1a5e - Revision history

OCA at 08:11, 22 May 2024

OCA — Wed, 22 May 2024 08:11:09 GMT

←Older revision		Revision as of 08:11, 22 May 2024
Line 21:		Line 21:
	</jmol>, as determined by [http://consurfdb.tau.ac.il/ ConSurfDB]. You may read the [[Conservation%2C_Evolutionary\|explanation]] of the method and the full data available from [http://bental.tau.ac.il/new_ConSurfDB/main_output.php?pdb_ID=1a5e ConSurf].		</jmol>, as determined by [http://consurfdb.tau.ac.il/ ConSurfDB]. You may read the [[Conservation%2C_Evolutionary\|explanation]] of the method and the full data available from [http://bental.tau.ac.il/new_ConSurfDB/main_output.php?pdb_ID=1a5e ConSurf].
	<div style="clear:both"></div>		<div style="clear:both"></div>
		+	<div style="background-color:#fffaf0;">
		+	== Publication Abstract from PubMed ==
		+	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.
		+
		+	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<ref>PMID:9660926</ref>
		+
		+	From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>
		+	</div>
		+	<div class="pdbe-citations 1a5e" style="background-color:#fffaf0;"></div>
	== References ==		== References ==
	<references/>		<references/>

OCA at 15:21, 13 March 2024

OCA — Wed, 13 Mar 2024 15:21:15 GMT

←Older revision		Revision as of 15:21, 13 March 2024
Line 1:		Line 1:

