1y98 - Revision history

OCA at 06:54, 23 August 2023

OCA — Wed, 23 Aug 2023 06:54:35 GMT

←Older revision		Revision as of 06:54, 23 August 2023
Line 3:		Line 3:
	<StructureSection load='1y98' size='340' side='right'caption='[[1y98]], [[Resolution\|resolution]] 2.50Å' scene=''>		<StructureSection load='1y98' size='340' side='right'caption='[[1y98]], [[Resolution\|resolution]] 2.50Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[1y98]] is a 2 chain structure with sequence from [~~http~~://en.wikipedia.org/wiki/~~Human Human~~]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1Y98 OCA]. For a <b>guided tour on the structure components</b> use [~~http~~://proteopedia.org/fgij/fg.htm?mol=1Y98 FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[1y98]] is a 2 chain structure with sequence from [https://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1Y98 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=1Y98 FirstGlance]. <br>
-	</td></tr><tr id='~~ligand~~'><td class="sblockLbl"><b>[[~~Ligand~~\|~~Ligands~~:]]</b></td><td class="sblockDat" id="~~ligandDat~~">~~<scene name='pdbligand=CO:COBALT+(II)+ION'>CO</scene>~~, ~~<scene name='pdbligand=SO4:SULFATE+ION'>SO4</scene>~~</td></tr>	+	</td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models\|Method:]]</b></td><td class="sblockDat" id="methodDat">X-ray diffraction, [[Resolution\|Resolution]] 2.5Å</td></tr>
-	<tr id='~~NonStdRes~~'><td class="sblockLbl"><b>[[~~Non-Standard_Residue~~\|~~NonStd Res~~:]]</b></td><td class="sblockDat"><scene name='pdbligand=~~SEP~~:~~PHOSPHOSERINE~~'>~~SEP~~</scene><~~/td></tr>~~	+	<tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=CO:COBALT+(II)+ION'>CO</scene>, <scene name='pdbligand=SEP:PHOSPHOSERINE'>SEP</scene>, <scene name='pdbligand=SO4:SULFATE+ION'>SO4</scene></td></tr>
-	~~<tr id~~='~~related'><td class~~=~~"sblockLbl"><b>[[Related_structure\|Related~~:~~]]</b~~></td>~~<td class="sblockDat"><div style='overflow: auto; max-height: 3em;'>[[1t29\|1t29]]~~, ~~[[1t15\|1t15]]~~<~~/div></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=1y98 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1y98 OCA], [https://pdbe.org/1y98 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=1y98 RCSB], [https://www.ebi.ac.uk/pdbsum/1y98 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=1y98 ProSAT]</span></td></tr>
-	~~<tr id~~='~~gene'><td class~~=~~"sblockLbl"><b>[[Gene\|Gene~~:~~]]</b~~></td>~~<td class="sblockDat">BRCA1 ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN])~~</td></tr>	+
-	<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[~~http~~://proteopedia.org/fgij/fg.htm?mol=1y98 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1y98 OCA], [~~http~~://pdbe.org/1y98 PDBe], [~~http~~://www.rcsb.org/pdb/explore.do?structureId=1y98 RCSB], [~~http~~://www.ebi.ac.uk/pdbsum/1y98 PDBsum], [~~http~~://prosat.h-its.org/prosat/prosatexe?pdbcode=1y98 ProSAT]</span></td></tr>	+
	</table>		</table>
	== Disease ==		== Disease ==
-	[~~[http~~://www.uniprot.org/uniprot/BRCA1_HUMAN BRCA1_HUMAN]] Defects in BRCA1 are a cause of susceptibility to breast cancer (BC) [MIM:[~~http~~://omim.org/entry/114480 114480]]. A common malignancy originating from breast epithelial tissue. Breast neoplasms can be distinguished by their histologic pattern. Invasive ductal carcinoma is by far the most common type. Breast cancer is etiologically and genetically heterogeneous. Important genetic factors have been indicated by familial occurrence and bilateral involvement. Mutations at more than one locus can be involved in different families or even in the same case. Note=Mutations in BRCA1 are thought to be responsible for 45% of inherited breast cancer. Moreover, BRCA1 carriers have a 4-fold increased risk of colon cancer, whereas male carriers face a 3-fold increased risk of prostate cancer. Cells lacking BRCA1 show defects in DNA repair by homologous recombination.<ref>PMID:11301010</ref> <ref>PMID:15133502</ref> <ref>PMID:7545954</ref> <ref>PMID:12427738</ref> <ref>PMID:18285836</ref> <ref>PMID:7939630</ref> <ref>PMID:7894491</ref> <ref>PMID:7894493</ref> <ref>PMID:8554067</ref> <ref>PMID:8776600</ref> <ref>PMID:8723683</ref> <ref>PMID:9760198</ref> <ref>PMID:9482581</ref> <ref>PMID:9609997</ref> <ref>PMID:10323242</ref> <ref>PMID:12442275</ref> <ref>PMID:12938098</ref> <ref>PMID:14722926</ref> Defects in BRCA1 are a cause of susceptibility to familial breast-ovarian cancer type 1 (BROVCA1) [MIM:[~~http~~://omim.org/entry/604370 604370]]. A condition associated with familial predisposition to cancer of the breast and ovaries. Characteristic features in affected families are an early age of onset of breast cancer (often before age 50), increased chance of bilateral cancers (cancer that develop in both breasts, or both ovaries, independently), frequent occurrence of breast cancer among men, increased incidence of tumors of other specific organs, such as the prostate. Note=Mutations in BRCA1 are thought to be responsible for more than 80% of inherited breast-ovarian cancer. Defects in BRCA1 are a cause of susceptibility to ovarian cancer (OC) [MIM:[~~http~~://omim.org/entry/167000 167000]]. The term ovarian cancer defines malignancies originating from ovarian tissue. Although many histologic types of ovarian tumors have been described, epithelial ovarian carcinoma is the most common form. Ovarian cancers are often asymptomatic and the recognized signs and symptoms, even of late-stage disease, are vague. Consequently, most patients are diagnosed with advanced disease. Defects in BRCA1 are a cause of susceptibility to pancreatic cancer type 4 (PNCA4) [MIM:[~~http~~://omim.org/entry/614320 614320]]. A malignant neoplasm of the pancreas. Tumors can arise from both the exocrine and endocrine portions of the pancreas, but 95% of them develop from the exocrine portion, including the ductal epithelium, acinar cells, connective tissue, and lymphatic tissue.	+	[https://www.uniprot.org/uniprot/BRCA1_HUMAN BRCA1_HUMAN] Defects in BRCA1 are a cause of susceptibility to breast cancer (BC) [MIM:[https://omim.org/entry/114480 114480]. A common malignancy originating from breast epithelial tissue. Breast neoplasms can be distinguished by their histologic pattern. Invasive ductal carcinoma is by far the most common type. Breast cancer is etiologically and genetically heterogeneous. Important genetic factors have been indicated by familial occurrence and bilateral involvement. Mutations at more than one locus can be involved in different families or even in the same case. Note=Mutations in BRCA1 are thought to be responsible for 45% of inherited breast cancer. Moreover, BRCA1 carriers have a 4-fold increased risk of colon cancer, whereas male carriers face a 3-fold increased risk of prostate cancer. Cells lacking BRCA1 show defects in DNA repair by homologous recombination.