P73
From Proteopedia
(Difference between revisions)
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{{STRUCTURE_2xwc| PDB=2xwc | SIZE=400| SCENE= |right|CAPTION=Monomer of the dimeric human p73 DNA-binding domain complex with Tris, glycerol and Zn+2 ion (grey), [[2xwc]] }} | {{STRUCTURE_2xwc| PDB=2xwc | SIZE=400| SCENE= |right|CAPTION=Monomer of the dimeric human p73 DNA-binding domain complex with Tris, glycerol and Zn+2 ion (grey), [[2xwc]] }} | ||
- | '''p73''' is a protein related to p53 tumor suppressor. It is involved in cell cycle regulation and induction of apoptosis. | + | '''p73''' is a protein related to p53 tumor suppressor. It is involved in cell cycle regulation and induction of apoptosis<ref>PMID:9891077</ref>. p73 has several variants differing in their C- or N-terminal. p73 contains DNA-binding domain (DBD residues 112-312); tetramerization domain (TD residues 351-398). |
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== 3D Structures of p73 == | == 3D Structures of p73 == | ||
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[[3vd0]], [[3vd1]], [[3vd2]], [[4g82]], [[4g83]], [[4guo]], [[4guq]] – hp73 DBD + DNA<br /> | [[3vd0]], [[3vd1]], [[3vd2]], [[4g82]], [[4g83]], [[4guo]], [[4guq]] – hp73 DBD + DNA<br /> | ||
[[4a63]] – hp73 DBD + apoptosis stimulating of p53 protein<br /> | [[4a63]] – hp73 DBD + apoptosis stimulating of p53 protein<br /> | ||
- | + | == References == | |
+ | <references/> | ||
[[Category:Topic Page]] | [[Category:Topic Page]] |
Revision as of 10:13, 13 June 2016
p73 is a protein related to p53 tumor suppressor. It is involved in cell cycle regulation and induction of apoptosis[1]. p73 has several variants differing in their C- or N-terminal. p73 contains DNA-binding domain (DBD residues 112-312); tetramerization domain (TD residues 351-398).
3D Structures of p73
Updated on 13-June-2016
1cok – hp73 C terminal – human – NMR
2kby – hp73 TD – NMR
2xwc – hp73 DBD (mutant)
3vd0, 3vd1, 3vd2, 4g82, 4g83, 4guo, 4guq – hp73 DBD + DNA
4a63 – hp73 DBD + apoptosis stimulating of p53 protein
References
- ↑ Di Como CJ, Gaiddon C, Prives C. p73 function is inhibited by tumor-derived p53 mutants in mammalian cells. Mol Cell Biol. 1999 Feb;19(2):1438-49. PMID:9891077