	==SOLUTION NMR STRUCTURE OF TUMOR SUPPRESSOR P16INK4A, 18 STRUCTURES==		==SOLUTION NMR STRUCTURE OF TUMOR SUPPRESSOR P16INK4A, 18 STRUCTURES==
-	<StructureSection load='1a5e' size='340' side='right'caption='[[1a5e~~]], [[NMR_Ensembles_of_Models \| 18 NMR models~~]]' scene=''>	+	<StructureSection load='1a5e' size='340' side='right'caption='[[1a5e]]' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[1a5e]] is a 1 chain structure with sequence from [https://en.wikipedia.org/wiki/~~Human Human~~]. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1A5E OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=1A5E FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[1a5e]] is a 1 chain structure with sequence from [https://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1A5E OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=1A5E FirstGlance]. <br>
-	</td></tr><tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=1a5e FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1a5e OCA], [https://pdbe.org/1a5e PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=1a5e RCSB], [https://www.ebi.ac.uk/pdbsum/1a5e PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=1a5e ProSAT]</span></td></tr>	+	</td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models\|Method:]]</b></td><td class="sblockDat" id="methodDat">Solution NMR</td></tr>
		+	<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=1a5e FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1a5e OCA], [https://pdbe.org/1a5e PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=1a5e RCSB], [https://www.ebi.ac.uk/pdbsum/1a5e PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=1a5e ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
-	[[https://www.uniprot.org/uniprot/~~CD2A1_HUMAN CD2A1_HUMAN]~~] Note=The association between cutaneous and uveal melanomas in some families suggests that mutations in CDKN2A may account for a proportion of uveal melanomas. However, CDKN2A mutations are rarely found in uveal melanoma patients. Defects in CDKN2A are the cause of cutaneous malignant melanoma type 2 (CMM2) [MIM:[https://omim.org/entry/155601 155601]]. Malignant melanoma is a malignant neoplasm of melanocytes, arising de novo or from a pre-existing benign nevus, which occurs most often in the skin but also may involve other sites.<ref>PMID:7987387</ref> <ref>PMID:8595405</ref> <ref>PMID:8653684</ref> <ref>PMID:8710906</ref> <ref>PMID:9328469</ref> <ref>PMID:9425228</ref> <ref>PMID:10651484</ref> <ref>PMID:11506491</ref> <ref>PMID:12019208</ref> <ref>PMID:10874641</ref> <ref>PMID:14646619</ref> <ref>PMID:19260062</ref> Defects in CDKN2A are the cause of familial atypical multiple mole melanoma-pancreatic carcinoma syndrome (FAMMMPC) [MIM:[https://omim.org/entry/606719 606719]]. Defects in CDKN2A are a cause of Li-Fraumeni syndrome (LFS) [MIM:[https://omim.org/entry/151623 151623]]. LFS is a highly penetrant familial cancer phenotype usually associated with inherited mutations in TP53.<ref>PMID:10484981</ref> Defects in CDKN2A are the cause of melanoma-astrocytoma syndrome (MASTS) [MIM:[https://omim.org/entry/155755 155755]]. The melanoma-astrocytoma syndrome is characterized by a dual predisposition to melanoma and neural system tumors, commonly astrocytoma.<ref>PMID:11136714</ref>	+	[https://www.uniprot.org/uniprot/CDN2A_HUMAN CDN2A_HUMAN] Note=The association between cutaneous and uveal melanomas in some families suggests that mutations in CDKN2A may account for a proportion of uveal melanomas. However, CDKN2A mutations are rarely found in uveal melanoma patients. Defects in CDKN2A are the cause of cutaneous malignant melanoma type 2 (CMM2) [MIM:[https://omim.org/entry/155601 155601]. Malignant melanoma is a malignant neoplasm of melanocytes, arising de novo or from a pre-existing benign nevus, which occurs most often in the skin but also may involve other sites.<ref>PMID:7987387</ref> <ref>PMID:8595405</ref> <ref>PMID:8653684</ref> <ref>PMID:8710906</ref> <ref>PMID:9328469</ref> <ref>PMID:9425228</ref> <ref>PMID:10651484</ref> <ref>PMID:11506491</ref> <ref>PMID:12019208</ref> <ref>PMID:10874641</ref> <ref>PMID:14646619</ref> <ref>PMID:19260062</ref> Defects in CDKN2A are the cause of familial atypical multiple mole melanoma-pancreatic carcinoma syndrome (FAMMMPC) [MIM:[https://omim.org/entry/606719 606719]. Defects in CDKN2A are a cause of Li-Fraumeni syndrome (LFS) [MIM:[https://omim.org/entry/151623 151623]. LFS is a highly penetrant familial cancer phenotype usually associated with inherited mutations in TP53.<ref>PMID:10484981</ref> Defects in CDKN2A are the cause of melanoma-astrocytoma syndrome (MASTS) [MIM:[https://omim.org/entry/155755 155755]. The melanoma-astrocytoma syndrome is characterized by a dual predisposition to melanoma and neural system tumors, commonly astrocytoma.<ref>PMID:11136714</ref>
	== Function ==		== Function ==
-	[[https://www.uniprot.org/uniprot/~~CD2A1_HUMAN CD2A1_HUMAN]~~] Acts as a negative regulator of the proliferation of normal cells by interacting strongly with CDK4 and CDK6. This inhibits their ability to interact with cyclins D and to phosphorylate the retinoblastoma protein.<ref>PMID:7972006</ref> <ref>PMID:16782892</ref>	+	[https://www.uniprot.org/uniprot/CDN2A_HUMAN CDN2A_HUMAN] Acts as a negative regulator of the proliferation of normal cells by interacting strongly with CDK4 and CDK6. This inhibits their ability to interact with cyclins D and to phosphorylate the retinoblastoma protein.<ref>PMID:7972006</ref> <ref>PMID:16782892</ref>
	== Evolutionary Conservation ==		== Evolutionary Conservation ==
	[[Image:Consurf_key_small.gif\|200px\|right]]		[[Image:Consurf_key_small.gif\|200px\|right]]
Line 20:		Line 21:
	</jmol>, as determined by [http://consurfdb.tau.ac.il/ ConSurfDB]. You may read the [[Conservation%2C_Evolutionary\|explanation]] of the method and the full data available from [http://bental.tau.ac.il/new_ConSurfDB/main_output.php?pdb_ID=1a5e ConSurf].		</jmol>, as determined by [http://consurfdb.tau.ac.il/ ConSurfDB]. You may read the [[Conservation%2C_Evolutionary\|explanation]] of the method and the full data available from [http://bental.tau.ac.il/new_ConSurfDB/main_output.php?pdb_ID=1a5e ConSurf].
	<div style="clear:both"></div>		<div style="clear:both"></div>
-	<div style="background-color:#fffaf0;">
-	== Publication Abstract from PubMed ==
-	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.
-
-	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<ref>PMID:9660926</ref>
-
-	From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>
-	</div>
-	<div class="pdbe-citations 1a5e" style="background-color:#fffaf0;"></div>
	== References ==		== References ==
	<references/>		<references/>
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
-	[[Category: ~~Human~~]]	+	[[Category: Homo sapiens]]
	[[Category: Large Structures]]		[[Category: Large Structures]]
-	[[Category: Byeon, I ~~J.L~~]]	+	[[Category: Byeon I-JL]]
-	[[Category: Ericson, K]]	+	[[Category: Ericson K]]
-	[[Category: Kim, H J]]	+	[[Category: Kim H-J]]
-	[[Category: Li, J]]	+	[[Category: Li J]]
-	[[Category: Maille, P O]]	+	[[Category: O'Maille P]]
-	[[Category: Selby~~, T L~~]]	+	[[Category: Selby TL]]
-	[[Category: Tevelev, A]]	+	[[Category: Tevelev A]]
-	[[Category: Tsai, M D]]	+	[[Category: Tsai M-D]]
-	~~[[Category: Ank repeat]]~~	+
-	~~[[Category: Anti-oncogene]]~~	+
-	~~[[Category: Cell cycle~~]]	+