<ref>PMID:11301010</ref> <ref>PMID:15133502</ref> <ref>PMID:7545954</ref> <ref>PMID:12427738</ref> <ref>PMID:18285836</ref> <ref>PMID:7939630</ref> <ref>PMID:7894491</ref> <ref>PMID:7894493</ref> <ref>PMID:8554067</ref> <ref>PMID:8776600</ref> <ref>PMID:8723683</ref> <ref>PMID:9760198</ref> <ref>PMID:9482581</ref> <ref>PMID:9609997</ref> <ref>PMID:10323242</ref> <ref>PMID:12442275</ref> <ref>PMID:12938098</ref> <ref>PMID:14722926</ref> Defects in BRCA1 are a cause of susceptibility to familial breast-ovarian cancer type 1 (BROVCA1) [MIM:[https://omim.org/entry/604370 604370]. A condition associated with familial predisposition to cancer of the breast and ovaries. Characteristic features in affected families are an early age of onset of breast cancer (often before age 50), increased chance of bilateral cancers (cancer that develop in both breasts, or both ovaries, independently), frequent occurrence of breast cancer among men, increased incidence of tumors of other specific organs, such as the prostate. Note=Mutations in BRCA1 are thought to be responsible for more than 80% of inherited breast-ovarian cancer. Defects in BRCA1 are a cause of susceptibility to ovarian cancer (OC) [MIM:[https://omim.org/entry/167000 167000]. The term ovarian cancer defines malignancies originating from ovarian tissue. Although many histologic types of ovarian tumors have been described, epithelial ovarian carcinoma is the most common form. Ovarian cancers are often asymptomatic and the recognized signs and symptoms, even of late-stage disease, are vague. Consequently, most patients are diagnosed with advanced disease. Defects in BRCA1 are a cause of susceptibility to pancreatic cancer type 4 (PNCA4) [MIM:[https://omim.org/entry/614320 614320]. A malignant neoplasm of the pancreas. Tumors can arise from both the exocrine and endocrine portions of the pancreas, but 95% of them develop from the exocrine portion, including the ductal epithelium, acinar cells, connective tissue, and lymphatic tissue.
	== Function ==		== Function ==
-	[~~[http~~://www.uniprot.org/uniprot/BRCA1_HUMAN BRCA1_HUMAN]] E3 ubiquitin-protein ligase that specifically mediates the formation of 'Lys-6'-linked polyubiquitin chains and plays a central role in DNA repair by facilitating cellular responses to DNA damage. It is unclear whether it also mediates the formation of other types of polyubiquitin chains. The E3 ubiquitin-protein ligase activity is required for its tumor suppressor function. The BRCA1-BARD1 heterodimer coordinates a diverse range of cellular pathways such as DNA damage repair, ubiquitination and transcriptional regulation to maintain genomic stability. Regulates centrosomal microtubule nucleation. Required for normal cell cycle progression from G2 to mitosis. Required for appropriate cell cycle arrests after ionizing irradiation in both the S-phase and the G2 phase of the cell cycle. Involved in transcriptional regulation of P21 in response to DNA damage. Required for FANCD2 targeting to sites of DNA damage. May function as a transcriptional regulator. Inhibits lipid synthesis by binding to inactive phosphorylated ACACA and preventing its dephosphorylation. Contributes to homologous recombination repair (HRR) via its direct interaction with PALB2, fine-tunes recombinational repair partly through its modulatory role in the PALB2-dependent loading of BRCA2-RAD51 repair machinery at DNA breaks. Component of the BRCA1-RBBP8 complex which regulates CHEK1 activation and controls cell cycle G2/M checkpoints on DNA damage via BRCA1-mediated ubiquitination of RBBP8.<ref>PMID:10500182</ref> <ref>PMID:10724175</ref> <ref>PMID:11836499</ref> <ref>PMID:12890688</ref> <ref>PMID:12887909</ref> <ref>PMID:14976165</ref> <ref>PMID:14990569</ref> <ref>PMID:16818604</ref> <ref>PMID:16326698</ref> <ref>PMID:18056443</ref> <ref>PMID:17525340</ref> <ref>PMID:19261748</ref> <ref>PMID:19369211</ref> <ref>PMID:20351172</ref> <ref>PMID:20364141</ref>	+	[https://www.uniprot.org/uniprot/BRCA1_HUMAN BRCA1_HUMAN] E3 ubiquitin-protein ligase that specifically mediates the formation of 'Lys-6'-linked polyubiquitin chains and plays a central role in DNA repair by facilitating cellular responses to DNA damage. It is unclear whether it also mediates the formation of other types of polyubiquitin chains. The E3 ubiquitin-protein ligase activity is required for its tumor suppressor function. The BRCA1-BARD1 heterodimer coordinates a diverse range of cellular pathways such as DNA damage repair, ubiquitination and transcriptional regulation to maintain genomic stability. Regulates centrosomal microtubule nucleation. Required for normal cell cycle progression from G2 to mitosis. Required for appropriate cell cycle arrests after ionizing irradiation in both the S-phase and the G2 phase of the cell cycle. Involved in transcriptional regulation of P21 in response to DNA damage. Required for FANCD2 targeting to sites of DNA damage. May function as a transcriptional regulator. Inhibits lipid synthesis by binding to inactive phosphorylated ACACA and preventing its dephosphorylation. Contributes to homologous recombination repair (HRR) via its direct interaction with PALB2, fine-tunes recombinational repair partly through its modulatory role in the PALB2-dependent loading of BRCA2-RAD51 repair machinery at DNA breaks. Component of the BRCA1-RBBP8 complex which regulates CHEK1 activation and controls cell cycle G2/M checkpoints on DNA damage via BRCA1-mediated ubiquitination of RBBP8.<ref>PMID:10500182</ref> <ref>PMID:10724175</ref> <ref>PMID:11836499</ref> <ref>PMID:12890688</ref> <ref>PMID:12887909</ref> <ref>PMID:14976165</ref> <ref>PMID:14990569</ref> <ref>PMID:16818604</ref> <ref>PMID:16326698</ref> <ref>PMID:18056443</ref> <ref>PMID:17525340</ref> <ref>PMID:19261748</ref> <ref>PMID:19369211</ref> <ref>PMID:20351172</ref> <ref>PMID:20364141</ref>
	== Evolutionary Conservation ==		== Evolutionary Conservation ==
	[[Image:Consurf_key_small.gif\|200px\|right]]		[[Image:Consurf_key_small.gif\|200px\|right]]
Line 40:		Line 38:
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
-	[[Category: ~~Human~~]]	+	[[Category: Homo sapiens]]
	[[Category: Large Structures]]		[[Category: Large Structures]]
-	[[Category: Birrane, G]]	+	[[Category: Birrane G]]
-	[[Category: Brown~~, R S~~]]	+	[[Category: Brown RS]]
-	[[Category: Ladias~~, J A.A~~]]	+	[[Category: Ladias JAA]]
-	[[Category: Varma~~, A K]]~~	+	[[Category: Varma AK]]
-	~~[[Category: Antitumor protein]]~~	+
-	~~[[Category: Brca1]]~~	+
-	~~[[Category: Brct]]~~	+
-	~~[[Category: Breast cancer]]~~	+
-	~~[[Category: Ctip]]~~	+
-	~~[[Category: Phosphopeptide~~]]	+

