TRP53

Trp53 is 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. Trp53 is postulated to bind to a p53-binding site and activate expression of downstream genes that inhibit growth and/or invasion, and thus play a role as a tumor suppressor. Mice deficient for Trp53 are developmentally normal but are susceptible to spontaneous tumors.

Transformation Related Protein 53

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.

Biological Process autophagy Source:Ensembl
Biological Process bone marrow development Source:Ensembl
Biological Process cellular response to actinomycin D Source:Ensembl
Biological Process cellular response to gamma radiation Source:Ensembl
Biological Process cellular response to glucose starvation Source:Ensembl
Biological Process cellular response to hypoxia Source:Ensembl
Biological Process cellular response to UV Source:Ensembl
Biological Process cellular response to xenobiotic stimulus Source:Ensembl
Biological Process chromatin assembly Source:Ensembl
Biological Process DNA damage response, signal transduction by p53 class mediator resulting in cell cycle arrest Source:Ensembl
Biological Process DNA damage response, signal transduction by p53 class mediator resulting in transcription of p21 class mediator Source:Ensembl
Biological Process ER overload response Source:Ensembl
Biological Process hematopoietic stem cell differentiation Source:Ensembl
Biological Process intrinsic apoptotic signaling pathway in response to DNA damage by p53 class mediator Source:Ensembl
Biological Process mRNA transcription Source:Ensembl
Biological Process negative regulation of apoptotic process Source:Ensembl
Biological Process negative regulation of cell growth Source:Ensembl
Biological Process negative regulation of fibroblast proliferation Source:Ensembl
Biological Process negative regulation of G1 to G0 transition Source:Ensembl
Biological Process negative regulation of pentose-phosphate shunt Source:Ensembl
Biological Process negative regulation of telomerase activity Source:Ensembl
Biological Process nervous system development Source:UniProt
Biological Process nucleotide-excision repair Source:Ensembl
Biological Process oligodendrocyte apoptotic process Source:Ensembl
Biological Process oxidative stress-induced premature senescence Source:Ensembl
Biological Process positive regulation of execution phase of apoptosis Source:Ensembl
Biological Process positive regulation of intrinsic apoptotic signaling pathway Source:Ensembl
Biological Process positive regulation of miRNA maturation Source:Ensembl
Biological Process positive regulation of miRNA transcription Source:Ensembl
Biological Process positive regulation of reactive oxygen species metabolic process Source:Ensembl
Biological Process positive regulation of release of cytochrome c from mitochondria Source:Ensembl
Biological Process positive regulation of RNA polymerase II transcription preinitiation complex assembly Source:Ensembl
Biological Process positive regulation of transcription from RNA polymerase II promoter in response to stress Source:Ensembl
Biological Process protein localization Source:Ensembl
Biological Process protein tetramerization Source:InterPro
Biological Process Ras protein signal transduction Source:Ensembl
Biological Process regulation of cell cycle G2/M phase transition Source:Ensembl
Biological Process regulation of transcription from RNA polymerase II promoter in response to DNA damage Source:Ensembl
Biological Process replicative senescence Source:Ensembl
Biological Process rhythmic process Source:UniProtKB-KW
Biological Process tumor necrosis factor-mediated signaling pathway Source:Ensembl
Biological Process viral process Source:Ensembl

Cytoplasm
Nucleus
Endoplasmic reticulum
Mitochondrion matrix
Nucleus, PML body