OCA at 10:21, 16 February 2022

OCA — Wed, 16 Feb 2022 10:21:03 GMT

←Older revision		Revision as of 10:21, 16 February 2022
Line 3:		Line 3:
	<StructureSection load='1a5e' size='340' side='right'caption='[[1a5e]], [[NMR_Ensembles_of_Models \| 18 NMR models]]' scene=''>		<StructureSection load='1a5e' size='340' side='right'caption='[[1a5e]], [[NMR_Ensembles_of_Models \| 18 NMR models]]' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[1a5e]] is a 1 chain structure. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1A5E OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=1A5E FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[1a5e]] is a 1 chain structure with sequence from [https://en.wikipedia.org/wiki/Human Human]. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1A5E OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=1A5E FirstGlance]. <br>
	</td></tr><tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=1a5e FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1a5e OCA], [https://pdbe.org/1a5e PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=1a5e RCSB], [https://www.ebi.ac.uk/pdbsum/1a5e PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=1a5e ProSAT]</span></td></tr>		</td></tr><tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=1a5e FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1a5e OCA], [https://pdbe.org/1a5e PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=1a5e RCSB], [https://www.ebi.ac.uk/pdbsum/1a5e PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=1a5e ProSAT]</span></td></tr>
	</table>		</table>
Line 33:		Line 33:
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
		+	[[Category: Human]]
	[[Category: Large Structures]]		[[Category: Large Structures]]
	[[Category: Byeon, I J.L]]		[[Category: Byeon, I J.L]]

OCA at 10:16, 17 February 2021

OCA — Wed, 17 Feb 2021 10:16:53 GMT

←Older revision		Revision as of 10:16, 17 February 2021
Line 3:		Line 3:
	<StructureSection load='1a5e' size='340' side='right'caption='[[1a5e]], [[NMR_Ensembles_of_Models \| 18 NMR models]]' scene=''>		<StructureSection load='1a5e' size='340' side='right'caption='[[1a5e]], [[NMR_Ensembles_of_Models \| 18 NMR models]]' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[1a5e]] is a 1 chain structure. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1A5E OCA]. For a <b>guided tour on the structure components</b> use [~~http~~://~~oca~~.~~weizmann.ac.il/oca-docs~~/fgij/fg.htm?mol=1A5E FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[1a5e]] is a 1 chain structure. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1A5E OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=1A5E FirstGlance]. <br>
-	</td></tr><tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><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~~://pdbe.org/1a5e PDBe], [~~http~~://www.rcsb.org/pdb/explore.do?structureId=1a5e RCSB], [~~http~~://www.ebi.ac.uk/pdbsum/1a5e PDBsum], [~~http~~://prosat.h-its.org/prosat/prosatexe?pdbcode=1a5e ProSAT]</span></td></tr>	+	</td></tr><tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=1a5e FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1a5e OCA], [https://pdbe.org/1a5e PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=1a5e RCSB], [https://www.ebi.ac.uk/pdbsum/1a5e PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=1a5e ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
-	[[~~http~~://www.uniprot.org/uniprot/CD2A1_HUMAN CD2A1_HUMAN]] Note=The association between cutaneous and uveal melanomas in some families suggests that mutations in CDKN2A may account for a proportion of uveal melanomas. However, CDKN2A mutations are rarely found in uveal melanoma patients. Defects in CDKN2A are the cause of cutaneous malignant melanoma type 2 (CMM2) [MIM:[~~http~~://omim.org/entry/155601 155601]]. Malignant melanoma is a malignant neoplasm of melanocytes, arising de novo or from a pre-existing benign nevus, which occurs most often in the skin but also may involve other sites.<ref>PMID:7987387</ref> <ref>PMID:8595405</ref> <ref>PMID:8653684</ref> <ref>PMID:8710906</ref> <ref>PMID:9328469</ref> <ref>PMID:9425228</ref> <ref>PMID:10651484</ref> <ref>PMID:11506491</ref> <ref>PMID:12019208</ref> <ref>PMID:10874641</ref> <ref>PMID:14646619</ref> <ref>PMID:19260062</ref> Defects in CDKN2A are the cause of familial atypical multiple mole melanoma-pancreatic carcinoma syndrome (FAMMMPC) [MIM:[~~http~~://omim.org/entry/606719 606719]]. Defects in CDKN2A are a cause of Li-Fraumeni syndrome (LFS) [MIM:[~~http~~://omim.org/entry/151623 151623]]. LFS is a highly penetrant familial cancer phenotype usually associated with inherited mutations in TP53.<ref>PMID:10484981</ref> Defects in CDKN2A are the cause of melanoma-astrocytoma syndrome (MASTS) [MIM:[~~http~~://omim.org/entry/155755 155755]]. The melanoma-astrocytoma syndrome is characterized by a dual predisposition to melanoma and neural system tumors, commonly astrocytoma.<ref>PMID:11136714</ref>	+	[[https://www.uniprot.org/uniprot/CD2A1_HUMAN CD2A1_HUMAN]] Note=The association between cutaneous and uveal melanomas in some families suggests that mutations in CDKN2A may account for a proportion of uveal melanomas. However, CDKN2A mutations are rarely found in uveal melanoma patients. Defects in CDKN2A are the cause of cutaneous malignant melanoma type 2 (CMM2) [MIM:[https://omim.org/entry/155601 155601]]. Malignant melanoma is a malignant neoplasm of melanocytes, arising de novo or from a pre-existing benign nevus, which occurs most often in the skin but also may involve other sites.<ref>PMID:7987387</ref> <ref>PMID:8595405</ref> <ref>PMID:8653684</ref> <ref>PMID:8710906</ref> <ref>PMID:9328469</ref> <ref>PMID:9425228</ref> <ref>PMID:10651484</ref> <ref>PMID:11506491</ref> <ref>PMID:12019208</ref> <ref>PMID:10874641</ref> <ref>PMID:14646619</ref> <ref>PMID:19260062</ref> Defects in CDKN2A are the cause of familial atypical multiple mole melanoma-pancreatic carcinoma syndrome (FAMMMPC) [MIM:[https://omim.org/entry/606719 606719]]. Defects in CDKN2A are a cause of Li-Fraumeni syndrome (LFS) [MIM:[https://omim.org/entry/151623 151623]]. LFS is a highly penetrant familial cancer phenotype usually associated with inherited mutations in TP53.<ref>PMID:10484981</ref> Defects in CDKN2A are the cause of melanoma-astrocytoma syndrome (MASTS) [MIM:[https://omim.org/entry/155755 155755]]. The melanoma-astrocytoma syndrome is characterized by a dual predisposition to melanoma and neural system tumors, commonly astrocytoma.<ref>PMID:11136714</ref>
	== Function ==		== Function ==
-	[[~~http~~://www.uniprot.org/uniprot/CD2A1_HUMAN CD2A1_HUMAN]] Acts as a negative regulator of the proliferation of normal cells by interacting strongly with CDK4 and CDK6. This inhibits their ability to interact with cyclins D and to phosphorylate the retinoblastoma protein.<ref>PMID:7972006</ref> <ref>PMID:16782892</ref>	+	[[https://www.uniprot.org/uniprot/CD2A1_HUMAN CD2A1_HUMAN]] Acts as a negative regulator of the proliferation of normal cells by interacting strongly with CDK4 and CDK6. This inhibits their ability to interact with cyclins D and to phosphorylate the retinoblastoma protein.<ref>PMID:7972006</ref> <ref>PMID:16782892</ref>
	== Evolutionary Conservation ==		== Evolutionary Conservation ==
	[[Image:Consurf_key_small.gif\|200px\|right]]		[[Image:Consurf_key_small.gif\|200px\|right]]