OCA at 08:41, 20 January 2021

OCA — Wed, 20 Jan 2021 08:41:55 GMT

←Older revision		Revision as of 08:41, 20 January 2021
Line 1:		Line 1:

	==Structure of the BRCT repeats of BRCA1 bound to a CtIP phosphopeptide.==		==Structure of the BRCT repeats of BRCA1 bound to a CtIP phosphopeptide.==
-	<StructureSection load='1y98' size='340' side='right' caption='[[1y98]], [[Resolution\|resolution]] 2.50Å' scene=''>	+	<StructureSection load='1y98' size='340' side='right'caption='[[1y98]], [[Resolution\|resolution]] 2.50Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[1y98]] is a 2 chain structure with sequence from [http://en.wikipedia.org/wiki/Human Human]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1Y98 OCA]. For a <b>guided tour on the structure components</b> use [http://~~oca~~.~~weizmann.ac.il/oca-docs~~/fgij/fg.htm?mol=1Y98 FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[1y98]] is a 2 chain structure with sequence from [http://en.wikipedia.org/wiki/Human Human]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1Y98 OCA]. For a <b>guided tour on the structure components</b> use [http://proteopedia.org/fgij/fg.htm?mol=1Y98 FirstGlance]. <br>
-	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=CO:COBALT+(II)+ION'>CO</scene>, <scene name='pdbligand=SO4:SULFATE+ION'>SO4</scene></td></tr>	+	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=CO:COBALT+(II)+ION'>CO</scene>, <scene name='pdbligand=SO4:SULFATE+ION'>SO4</scene></td></tr>
	<tr id='NonStdRes'><td class="sblockLbl"><b>[[Non-Standard_Residue\|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=SEP:PHOSPHOSERINE'>SEP</scene></td></tr>		<tr id='NonStdRes'><td class="sblockLbl"><b>[[Non-Standard_Residue\|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=SEP:PHOSPHOSERINE'>SEP</scene></td></tr>
-	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1t29\|1t29]], [[1t15\|1t15]]</td></tr>	+	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat"><div style='overflow: auto; max-height: 3em;'>[[1t29\|1t29]], [[1t15\|1t15]]</div></td></tr>
	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">BRCA1 ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN])</td></tr>		<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">BRCA1 ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN])</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=1y98 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1y98 OCA], [http://pdbe.org/1y98 PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=1y98 RCSB], [http://www.ebi.ac.uk/pdbsum/1y98 PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=1y98 ProSAT]</span></td></tr>	+	<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[http://proteopedia.org/fgij/fg.htm?mol=1y98 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1y98 OCA], [http://pdbe.org/1y98 PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=1y98 RCSB], [http://www.ebi.ac.uk/pdbsum/1y98 PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=1y98 ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
Line 35:		Line 35:

	==See Also==		==See Also==
-	*[[BRCA\|BRCA]]	+	*[[BRCA 3D structures\|BRCA 3D structures]]
	== References ==		== References ==
	<references/>		<references/>
Line 41:		Line 41:
	</StructureSection>		</StructureSection>
	[[Category: Human]]		[[Category: Human]]
		+	[[Category: Large Structures]]
	[[Category: Birrane, G]]		[[Category: Birrane, G]]
	[[Category: Brown, R S]]		[[Category: Brown, R S]]

OCA at 06:37, 25 April 2018

OCA — Wed, 25 Apr 2018 06:37:15 GMT

←Older revision		Revision as of 06:37, 25 April 2018
Line 1:		Line 1:
		+
	==Structure of the BRCT repeats of BRCA1 bound to a CtIP phosphopeptide.==		==Structure of the BRCT repeats of BRCA1 bound to a CtIP phosphopeptide.==
	<StructureSection load='1y98' size='340' side='right' caption='[[1y98]], [[Resolution\|resolution]] 2.50Å' scene=''>		<StructureSection load='1y98' size='340' side='right' caption='[[1y98]], [[Resolution\|resolution]] 2.50Å' scene=''>
Line 7:		Line 8:
	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1t29\|1t29]], [[1t15\|1t15]]</td></tr>		<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1t29\|1t29]], [[1t15\|1t15]]</td></tr>
	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">BRCA1 ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN])</td></tr>		<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">BRCA1 ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN])</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=1y98 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1y98 OCA], [http://pdbe.org/1y98 PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=1y98 RCSB], [http://www.ebi.ac.uk/pdbsum/1y98 PDBsum]</span></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=1y98 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1y98 OCA], [http://pdbe.org/1y98 PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=1y98 RCSB], [http://www.ebi.ac.uk/pdbsum/1y98 PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=1y98 ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
Line 17:		Line 18:
	Check<jmol>		Check<jmol>
	<jmolCheckbox>		<jmolCheckbox>
-	<scriptWhenChecked>select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/y9/1y98_consurf.spt"</scriptWhenChecked>	+	<scriptWhenChecked>; select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/y9/1y98_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 32:		Line 33:
	</div>		</div>
	<div class="pdbe-citations 1y98" style="background-color:#fffaf0;"></div>		<div class="pdbe-citations 1y98" style="background-color:#fffaf0;"></div>
		+
		+	==See Also==
		+	*[[BRCA\|BRCA]]
	== References ==		== References ==
	<references/>		<references/>

OCA at 06:11, 10 February 2016

OCA — Wed, 10 Feb 2016 06:11:38 GMT

←Older revision		Revision as of 06:11, 10 February 2016
Line 21:		Line 21:
	<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=1y98 ConSurf].
	<div style="clear:both"></div>		<div style="clear:both"></div>
	<div style="background-color:#fffaf0;">		<div style="background-color:#fffaf0;">

