User:JonSDSUGrad/Sandbox/TEST6 TP53

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tumor protein p53 (Li-Fraumeni syndrome)
PDB rendering based on 1a1u.
Available structures: 1a1u, 1aie, 1c26, 1gzh, 1hs5, 1kzy, 1olg, 1olh, 1pes, 1pet, 1sae, 1saf, 1sag, 1sah, 1sai, 1saj, 1sak, 1sal, 1tsr, 1tup, 1uol, 1ycs, 2ac0, 2ady, 2ahi, 2ata, 2b3g, 2bim, 2bin, 2bio, 2bip, 2biq, 2fej, 2gs0, 2h1l, 2j1w, 2j1x, 2j1y, 2j1z, 2j20, 2j21, 2ocj, 3sak
Identifiers
Symbol(s) TP53; LFS1; TRP53; p53
External IDs OMIM: 191170 MGI98834 HomoloGene460
Orthologs
Human Mouse
Entrez 7157 22059
Ensembl ENSG00000141510 ENSMUSG00000059552
Uniprot P04637 n/a
Refseq NM_000546 (mRNA)
NP_000537 (protein)
NM_011640 (mRNA)
NP_035770 (protein)
Location Chr 17: 7.51 - 7.53 Mb Chr 11: 69.4 - 69.41 Mb
Pubmed search [1] [2]

[edit] Summary

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.[1]

[edit] References

  1. ^ Entrez Gene: TP53 tumor protein p53 (Li-Fraumeni syndrome). Retrieved on 2007-08-07.

[edit] Further Reading