OCA at 13:56, 10 May 2019

OCA — Fri, 10 May 2019 13:56:30 GMT

←Older revision		Revision as of 13:56, 10 May 2019
Line 1:		Line 1:

	==SOLUTION NMR STRUCTURE OF TUMOR SUPPRESSOR P16INK4A, 18 STRUCTURES==		==SOLUTION NMR STRUCTURE OF TUMOR SUPPRESSOR P16INK4A, 18 STRUCTURES==
-	<StructureSection load='1a5e' size='340' side='right' caption='[[1a5e]], [[NMR_Ensembles_of_Models \| 18 NMR models]]' scene=''>	+	<StructureSection load='1a5e' size='340' side='right'caption='[[1a5e]], [[NMR_Ensembles_of_Models \| 18 NMR models]]' scene=''>
	== Structural highlights ==		== Structural highlights ==
	<table><tr><td colspan='2'>[[1a5e]] is a 1 chain structure. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1A5E OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1A5E FirstGlance]. <br>		<table><tr><td colspan='2'>[[1a5e]] is a 1 chain structure. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1A5E OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1A5E FirstGlance]. <br>
Line 14:		Line 14:
	Check<jmol>		Check<jmol>
	<jmolCheckbox>		<jmolCheckbox>
-	<scriptWhenChecked>select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/a5/1a5e_consurf.spt"</scriptWhenChecked>	+	<scriptWhenChecked>; select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/a5/1a5e_consurf.spt"</scriptWhenChecked>
	<scriptWhenUnchecked>script /wiki/extensions/Proteopedia/spt/initialview01.spt</scriptWhenUnchecked>		<scriptWhenUnchecked>script /wiki/extensions/Proteopedia/spt/initialview01.spt</scriptWhenUnchecked>
	<text>to colour the structure by Evolutionary Conservation</text>		<text>to colour the structure by Evolutionary Conservation</text>
Line 33:		Line 33:
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
		+	[[Category: Large Structures]]
	[[Category: Byeon, I J.L]]		[[Category: Byeon, I J.L]]
	[[Category: Ericson, K]]		[[Category: Ericson, K]]