OCA at 06:08, 11 September 2015

OCA — Fri, 11 Sep 2015 06:08:59 GMT

←Older revision		Revision as of 06:08, 11 September 2015
Line 2:		Line 2:
	<StructureSection load='1y98' size='340' side='right' caption='[[1y98]], [[Resolution\|resolution]] 2.50Å' scene=''>		<StructureSection load='1y98' size='340' side='right' caption='[[1y98]], [[Resolution\|resolution]] 2.50Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[1y98]] is a 2 chain structure with sequence from [http://en.wikipedia.org/wiki/~~Homo_sapiens Homo sapiens~~]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1Y98 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1Y98 FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[1y98]] is a 2 chain structure with sequence from [http://en.wikipedia.org/wiki/Human Human]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1Y98 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1Y98 FirstGlance]. <br>
	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=CO:COBALT+(II)+ION'>CO</scene>, <scene name='pdbligand=SO4:SULFATE+ION'>SO4</scene></td></tr>		</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=CO:COBALT+(II)+ION'>CO</scene>, <scene name='pdbligand=SO4:SULFATE+ION'>SO4</scene></td></tr>
	<tr id='NonStdRes'><td class="sblockLbl"><b>[[Non-Standard_Residue\|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=SEP:PHOSPHOSERINE'>SEP</scene></td></tr>		<tr id='NonStdRes'><td class="sblockLbl"><b>[[Non-Standard_Residue\|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=SEP:PHOSPHOSERINE'>SEP</scene></td></tr>
	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1t29\|1t29]], [[1t15\|1t15]]</td></tr>		<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1t29\|1t29]], [[1t15\|1t15]]</td></tr>
-	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">BRCA1 ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 ~~Homo sapiens~~])</td></tr>	+	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">BRCA1 ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN])</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=1y98 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1y98 OCA], [http://www.rcsb.org/pdb/explore.do?structureId=1y98 RCSB], [http://www.ebi.ac.uk/pdbsum/1y98 PDBsum]</span></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=1y98 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1y98 OCA], [http://pdbe.org/1y98 PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=1y98 RCSB], [http://www.ebi.ac.uk/pdbsum/1y98 PDBsum]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
Line 31:		Line 31:
	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 1y98" style="background-color:#fffaf0;"></div>
	== References ==		== References ==
	<references/>		<references/>
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
-	[[Category: ~~Homo sapiens~~]]	+	[[Category: Human]]
	[[Category: Birrane, G]]		[[Category: Birrane, G]]
	[[Category: Brown, R S]]		[[Category: Brown, R S]]

OCA at 09:12, 8 January 2015

OCA — Thu, 08 Jan 2015 09:12:52 GMT

←Older revision		Revision as of 09:12, 8 January 2015
Line 3:		Line 3:
	== Structural highlights ==		== Structural highlights ==
	<table><tr><td colspan='2'>[[1y98]] is a 2 chain structure with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1Y98 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1Y98 FirstGlance]. <br>		<table><tr><td colspan='2'>[[1y98]] is a 2 chain structure with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1Y98 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1Y98 FirstGlance]. <br>
-	</td></tr><tr><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=CO:COBALT+(II)+ION'>CO</scene>, <scene name='pdbligand=SO4:SULFATE+ION'>SO4</scene><br>	+	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=CO:COBALT+(II)+ION'>CO</scene>, <scene name='pdbligand=SO4:SULFATE+ION'>SO4</scene></td></tr>
-	<tr><td class="sblockLbl"><b>[[Non-Standard_Residue\|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=SEP:PHOSPHOSERINE'>SEP</scene></td></tr>	+	<tr id='NonStdRes'><td class="sblockLbl"><b>[[Non-Standard_Residue\|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=SEP:PHOSPHOSERINE'>SEP</scene></td></tr>
-	<tr><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1t29\|1t29]], [[1t15\|1t15]]</td></tr>	+	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1t29\|1t29]], [[1t15\|1t15]]</td></tr>
-	<tr><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">BRCA1 ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 Homo sapiens])</td></tr>	+	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">BRCA1 ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 Homo sapiens])</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=1y98 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1y98 OCA], [http://www.rcsb.org/pdb/explore.do?structureId=1y98 RCSB], [http://www.ebi.ac.uk/pdbsum/1y98 PDBsum]</span></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=1y98 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1y98 OCA], [http://www.rcsb.org/pdb/explore.do?structureId=1y98 RCSB], [http://www.ebi.ac.uk/pdbsum/1y98 PDBsum]</span></td></tr>
-	<table>	+	</table>
	== Disease ==		== Disease ==
