulation of transcription, DNA-dependent; negative regulation of transforming growth factor beta receptor signaling pathway; neuron apoptosis; Notch signaling pathway; nucleotide-excision repair; positive regulation of apoptosis; positive regulation of histone deacetylation; positive regulation of neuron apoptosis; positive regulation of peptidyl-tyrosine phosphorylation; positive regulation of protein oligomerization; positive regulation of transcription from RNA polymerase II promoter; positive regulation of transcription, DNA-dependent; programmed cell death; protein complex assembly; protein import into nucleus, translocation; protein localization; protein tetramerization; Ras protein signal transduction; regulation of apoptosis; regulation of mitochondrial membrane permeability; regulation of tissue remodeling; regulation of transcription, DNA-dependent; release of cytochrome c from mitochondria; response to antibiotic; response to DNA damage stimulus; response to gamma radiation; response to salt stress; response to X-ray; rRNA transcription; somitogenesis; T cell differentiation in the thymus; T cell lineage commitment; T cell proliferation during immune response; transcription initiation from RNA polymerase II promoter; transforming growth factor beta receptor signaling pathway; viral reproduction. Disease: Adrenocortical Carcinoma, Hereditary; Basal Cell Carcinoma, Susceptibility To, 7; Breast Cancer; Colorectal Cancer; Glioma Susceptibility 1; Hepatocellular Carcinoma; Li-fraumeni Syndrome 1; Nasopharyngeal Carcinoma; Osteogenic Sarcoma; Pancreatic Cancer; Papilloma Of Choroid Plexus

0.05 mg

160 USD

0.1 mg

235