OCA at 09:09, 9 August 2017

OCA — Wed, 09 Aug 2017 09:09:42 GMT

←Older revision		Revision as of 09:09, 9 August 2017
Line 1:		Line 1:
		+
	==SOLUTION NMR STRUCTURE OF TUMOR SUPPRESSOR P16INK4A, 18 STRUCTURES==		==SOLUTION NMR STRUCTURE OF TUMOR SUPPRESSOR P16INK4A, 18 STRUCTURES==
	<StructureSection load='1a5e' size='340' side='right' caption='[[1a5e]], [[NMR_Ensembles_of_Models \| 18 NMR models]]' scene=''>		<StructureSection load='1a5e' size='340' side='right' caption='[[1a5e]], [[NMR_Ensembles_of_Models \| 18 NMR models]]' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[1a5e]] is a 1 chain structure ~~with sequence from [http://en.wikipedia.org/wiki/Human Human]~~. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1A5E OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1A5E FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[1a5e]] is a 1 chain structure. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1A5E OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1A5E FirstGlance]. <br>
-	</td></tr><tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><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://pdbe.org/1a5e PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=1a5e RCSB], [http://www.ebi.ac.uk/pdbsum/1a5e PDBsum]</span></td></tr>	+	</td></tr><tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><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://pdbe.org/1a5e PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=1a5e RCSB], [http://www.ebi.ac.uk/pdbsum/1a5e PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=1a5e ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
Line 17:		Line 18:
	<text>to colour the structure by Evolutionary Conservation</text>		<text>to colour the structure by Evolutionary Conservation</text>
	</jmolCheckbox>		</jmolCheckbox>
-	</jmol>, as determined by [http://consurfdb.tau.ac.il/ ConSurfDB]. You may read the [[Conservation%2C_Evolutionary\|explanation]] of the method and the full data available from [http://bental.tau.ac.il/new_ConSurfDB/~~chain_selection~~.php?pdb_ID=~~2ata~~ ConSurf].	+	</jmol>, as determined by [http://consurfdb.tau.ac.il/ ConSurfDB]. You may read the [[Conservation%2C_Evolutionary\|explanation]] of the method and the full data available from [http://bental.tau.ac.il/new_ConSurfDB/main_output.php?pdb_ID=1a5e ConSurf].
	<div style="clear:both"></div>		<div style="clear:both"></div>
	<div style="background-color:#fffaf0;">		<div style="background-color:#fffaf0;">
Line 32:		Line 33:
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
-	[[Category: Human]]
	[[Category: Byeon, I J.L]]		[[Category: Byeon, I J.L]]
	[[Category: Ericson, K]]		[[Category: Ericson, K]]

OCA at 15:41, 9 September 2015

OCA — Wed, 09 Sep 2015 15:41:17 GMT

←Older revision		Revision as of 15:41, 9 September 2015
Line 2:		Line 2:
	<StructureSection load='1a5e' size='340' side='right' caption='[[1a5e]], [[NMR_Ensembles_of_Models \| 18 NMR models]]' scene=''>		<StructureSection load='1a5e' size='340' side='right' caption='[[1a5e]], [[NMR_Ensembles_of_Models \| 18 NMR models]]' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[1a5e]] is a 1 chain structure with sequence from [http://en.wikipedia.org/wiki/~~Homo_sapiens Homo sapiens~~]. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1A5E OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1A5E FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[1a5e]] is a 1 chain structure with sequence from [http://en.wikipedia.org/wiki/Human Human]. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1A5E OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1A5E FirstGlance]. <br>
-	</td></tr><tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><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.rcsb.org/pdb/explore.do?structureId=1a5e RCSB], [http://www.ebi.ac.uk/pdbsum/1a5e PDBsum]</span></td></tr>	+	</td></tr><tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><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://pdbe.org/1a5e PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=1a5e RCSB], [http://www.ebi.ac.uk/pdbsum/1a5e PDBsum]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
Line 27:		Line 27:
	From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>		From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>
	</div>		</div>
		+	<div class="pdbe-citations 1a5e" style="background-color:#fffaf0;"></div>
	== References ==		== References ==
	<references/>		<references/>
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
-	[[Category: ~~Homo sapiens~~]]	+	[[Category: Human]]
	[[Category: Byeon, I J.L]]		[[Category: Byeon, I J.L]]
	[[Category: Ericson, K]]		[[Category: Ericson, K]]