	[[http://www.uniprot.org/uniprot/BRCA1_HUMAN BRCA1_HUMAN]] Defects in BRCA1 are a cause of susceptibility to breast cancer (BC) [MIM:[http://omim.org/entry/114480 114480]]. A common malignancy originating from breast epithelial tissue. Breast neoplasms can be distinguished by their histologic pattern. Invasive ductal carcinoma is by far the most common type. Breast cancer is etiologically and genetically heterogeneous. Important genetic factors have been indicated by familial occurrence and bilateral involvement. Mutations at more than one locus can be involved in different families or even in the same case. Note=Mutations in BRCA1 are thought to be responsible for 45% of inherited breast cancer. Moreover, BRCA1 carriers have a 4-fold increased risk of colon cancer, whereas male carriers face a 3-fold increased risk of prostate cancer. Cells lacking BRCA1 show defects in DNA repair by homologous recombination.<ref>PMID:11301010</ref> <ref>PMID:15133502</ref> <ref>PMID:7545954</ref> <ref>PMID:12427738</ref> <ref>PMID:18285836</ref> <ref>PMID:7939630</ref> <ref>PMID:7894491</ref> <ref>PMID:7894493</ref> <ref>PMID:8554067</ref> <ref>PMID:8776600</ref> <ref>PMID:8723683</ref> <ref>PMID:9760198</ref> <ref>PMID:9482581</ref> <ref>PMID:9609997</ref> <ref>PMID:10323242</ref> <ref>PMID:12442275</ref> <ref>PMID:12938098</ref> <ref>PMID:14722926</ref> Defects in BRCA1 are a cause of susceptibility to familial breast-ovarian cancer type 1 (BROVCA1) [MIM:[http://omim.org/entry/604370 604370]]. A condition associated with familial predisposition to cancer of the breast and ovaries. Characteristic features in affected families are an early age of onset of breast cancer (often before age 50), increased chance of bilateral cancers (cancer that develop in both breasts, or both ovaries, independently), frequent occurrence of breast cancer among men, increased incidence of tumors of other specific organs, such as the prostate. Note=Mutations in BRCA1 are thought to be responsible for more than 80% of inherited breast-ovarian cancer. Defects in BRCA1 are a cause of susceptibility to ovarian cancer (OC) [MIM:[http://omim.org/entry/167000 167000]]. The term ovarian cancer defines malignancies originating from ovarian tissue. Although many histologic types of ovarian tumors have been described, epithelial ovarian carcinoma is the most common form. Ovarian cancers are often asymptomatic and the recognized signs and symptoms, even of late-stage disease, are vague. Consequently, most patients are diagnosed with advanced disease. Defects in BRCA1 are a cause of susceptibility to pancreatic cancer type 4 (PNCA4) [MIM:[http://omim.org/entry/614320 614320]]. A malignant neoplasm of the pancreas. Tumors can arise from both the exocrine and endocrine portions of the pancreas, but 95% of them develop from the exocrine portion, including the ductal epithelium, acinar cells, connective tissue, and lymphatic tissue.		[[http://www.uniprot.org/uniprot/BRCA1_HUMAN BRCA1_HUMAN]] Defects in BRCA1 are a cause of susceptibility to breast cancer (BC) [MIM:[http://omim.org/entry/114480 114480]]. A common malignancy originating from breast epithelial tissue. Breast neoplasms can be distinguished by their histologic pattern. Invasive ductal carcinoma is by far the most common type. Breast cancer is etiologically and genetically heterogeneous. Important genetic factors have been indicated by familial occurrence and bilateral involvement. Mutations at more than one locus can be involved in different families or even in the same case. Note=Mutations in BRCA1 are thought to be responsible for 45% of inherited breast cancer. Moreover, BRCA1 carriers have a 4-fold increased risk of colon cancer, whereas male carriers face a 3-fold increased risk of prostate cancer. Cells lacking BRCA1 show defects in DNA repair by homologous recombination.<ref>PMID:11301010</ref> <ref>PMID:15133502</ref> <ref>PMID:7545954</ref> <ref>PMID:12427738</ref> <ref>PMID:18285836</ref> <ref>PMID:7939630</ref> <ref>PMID:7894491</ref> <ref>PMID:7894493</ref> <ref>PMID:8554067</ref> <ref>PMID:8776600</ref> <ref>PMID:8723683</ref> <ref>PMID:9760198</ref> <ref>PMID:9482581</ref> <ref>PMID:9609997</ref> <ref>PMID:10323242</ref> <ref>PMID:12442275</ref> <ref>PMID:12938098</ref> <ref>PMID:14722926</ref> Defects in BRCA1 are a cause of susceptibility to familial breast-ovarian cancer type 1 (BROVCA1) [MIM:[http://omim.org/entry/604370 604370]]. A condition associated with familial predisposition to cancer of the breast and ovaries. Characteristic features in affected families are an early age of onset of breast cancer (often before age 50), increased chance of bilateral cancers (cancer that develop in both breasts, or both ovaries, independently), frequent occurrence of breast cancer among men, increased incidence of tumors of other specific organs, such as the prostate. Note=Mutations in BRCA1 are thought to be responsible for more than 80% of inherited breast-ovarian cancer. Defects in BRCA1 are a cause of susceptibility to ovarian cancer (OC) [MIM:[http://omim.org/entry/167000 167000]]. The term ovarian cancer defines malignancies originating from ovarian tissue. Although many histologic types of ovarian tumors have been described, epithelial ovarian carcinoma is the most common form. Ovarian cancers are often asymptomatic and the recognized signs and symptoms, even of late-stage disease, are vague. Consequently, most patients are diagnosed with advanced disease. Defects in BRCA1 are a cause of susceptibility to pancreatic cancer type 4 (PNCA4) [MIM:[http://omim.org/entry/614320 614320]]. A malignant neoplasm of the pancreas. Tumors can arise from both the exocrine and endocrine portions of the pancreas, but 95% of them develop from the exocrine portion, including the ductal epithelium, acinar cells, connective tissue, and lymphatic tissue.
Line 36:		Line 36:
	</StructureSection>		</StructureSection>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
-	[[Category: Birrane, G.]]	+	[[Category: Birrane, G]]
-	[[Category: Brown, R S.]]	+	[[Category: Brown, R S]]
-	[[Category: Ladias, J A.A.]]	+	[[Category: Ladias, J A.A]]
-	[[Category: Varma, A K.]]	+	[[Category: Varma, A K]]
	[[Category: Antitumor protein]]		[[Category: Antitumor protein]]
	[[Category: Brca1]]		[[Category: Brca1]]

