1a5e
From Proteopedia
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|ACTIVITY= | |ACTIVITY= | ||
|GENE= | |GENE= | ||
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| + | |RESOURCES=<span class='plainlinks'>[http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1a5e FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1a5e OCA], [http://www.ebi.ac.uk/pdbsum/1a5e PDBsum], [http://www.rcsb.org/pdb/explore.do?structureId=1a5e RCSB]</span> | ||
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==Overview== | ==Overview== | ||
The solution structure of the tumor suppressor p16INK4A has been determined by NMR, and important recognition regions of both cdk4 and p16INK4A have been identified. The tertiary structure of p16INK4A contains four helix-turn-helix motifs linked by three loops. Twelve tumorigenic mutants of p16INK4A have been constructed and analyzed for their structure and activity, and new mutants have been designed rationally. A fragment of 58 residues at the N terminus of cdk4 important for p16INK4A binding has been identified. The importance of this region was further verified by mutational analysis of cdk4. These results and docking experiments have been used to assess possible modes of binding between p16INK4A and cdk4. | The solution structure of the tumor suppressor p16INK4A has been determined by NMR, and important recognition regions of both cdk4 and p16INK4A have been identified. The tertiary structure of p16INK4A contains four helix-turn-helix motifs linked by three loops. Twelve tumorigenic mutants of p16INK4A have been constructed and analyzed for their structure and activity, and new mutants have been designed rationally. A fragment of 58 residues at the N terminus of cdk4 important for p16INK4A binding has been identified. The importance of this region was further verified by mutational analysis of cdk4. These results and docking experiments have been used to assess possible modes of binding between p16INK4A and cdk4. | ||
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| - | ==Disease== | ||
| - | Known diseases associated with this structure: Li Fraumeni syndrome OMIM:[[http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=600160 600160]], Melanoma and neural system tumor syndrome OMIM:[[http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=600160 600160]], Melanoma, cutaneous malignant, 2 OMIM:[[http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=600160 600160]], Orolaryngeal cancer, multiple, OMIM:[[http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=600160 600160]], Pancreatic cancer/melanoma syndrome OMIM:[[http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=600160 600160]] | ||
==About this Structure== | ==About this Structure== | ||
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[[Category: repeat]] | [[Category: repeat]] | ||
| - | ''Page seeded by [http://oca.weizmann.ac.il/oca OCA ] on | + | ''Page seeded by [http://oca.weizmann.ac.il/oca OCA ] on Sun Mar 30 18:33:36 2008'' |
Revision as of 15:33, 30 March 2008
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| Resources: | FirstGlance, OCA, PDBsum, RCSB | ||||||
| Coordinates: | save as pdb, mmCIF, xml | ||||||
SOLUTION NMR STRUCTURE OF TUMOR SUPPRESSOR P16INK4A, 18 STRUCTURES
Overview
The solution structure of the tumor suppressor p16INK4A has been determined by NMR, and important recognition regions of both cdk4 and p16INK4A have been identified. The tertiary structure of p16INK4A contains four helix-turn-helix motifs linked by three loops. Twelve tumorigenic mutants of p16INK4A have been constructed and analyzed for their structure and activity, and new mutants have been designed rationally. A fragment of 58 residues at the N terminus of cdk4 important for p16INK4A binding has been identified. The importance of this region was further verified by mutational analysis of cdk4. These results and docking experiments have been used to assess possible modes of binding between p16INK4A and cdk4.
About this Structure
1A5E is a Single protein structure of sequence from Homo sapiens. Full crystallographic information is available from OCA.
Reference
Tumor suppressor p16INK4A: determination of solution structure and analyses of its interaction with cyclin-dependent kinase 4., Byeon IJ, Li J, Ericson K, Selby TL, Tevelev A, Kim HJ, O'Maille P, Tsai MD, Mol Cell. 1998 Feb;1(3):421-31. PMID:9660926
Page seeded by OCA on Sun Mar 30 18:33:36 2008
Categories: Homo sapiens | Single protein | Byeon, I J.L. | Ericson, K. | Kim, H J. | Li, J. | Maille, P O. | Selby, T L. | Tevelev, A. | Tsai, M D. | Ank repeat | Anti-oncogene | Cell cycle | Repeat