OCA at 10:29, 22 December 2014

OCA — Mon, 22 Dec 2014 10:29:47 GMT

←Older revision		Revision as of 10:29, 22 December 2014
Line 3:		Line 3:
	== Structural highlights ==		== Structural highlights ==
	<table><tr><td colspan='2'>[[1a5e]] is a 1 chain structure with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1A5E OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1A5E FirstGlance]. <br>		<table><tr><td colspan='2'>[[1a5e]] is a 1 chain structure with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1A5E OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1A5E FirstGlance]. <br>
-	</td></tr><tr><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><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.rcsb.org/pdb/explore.do?structureId=1a5e RCSB], [http://www.ebi.ac.uk/pdbsum/1a5e PDBsum]</span></td></tr>	+	</td></tr><tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><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.rcsb.org/pdb/explore.do?structureId=1a5e RCSB], [http://www.ebi.ac.uk/pdbsum/1a5e PDBsum]</span></td></tr>
-	<table>	+	</table>
	== Disease ==		== Disease ==
	[[http://www.uniprot.org/uniprot/CD2A1_HUMAN CD2A1_HUMAN]] Note=The association between cutaneous and uveal melanomas in some families suggests that mutations in CDKN2A may account for a proportion of uveal melanomas. However, CDKN2A mutations are rarely found in uveal melanoma patients. Defects in CDKN2A are the cause of cutaneous malignant melanoma type 2 (CMM2) [MIM:[http://omim.org/entry/155601 155601]]. Malignant melanoma is a malignant neoplasm of melanocytes, arising de novo or from a pre-existing benign nevus, which occurs most often in the skin but also may involve other sites.<ref>PMID:7987387</ref> <ref>PMID:8595405</ref> <ref>PMID:8653684</ref> <ref>PMID:8710906</ref> <ref>PMID:9328469</ref> <ref>PMID:9425228</ref> <ref>PMID:10651484</ref> <ref>PMID:11506491</ref> <ref>PMID:12019208</ref> <ref>PMID:10874641</ref> <ref>PMID:14646619</ref> <ref>PMID:19260062</ref> Defects in CDKN2A are the cause of familial atypical multiple mole melanoma-pancreatic carcinoma syndrome (FAMMMPC) [MIM:[http://omim.org/entry/606719 606719]]. Defects in CDKN2A are a cause of Li-Fraumeni syndrome (LFS) [MIM:[http://omim.org/entry/151623 151623]]. LFS is a highly penetrant familial cancer phenotype usually associated with inherited mutations in TP53.<ref>PMID:10484981</ref> Defects in CDKN2A are the cause of melanoma-astrocytoma syndrome (MASTS) [MIM:[http://omim.org/entry/155755 155755]]. The melanoma-astrocytoma syndrome is characterized by a dual predisposition to melanoma and neural system tumors, commonly astrocytoma.<ref>PMID:11136714</ref>		[[http://www.uniprot.org/uniprot/CD2A1_HUMAN CD2A1_HUMAN]] Note=The association between cutaneous and uveal melanomas in some families suggests that mutations in CDKN2A may account for a proportion of uveal melanomas. However, CDKN2A mutations are rarely found in uveal melanoma patients. Defects in CDKN2A are the cause of cutaneous malignant melanoma type 2 (CMM2) [MIM:[http://omim.org/entry/155601 155601]]. Malignant melanoma is a malignant neoplasm of melanocytes, arising de novo or from a pre-existing benign nevus, which occurs most often in the skin but also may involve other sites.<ref>PMID:7987387</ref> <ref>PMID:8595405</ref> <ref>PMID:8653684</ref> <ref>PMID:8710906</ref> <ref>PMID:9328469</ref> <ref>PMID:9425228</ref> <ref>PMID:10651484</ref> <ref>PMID:11506491</ref> <ref>PMID:12019208</ref> <ref>PMID:10874641</ref> <ref>PMID:14646619</ref> <ref>PMID:19260062</ref> Defects in CDKN2A are the cause of familial atypical multiple mole melanoma-pancreatic carcinoma syndrome (FAMMMPC) [MIM:[http://omim.org/entry/606719 606719]]. Defects in CDKN2A are a cause of Li-Fraumeni syndrome (LFS) [MIM:[http://omim.org/entry/151623 151623]]. LFS is a highly penetrant familial cancer phenotype usually associated with inherited mutations in TP53.<ref>PMID:10484981</ref> Defects in CDKN2A are the cause of melanoma-astrocytoma syndrome (MASTS) [MIM:[http://omim.org/entry/155755 155755]]. The melanoma-astrocytoma syndrome is characterized by a dual predisposition to melanoma and neural system tumors, commonly astrocytoma.<ref>PMID:11136714</ref>
Line 32:		Line 32:
	</StructureSection>		</StructureSection>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
-	[[Category: Byeon, I J.L.]]	+	[[Category: Byeon, I J.L]]
-	[[Category: Ericson, K.]]	+	[[Category: Ericson, K]]
-	[[Category: Kim, H J.]]	+	[[Category: Kim, H J]]
-	[[Category: Li, J.]]	+	[[Category: Li, J]]
-	[[Category: Maille, P O.]]	+	[[Category: Maille, P O]]
-	[[Category: Selby, T L.]]	+	[[Category: Selby, T L]]
-	[[Category: Tevelev, A.]]	+	[[Category: Tevelev, A]]
-	[[Category: Tsai, M D.]]	+	[[Category: Tsai, M D]]
	[[Category: Ank repeat]]		[[Category: Ank repeat]]
	[[Category: Anti-oncogene]]		[[Category: Anti-oncogene]]
	[[Category: Cell cycle]]		[[Category: Cell cycle]]