OCA at 19:29, 29 September 2014

OCA — Mon, 29 Sep 2014 19:29:23 GMT

←Older revision		Revision as of 19:29, 29 September 2014
Line 1:		Line 1:
-	~~{{STRUCTURE_1y98~~\| ~~PDB~~=1y98 \| ~~SCENE~~= }}	+	==Structure of the BRCT repeats of BRCA1 bound to a CtIP phosphopeptide.==
-	===~~Structure~~ of the ~~BRCT repeats~~ of BRCA1 ~~bound~~ to a ~~CtIP phosphopeptide~~.===	+	<StructureSection load='1y98' size='340' side='right' caption='[[1y98]], [[Resolution\|resolution]] 2.50Å' scene=''>
-	~~{{ABSTRACT_PUBMED_16101277}}~~	+	== Structural highlights ==
		+	<table><tr><td colspan='2'>[[1y98]] is a 2 chain structure with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1Y98 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1Y98 FirstGlance]. <br>
		+	</td></tr><tr><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=CO:COBALT+(II)+ION'>CO</scene>, <scene name='pdbligand=SO4:SULFATE+ION'>SO4</scene><br>
		+	<tr><td class="sblockLbl"><b>[[Non-Standard_Residue\|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=SEP:PHOSPHOSERINE'>SEP</scene></td></tr>
		+	<tr><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1t29\|1t29]], [[1t15\|1t15]]</td></tr>
		+	<tr><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">BRCA1 ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 Homo sapiens])</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=1y98 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1y98 OCA], [http://www.rcsb.org/pdb/explore.do?structureId=1y98 RCSB], [http://www.ebi.ac.uk/pdbsum/1y98 PDBsum]</span></td></tr>
		+	<table>
		+	== Disease ==
		+	[[http://www.uniprot.org/uniprot/BRCA1_HUMAN BRCA1_HUMAN]] Defects in BRCA1 are a cause of susceptibility to breast cancer (BC) [MIM:[http://omim.org/entry/114480 114480]]. A common malignancy originating from breast epithelial tissue. Breast neoplasms can be distinguished by their histologic pattern. Invasive ductal carcinoma is by far the most common type. Breast cancer is etiologically and genetically heterogeneous. Important genetic factors have been indicated by familial occurrence and bilateral involvement. Mutations at more than one locus can be involved in different families or even in the same case. Note=Mutations in BRCA1 are thought to be responsible for 45% of inherited breast cancer. Moreover, BRCA1 carriers have a 4-fold increased risk of colon cancer, whereas male carriers face a 3-fold increased risk of prostate cancer. Cells lacking BRCA1 show defects in DNA repair by homologous recombination.<ref>PMID:11301010</ref> <ref>PMID:15133502</ref> <ref>PMID:7545954</ref> <ref>PMID:12427738</ref> <ref>PMID:18285836</ref> <ref>PMID:7939630</ref> <ref>PMID:7894491</ref> <ref>PMID:7894493</ref> <ref>PMID:8554067</ref> <ref>PMID:8776600</ref> <ref>PMID:8723683</ref> <ref>PMID:9760198</ref> <ref>PMID:9482581</ref> <ref>PMID:9609997</ref> <ref>PMID:10323242</ref> <ref>PMID:12442275</ref> <ref>PMID:12938098</ref> <ref>PMID:14722926</ref> Defects in BRCA1 are a cause of susceptibility to familial breast-ovarian cancer type 1 (BROVCA1) [MIM:[http://omim.org/entry/604370 604370]]. A condition associated with familial predisposition to cancer of the breast and ovaries. Characteristic features in affected families are an early age of onset of breast cancer (often before age 50), increased chance of bilateral cancers (cancer that develop in both breasts, or both ovaries, independently), frequent occurrence of breast cancer among men, increased incidence of tumors of other specific organs, such as the prostate. Note=Mutations in BRCA1 are thought to be responsible for more than 80% of inherited breast-ovarian cancer. Defects in BRCA1 are a cause of susceptibility to ovarian cancer (OC) [MIM:[http://omim.org/entry/167000 167000]]. The term ovarian cancer defines malignancies originating from ovarian tissue. Although many histologic types of ovarian tumors have been described, epithelial ovarian carcinoma is the most common form. Ovarian cancers are often asymptomatic and the recognized signs and symptoms, even of late-stage disease, are vague. Consequently, most patients are diagnosed with advanced disease. Defects in BRCA1 are a cause of susceptibility to pancreatic cancer type 4 (PNCA4) [MIM:[http://omim.org/entry/614320 614320]]. A malignant neoplasm of the pancreas. Tumors can arise from both the exocrine and endocrine portions of the pancreas, but 95% of them develop from the exocrine portion, including the ductal epithelium, acinar cells, connective tissue, and lymphatic tissue.
		+	== Function ==
		+	[[http://www.uniprot.org/uniprot/BRCA1_HUMAN BRCA1_HUMAN]] E3 ubiquitin-protein ligase that specifically mediates the formation of 'Lys-6'-linked polyubiquitin chains and plays a central role in DNA repair by facilitating cellular responses to DNA damage. It is unclear whether it also mediates the formation of other types of polyubiquitin chains. The E3 ubiquitin-protein ligase activity is required for its tumor suppressor function. The BRCA1-BARD1 heterodimer coordinates a diverse range of cellular pathways such as DNA damage repair, ubiquitination and transcriptional regulation to maintain genomic stability. Regulates centrosomal microtubule nucleation. Required for normal cell cycle progression from G2 to mitosis. Required for appropriate cell cycle arrests after ionizing irradiation in both the S-phase and the G2 phase of the cell cycle. Involved in transcriptional regulation of P21 in response to DNA damage. Required for FANCD2 targeting to sites of DNA damage. May function as a transcriptional regulator. Inhibits lipid synthesis by binding to inactive phosphorylated ACACA and preventing its dephosphorylation. Contributes to homologous recombination repair (HRR) via its direct interaction with PALB2, fine-tunes recombinational repair partly through its modulatory role in the PALB2-dependent loading of BRCA2-RAD51 repair machinery at DNA breaks. Component of the BRCA1-RBBP8 complex which regulates CHEK1 activation and controls cell cycle G2/M checkpoints on DNA damage via BRCA1-mediated ubiquitination of RBBP8.<ref>PMID:10500182</ref> <ref>PMID:10724175</ref> <ref>PMID:11836499</ref> <ref>PMID:12890688</ref> <ref>PMID:12887909</ref> <ref>PMID:14976165</ref> <ref>PMID:14990569</ref> <ref>PMID:16818604</ref> <ref>PMID:16326698</ref> <ref>PMID:18056443</ref> <ref>PMID:17525340</ref> <ref>PMID:19261748</ref> <ref>PMID:19369211</ref> <ref>PMID:20351172</ref> <ref>PMID:20364141</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/y9/1y98_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 breast and ovarian tumor suppressor BRCA1 has important functions in cell cycle checkpoint control and DNA repair. Two tandem BRCA1 C-terminal (BRCT) domains are essential for the tumor suppression activity of BRCA1 and interact in a phosphorylation-dependent manner with proteins involved in DNA damage-induced checkpoint control, including the DNA helicase BACH1 and the CtBP-interacting protein (CtIP). The crystal structure of the BRCA1 BRCT repeats bound to the PTRVSpSPVFGAT phosphopeptide corresponding to residues 322-333 of human CtIP was determined at 2.5 A resolution. The peptide binds to a cleft formed by the interface of the two BRCTs in a two-pronged manner, with phospho-Ser327 and Phe330 anchoring the peptide through extensive contacts with BRCA1 residues. Several hydrogen bonds and salt bridges that stabilize the BRCA1-BACH1 complex are missing in the BRCA1-CtIP interaction, offering a structural basis for the approximately 5-fold lower affinity of BRCA1 for CtIP compared to that of BACH1, as determined by isothermal titration calorimetry. Importantly, the side chain of Arg1775 in the cancer-associated BRCA1 mutation M1775R sterically clashes with the phenyl ring of CtIP Phe330, disrupting the BRCA1-CtIP interaction. These results provide new insights into the molecular mechanisms underlying the dynamic selection of target proteins involved in DNA repair and cell cycle control by BRCA1 and reveal how certain cancer-associated mutations affect these interactions.

-	~~==Disease==~~	+	Structural basis for cell cycle checkpoint control by the BRCA1-CtIP complex.,Varma AK, Brown RS, Birrane G, Ladias JA Biochemistry. 2005 Aug 23;44(33):10941-6. PMID:16101277<ref>PMID:16101277</ref>
-	[[http://www.uniprot.org/uniprot/BRCA1_HUMAN BRCA1_HUMAN]] Defects in BRCA1 are a cause of susceptibility to breast cancer (BC) [MIM:[http://omim.org/entry/114480 114480]]. A common malignancy originating from breast epithelial tissue. Breast neoplasms can be distinguished by ~~their histologic pattern. Invasive ductal carcinoma is by far~~ the most common type. Breast cancer is etiologically and genetically heterogeneous. Important genetic factors have been indicated by familial occurrence and bilateral involvement. Mutations at more than one locus can be involved in different families or even in the same case. Note=Mutations in BRCA1 ~~are thought to be responsible for 45% of inherited breast cancer~~. ~~Moreover~~, ~~BRCA1 carriers have a 4-fold increased risk of colon cancer~~, ~~whereas male carriers face a 3~~-~~fold increased risk of prostate cancer~~. ~~Cells lacking BRCA1 show defects in DNA repair by homologous recombination.<ref>~~PMID:~~11301010</ref>~~<ref>PMID:~~15133502~~</ref><ref>PMID:7545954</ref><ref>PMID:12427738</ref><ref>PMID:18285836</ref><ref>PMID:7939630</ref><ref>PMID:7894491</ref><ref>PMID:7894493</ref><ref>PMID:8554067</ref><ref>PMID:8776600</ref><ref>PMID:8723683</ref><ref>PMID:9760198</ref><ref>PMID:9482581</ref><ref>PMID:9609997</ref><ref>PMID:10323242</ref><ref>PMID:12442275</ref><ref>PMID:12938098</ref><ref>PMID:14722926</ref> Defects in BRCA1 are a cause of susceptibility to familial breast-ovarian cancer type 1 (BROVCA1) [MIM:[http://omim.org/entry/604370 604370]]. A condition associated with familial predisposition to cancer of the breast and ovaries. Characteristic features in affected families are an early age of onset of breast cancer (often before age 50), increased chance of bilateral cancers (cancer that develop in both breasts, or both ovaries, independently), frequent occurrence of breast cancer among men, increased incidence of tumors of other specific organs, such as the prostate. Note=Mutations in BRCA1 are thought to be responsible for more than 80% of inherited breast-ovarian cancer. Defects in BRCA1 are a cause of susceptibility to ovarian cancer (OC) [MIM:[http://omim.org/entry/167000 167000]]. The term ovarian cancer defines malignancies originating from ovarian tissue. Although many histologic types of ovarian tumors have been described, epithelial ovarian carcinoma is the most common form. Ovarian cancers are often asymptomatic and the recognized signs and symptoms, even of late-stage disease, are vague. Consequently, most patients are diagnosed with advanced disease. Defects in BRCA1 are a cause of susceptibility to pancreatic cancer type 4 (PNCA4) [MIM:[http://omim.org/entry/614320 614320]]. A malignant neoplasm of the pancreas. Tumors can arise from both the exocrine and endocrine portions of the pancreas, but 95% of them develop from the exocrine portion, including the ductal epithelium, acinar cells, connective tissue, and lymphatic tissue.	+

-	~~==Function==~~	+	From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>
-	~~[[http:~~/~~/www.uniprot.org/uniprot/BRCA1_HUMAN BRCA1_HUMAN]] E3 ubiquitin-protein ligase that specifically mediates the formation~~ of ~~'Lys-6'-linked polyubiquitin chains and plays a central role in DNA repair by facilitating cellular responses to DNA damage. It is unclear whether it also mediates~~ the ~~formation of other types of polyubiquitin chains~~. The E3 ubiquitin-protein ligase activity is required for its tumor suppressor function. The BRCA1-BARD1 heterodimer coordinates a diverse range of cellular pathways such as DNA damage repair, ubiquitination and transcriptional regulation to maintain genomic stability. Regulates centrosomal microtubule nucleation. Required for normal cell cycle progression from G2 to mitosis. Required for appropriate cell cycle arrests after ionizing irradiation in both the S~~-phase and the G2 phase of the cell cycle~~. ~~Involved in transcriptional regulation~~ of P21 in response to DNA damage. Required for FANCD2 targeting to sites of DNA damage. May function as a transcriptional regulator. Inhibits lipid synthesis by binding to inactive phosphorylated ACACA and preventing its dephosphorylation. Contributes to homologous recombination repair (HRR) via its direct interaction with PALB2, fine-tunes recombinational repair partly through its modulatory role in the PALB2-dependent loading of BRCA2-RAD51 repair machinery at DNA breaks. Component of the BRCA1-RBBP8 complex which regulates CHEK1 activation and controls cell cycle G2/M checkpoints on DNA damage via BRCA1-mediated ubiquitination of RBBP8.<~~ref~~>~~PMID:10500182~~</~~ref~~><ref>PMID:10724175</ref><ref>PMID:11836499</ref><ref>PMID:12890688</ref><ref>PMID:12887909</ref><ref>PMID:14976165</ref><ref>PMID:14990569</ref><ref>PMID:16818604</ref><ref>PMID:16326698</ref><ref>PMID:18056443</ref><ref>PMID:17525340</ref><ref>PMID:19261748</ref><ref>PMID:19369211</ref><ref>PMID:20351172</ref><ref>PMID:20364141</ref>	+	</div>
-		+	== References ==
-	==~~About this Structure==~~	+	<references/>
-	[[1y98]] is a 2 chain structure with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1Y98 OCA].	+	__TOC__
-		+	</StructureSection>
-	~~==Reference~~==	+
-	~~<ref group="xtra">PMID:016101277</ref>~~<references ~~group="xtra"~~/><~~references~~/>	+
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
	[[Category: Birrane, G.]]		[[Category: Birrane, G.]]

OCA at 01:18, 25 March 2013

OCA — Mon, 25 Mar 2013 01:18:06 GMT

←Older revision		Revision as of 01:18, 25 March 2013
Line 1:		Line 1:
-	[[Image:1y98.png\|left\|200px]]
-
	{{STRUCTURE_1y98\| PDB=1y98 \| SCENE= }}		{{STRUCTURE_1y98\| PDB=1y98 \| SCENE= }}
-
	===Structure of the BRCT repeats of BRCA1 bound to a CtIP phosphopeptide.===		===Structure of the BRCT repeats of BRCA1 bound to a CtIP phosphopeptide.===
		+	{{ABSTRACT_PUBMED_16101277}}