OCA at 16:47, 29 September 2014

OCA — Mon, 29 Sep 2014 16:47:03 GMT

←Older revision		Revision as of 16:47, 29 September 2014
Line 1:		Line 1:
-	~~{{STRUCTURE_1a5e\| PDB=1a5e \| SCENE= }}~~	+	==SOLUTION NMR STRUCTURE OF TUMOR SUPPRESSOR P16INK4A, 18 STRUCTURES==
-	===SOLUTION NMR STRUCTURE OF TUMOR SUPPRESSOR P16INK4A, 18 STRUCTURES===	+	<StructureSection load='1a5e' size='340' side='right' caption='[[1a5e]], [[NMR_Ensembles_of_Models \| 18 NMR models]]' scene=''>
-	~~{{ABSTRACT_PUBMED_9660926}}~~	+	== Structural highlights ==
		+	<table><tr><td colspan='2'>[[1a5e]] is a 1 chain structure with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1A5E OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1A5E FirstGlance]. <br>
		+	</td></tr><tr><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><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.rcsb.org/pdb/explore.do?structureId=1a5e RCSB], [http://www.ebi.ac.uk/pdbsum/1a5e PDBsum]</span></td></tr>
		+	<table>
		+	== Disease ==
		+	[[http://www.uniprot.org/uniprot/CD2A1_HUMAN CD2A1_HUMAN]] Note=The association between cutaneous and uveal melanomas in some families suggests that mutations in CDKN2A may account for a proportion of uveal melanomas. However, CDKN2A mutations are rarely found in uveal melanoma patients. Defects in CDKN2A are the cause of cutaneous malignant melanoma type 2 (CMM2) [MIM:[http://omim.org/entry/155601 155601]]. Malignant melanoma is a malignant neoplasm of melanocytes, arising de novo or from a pre-existing benign nevus, which occurs most often in the skin but also may involve other sites.<ref>PMID:7987387</ref> <ref>PMID:8595405</ref> <ref>PMID:8653684</ref> <ref>PMID:8710906</ref> <ref>PMID:9328469</ref> <ref>PMID:9425228</ref> <ref>PMID:10651484</ref> <ref>PMID:11506491</ref> <ref>PMID:12019208</ref> <ref>PMID:10874641</ref> <ref>PMID:14646619</ref> <ref>PMID:19260062</ref> Defects in CDKN2A are the cause of familial atypical multiple mole melanoma-pancreatic carcinoma syndrome (FAMMMPC) [MIM:[http://omim.org/entry/606719 606719]]. Defects in CDKN2A are a cause of Li-Fraumeni syndrome (LFS) [MIM:[http://omim.org/entry/151623 151623]]. LFS is a highly penetrant familial cancer phenotype usually associated with inherited mutations in TP53.<ref>PMID:10484981</ref> Defects in CDKN2A are the cause of melanoma-astrocytoma syndrome (MASTS) [MIM:[http://omim.org/entry/155755 155755]]. The melanoma-astrocytoma syndrome is characterized by a dual predisposition to melanoma and neural system tumors, commonly astrocytoma.<ref>PMID:11136714</ref>
		+	== Function ==
		+	[[http://www.uniprot.org/uniprot/CD2A1_HUMAN CD2A1_HUMAN]] Acts as a negative regulator of the proliferation of normal cells by interacting strongly with CDK4 and CDK6. This inhibits their ability to interact with cyclins D and to phosphorylate the retinoblastoma protein.<ref>PMID:7972006</ref> <ref>PMID:16782892</ref>
		+	== Evolutionary Conservation ==
		+	[[Image:Consurf_key_small.gif\|200px\|right]]
		+	Check<jmol>
		+	<jmolCheckbox>
		+	<scriptWhenChecked>select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/a5/1a5e_consurf.spt"</scriptWhenChecked>
		+	<scriptWhenUnchecked>script /wiki/extensions/Proteopedia/spt/initialview01.spt</scriptWhenUnchecked>
		+	<text>to colour the structure by Evolutionary Conservation</text>
		+	</jmolCheckbox>
		+	</jmol>, as determined by [http://consurfdb.tau.ac.il/ ConSurfDB]. You may read the [[Conservation%2C_Evolutionary\|explanation]] of the method and the full data available from [http://bental.tau.ac.il/new_ConSurfDB/chain_selection.php?pdb_ID=2ata ConSurf].
		+	<div style="clear:both"></div>
		+	<div style="background-color:#fffaf0;">
		+	== Publication Abstract from PubMed ==
		+	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.

-	~~==Disease==~~	+	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<ref>PMID:9660926</ref>
-	~~[[http~~:~~//www.uniprot.org/uniprot/CD2A1_HUMAN CD2A1_HUMAN]] Note=The association between cutaneous~~ and ~~uveal melanomas in some families suggests that mutations in CDKN2A may account for a proportion~~ of ~~uveal melanomas~~. ~~However~~, CDKN2A mutations are rarely found in uveal melanoma patients. Defects in CDKN2A are the cause of cutaneous malignant melanoma type 2 (CMM2) [MIM:[http://omim.org/entry/155601 155601]]. Malignant melanoma is a malignant neoplasm of melanocytes, ~~arising de novo or from a pre-existing benign nevus~~, ~~which occurs most often in the skin but also may involve other sites~~.<ref>PMID:7987387</ref><ref>PMID:8595405</ref><ref>PMID:8653684</ref><ref>PMID:8710906</ref><ref>PMID:9328469</ref><ref>PMID:9425228</ref><ref>PMID:10651484</ref><ref>PMID:11506491</ref><ref>PMID:12019208</ref><ref>PMID:10874641</ref><ref>PMID:14646619</ref><ref>PMID:19260062</ref> Defects in CDKN2A are the cause of familial atypical multiple mole melanoma-pancreatic carcinoma syndrome (~~FAMMMPC~~) ~~[MIM~~:~~[http://omim.org/entry/606719 606719]]. Defects in CDKN2A are a cause of Li~~-~~Fraumeni syndrome (LFS) [MIM:[http://omim~~.~~org/entry/151623 151623]]. LFS is a highly penetrant familial cancer phenotype usually associated with inherited mutations in TP53.<ref>~~PMID:10484981</ref> Defects in CDKN2A are the cause of melanoma-astrocytoma syndrome (MASTS) [MIM:[http://omim.org/entry/155755 155755]]. The melanoma-astrocytoma syndrome is characterized by a dual predisposition to melanoma and neural system tumors, commonly astrocytoma.<ref>PMID:~~11136714~~</ref>	+