-	~~{{ABSTRACT_PUBMED_16101277}}~~	+	==Disease==
		+	[[http://www.uniprot.org/uniprot/BRCA1_HUMAN BRCA1_HUMAN]] Defects in BRCA1 are a cause of susceptibility to breast cancer (BC) [MIM:[http://omim.org/entry/114480 114480]]. A common malignancy originating from breast epithelial tissue. Breast neoplasms can be distinguished by their histologic pattern. Invasive ductal carcinoma is by far the most common type. Breast cancer is etiologically and genetically heterogeneous. Important genetic factors have been indicated by familial occurrence and bilateral involvement. Mutations at more than one locus can be involved in different families or even in the same case. Note=Mutations in BRCA1 are thought to be responsible for 45% of inherited breast cancer. Moreover, BRCA1 carriers have a 4-fold increased risk of colon cancer, whereas male carriers face a 3-fold increased risk of prostate cancer. Cells lacking BRCA1 show defects in DNA repair by homologous recombination.<ref>PMID:11301010</ref><ref>PMID:15133502</ref><ref>PMID:7545954</ref><ref>PMID:12427738</ref><ref>PMID:18285836</ref><ref>PMID:7939630</ref><ref>PMID:7894491</ref><ref>PMID:7894493</ref><ref>PMID:8554067</ref><ref>PMID:8776600</ref><ref>PMID:8723683</ref><ref>PMID:9760198</ref><ref>PMID:9482581</ref><ref>PMID:9609997</ref><ref>PMID:10323242</ref><ref>PMID:12442275</ref><ref>PMID:12938098</ref><ref>PMID:14722926</ref> Defects in BRCA1 are a cause of susceptibility to familial breast-ovarian cancer type 1 (BROVCA1) [MIM:[http://omim.org/entry/604370 604370]]. A condition associated with familial predisposition to cancer of the breast and ovaries. Characteristic features in affected families are an early age of onset of breast cancer (often before age 50), increased chance of bilateral cancers (cancer that develop in both breasts, or both ovaries, independently), frequent occurrence of breast cancer among men, increased incidence of tumors of other specific organs, such as the prostate. Note=Mutations in BRCA1 are thought to be responsible for more than 80% of inherited breast-ovarian cancer. Defects in BRCA1 are a cause of susceptibility to ovarian cancer (OC) [MIM:[http://omim.org/entry/167000 167000]]. The term ovarian cancer defines malignancies originating from ovarian tissue. Although many histologic types of ovarian tumors have been described, epithelial ovarian carcinoma is the most common form. Ovarian cancers are often asymptomatic and the recognized signs and symptoms, even of late-stage disease, are vague. Consequently, most patients are diagnosed with advanced disease. Defects in BRCA1 are a cause of susceptibility to pancreatic cancer type 4 (PNCA4) [MIM:[http://omim.org/entry/614320 614320]]. A malignant neoplasm of the pancreas. Tumors can arise from both the exocrine and endocrine portions of the pancreas, but 95% of them develop from the exocrine portion, including the ductal epithelium, acinar cells, connective tissue, and lymphatic tissue.
		+
		+	==Function==
		+	[[http://www.uniprot.org/uniprot/BRCA1_HUMAN BRCA1_HUMAN]] E3 ubiquitin-protein ligase that specifically mediates the formation of 'Lys-6'-linked polyubiquitin chains and plays a central role in DNA repair by facilitating cellular responses to DNA damage. It is unclear whether it also mediates the formation of other types of polyubiquitin chains. The E3 ubiquitin-protein ligase activity is required for its tumor suppressor function. The BRCA1-BARD1 heterodimer coordinates a diverse range of cellular pathways such as DNA damage repair, ubiquitination and transcriptional regulation to maintain genomic stability. Regulates centrosomal microtubule nucleation. Required for normal cell cycle progression from G2 to mitosis. Required for appropriate cell cycle arrests after ionizing irradiation in both the S-phase and the G2 phase of the cell cycle. Involved in transcriptional regulation of P21 in response to DNA damage. Required for FANCD2 targeting to sites of DNA damage. May function as a transcriptional regulator. Inhibits lipid synthesis by binding to inactive phosphorylated ACACA and preventing its dephosphorylation. Contributes to homologous recombination repair (HRR) via its direct interaction with PALB2, fine-tunes recombinational repair partly through its modulatory role in the PALB2-dependent loading of BRCA2-RAD51 repair machinery at DNA breaks. Component of the BRCA1-RBBP8 complex which regulates CHEK1 activation and controls cell cycle G2/M checkpoints on DNA damage via BRCA1-mediated ubiquitination of RBBP8.<ref>PMID:10500182</ref><ref>PMID:10724175</ref><ref>PMID:11836499</ref><ref>PMID:12890688</ref><ref>PMID:12887909</ref><ref>PMID:14976165</ref><ref>PMID:14990569</ref><ref>PMID:16818604</ref><ref>PMID:16326698</ref><ref>PMID:18056443</ref><ref>PMID:17525340</ref><ref>PMID:19261748</ref><ref>PMID:19369211</ref><ref>PMID:20351172</ref><ref>PMID:20364141</ref>

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

	==Reference==		==Reference==
-	<ref group="xtra">PMID:016101277</ref><references group="xtra"/>	+	<ref group="xtra">PMID:016101277</ref><references group="xtra"/><references/>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
	[[Category: Birrane, G.]]		[[Category: Birrane, G.]]

OCA: Protected "1y98" [edit=sysop:move=sysop]

OCA — Sat, 05 Jan 2013 17:14:45 GMT

Protected "1y98" [edit=sysop:move=sysop]

←Older revision

Revision as of 17:14, 5 January 2013

OCA at 17:14, 5 January 2013

OCA — Sat, 05 Jan 2013 17:14:43 GMT

←Older revision		Revision as of 17:14, 5 January 2013
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-	{{Seed}}
	[[Image:1y98.png\|left\|200px]]		[[Image:1y98.png\|left\|200px]]

-	<!--
-	The line below this paragraph, containing "STRUCTURE_1y98", creates the "Structure Box" on the page.
-	You may change the PDB parameter (which sets the PDB file loaded into the applet)
-	or the SCENE parameter (which sets the initial scene displayed when the page is loaded),
-	or leave the SCENE parameter empty for the default display.
-	-->
	{{STRUCTURE_1y98\| PDB=1y98 \| SCENE= }}		{{STRUCTURE_1y98\| PDB=1y98 \| SCENE= }}

	===Structure of the BRCT repeats of BRCA1 bound to a CtIP phosphopeptide.===		===Structure of the BRCT repeats of BRCA1 bound to a CtIP phosphopeptide.===

-
-	<!--
-	The line below this paragraph, {{ABSTRACT_PUBMED_16101277}}, adds the Publication Abstract to the page
-	(as it appears on PubMed at http://www.pubmed.gov), where 16101277 is the PubMed ID number.
-	-->
	{{ABSTRACT_PUBMED_16101277}}		{{ABSTRACT_PUBMED_16101277}}
-
-	==Disease==
-	Known disease associated with this structure: Breast cancer-1 OMIM:[[http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=113705 113705]], Breast-ovarian cancer OMIM:[[http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=113705 113705]], Ovarian cancer OMIM:[[http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=113705 113705]], Papillary serous carcinoma of the peritoneum OMIM:[[http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=113705 113705]]

	==About this Structure==		==About this Structure==
-	~~1Y98~~ is a 2 ~~chains~~ structure ~~of sequences~~ from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1Y98 OCA].	+	[[1y98]] is a 2 chain structure with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1Y98 OCA].

	==Reference==		==Reference==
-	<ref group="xtra">PMID:~~16101277~~</ref><references group="xtra"/>	+	<ref group="xtra">PMID:016101277</ref><references group="xtra"/>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
	[[Category: Birrane, G.]]		[[Category: Birrane, G.]]
Line 32:		Line 17:
	[[Category: Ladias, J A.A.]]		[[Category: Ladias, J A.A.]]
	[[Category: Varma, A K.]]		[[Category: Varma, A K.]]
		+	[[Category: Antitumor protein]]
	[[Category: Brca1]]		[[Category: Brca1]]
	[[Category: Brct]]		[[Category: Brct]]
Line 37:		Line 23:
	[[Category: Ctip]]		[[Category: Ctip]]
	[[Category: Phosphopeptide]]		[[Category: Phosphopeptide]]
-
-	''Page seeded by [http://oca.weizmann.ac.il/oca OCA ] on Tue Feb 17 16:02:38 2009''