-	~~==Function==~~	+	From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>
-	~~[[http://www.uniprot.org/uniprot~~/~~CD2A1_HUMAN CD2A1_HUMAN]] Acts as~~ a ~~negative regulator~~ of the ~~proliferation~~ of ~~normal cells by interacting strongly with CDK4 and CDK6. This inhibits their ability to interact with cyclins D and to phosphorylate the retinoblastoma protein~~.<~~ref~~>~~PMID:7972006~~</~~ref~~>~~<ref>PMID:16782892</ref>~~	+	</div>
-		+	== References ==
-	==~~About this Structure==~~	+	<references/>
-	[[1a5e]] is a 1 chain structure with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1A5E OCA].	+	__TOC__
-		+	</StructureSection>
-	~~==Reference~~==	+
-	~~<ref group="xtra">PMID:009660926</ref>~~<references ~~group="xtra"~~/><~~references~~/>	+
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
	[[Category: Byeon, I J.L.]]		[[Category: Byeon, I J.L.]]

OCA at 05:21, 25 March 2013

OCA — Mon, 25 Mar 2013 05:21:16 GMT

←Older revision		Revision as of 05:21, 25 March 2013
Line 1:		Line 1:
-	[[Image:1a5e.png\|left\|200px]]
-
	{{STRUCTURE_1a5e\| PDB=1a5e \| SCENE= }}		{{STRUCTURE_1a5e\| PDB=1a5e \| SCENE= }}
-
	===SOLUTION NMR STRUCTURE OF TUMOR SUPPRESSOR P16INK4A, 18 STRUCTURES===		===SOLUTION NMR STRUCTURE OF TUMOR SUPPRESSOR P16INK4A, 18 STRUCTURES===
		+	{{ABSTRACT_PUBMED_9660926}}

-	~~{{ABSTRACT_PUBMED_9660926}}~~	+	==Disease==
		+	[[http://www.uniprot.org/uniprot/CD2A1_HUMAN CD2A1_HUMAN]] Note=The association between cutaneous and uveal melanomas in some families suggests that mutations in CDKN2A may account for a proportion of uveal melanomas. However, CDKN2A mutations are rarely found in uveal melanoma patients. Defects in CDKN2A are the cause of cutaneous malignant melanoma type 2 (CMM2) [MIM:[http://omim.org/entry/155601 155601]]. Malignant melanoma is a malignant neoplasm of melanocytes, arising de novo or from a pre-existing benign nevus, which occurs most often in the skin but also may involve other sites.<ref>PMID:7987387</ref><ref>PMID:8595405</ref><ref>PMID:8653684</ref><ref>PMID:8710906</ref><ref>PMID:9328469</ref><ref>PMID:9425228</ref><ref>PMID:10651484</ref><ref>PMID:11506491</ref><ref>PMID:12019208</ref><ref>PMID:10874641</ref><ref>PMID:14646619</ref><ref>PMID:19260062</ref> Defects in CDKN2A are the cause of familial atypical multiple mole melanoma-pancreatic carcinoma syndrome (FAMMMPC) [MIM:[http://omim.org/entry/606719 606719]]. Defects in CDKN2A are a cause of Li-Fraumeni syndrome (LFS) [MIM:[http://omim.org/entry/151623 151623]]. LFS is a highly penetrant familial cancer phenotype usually associated with inherited mutations in TP53.<ref>PMID:10484981</ref> Defects in CDKN2A are the cause of melanoma-astrocytoma syndrome (MASTS) [MIM:[http://omim.org/entry/155755 155755]]. The melanoma-astrocytoma syndrome is characterized by a dual predisposition to melanoma and neural system tumors, commonly astrocytoma.<ref>PMID:11136714</ref>
		+
		+	==Function==
		+	[[http://www.uniprot.org/uniprot/CD2A1_HUMAN CD2A1_HUMAN]] Acts as a negative regulator of the proliferation of normal cells by interacting strongly with CDK4 and CDK6. This inhibits their ability to interact with cyclins D and to phosphorylate the retinoblastoma protein.<ref>PMID:7972006</ref><ref>PMID:16782892</ref>

	==About this Structure==		==About this Structure==
Line 11:		Line 13:

	==Reference==		==Reference==
-	<ref group="xtra">PMID:009660926</ref><references group="xtra"/>	+	<ref group="xtra">PMID:009660926</ref><references group="xtra"/><references/>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
	[[Category: Byeon, I J.L.]]		[[Category: Byeon, I J.L.]]