3nh7 - Revision history

OCA at 16:46, 1 November 2023

OCA — Wed, 01 Nov 2023 16:46:25 GMT

←Older revision		Revision as of 16:46, 1 November 2023
Line 3:		Line 3:
	<StructureSection load='3nh7' size='340' side='right'caption='[[3nh7]], [[Resolution\|resolution]] 2.70Å' scene=''>		<StructureSection load='3nh7' size='340' side='right'caption='[[3nh7]], [[Resolution\|resolution]] 2.70Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[3nh7]] is a 12 chain structure with sequence from [https://en.wikipedia.org/wiki/~~Human Human~~]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3NH7 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=3NH7 FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[3nh7]] is a 12 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=3NH7 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=3NH7 FirstGlance]. <br>
-	</td></tr><tr id='~~related~~'><td class="sblockLbl"><b>[[~~Related_structure~~\|~~Related~~:]]</b></td><td class="sblockDat"~~><div style='overflow: auto; max-height: 3em;'>[[1rew\|1rew]], [[2k3g\|2k3g]]</div></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]] 2.7Å</td></tr>
-	~~<tr~~ id~~='gene'><td class~~="~~sblockLbl~~">~~<b>~~[[~~Gene~~\|~~Gene:~~]]~~</b></td><td class="sblockDat">BMPR1A ([https://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN])</td></tr>~~	+
-	<tr id='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[https://en.wikipedia.org/wiki/Receptor_protein_serine/threonine_kinase Receptor protein serine/threonine kinase], with EC number [https://www.brenda-enzymes.info/php/result_flat.php4?ecno=2.7~~.11.30 2.7.11.30] </span>~~</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=3nh7 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3nh7 OCA], [https://pdbe.org/3nh7 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=3nh7 RCSB], [https://www.ebi.ac.uk/pdbsum/3nh7 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=3nh7 ProSAT]</span></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=3nh7 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3nh7 OCA], [https://pdbe.org/3nh7 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=3nh7 RCSB], [https://www.ebi.ac.uk/pdbsum/3nh7 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=3nh7 ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
-	[[https://www.uniprot.org/uniprot/BMR1A_HUMAN BMR1A_HUMAN]] Defects in BMPR1A are a cause of juvenile polyposis syndrome (JPS) [MIM:[https://omim.org/entry/174900 174900]]; also known as juvenile intestinal polyposis (JIP). JPS is an autosomal dominant gastrointestinal hamartomatous polyposis syndrome in which patients are at risk for developing gastrointestinal cancers. The lesions are typified by a smooth histological appearance, predominant stroma, cystic spaces and lack of a smooth muscle core. Multiple juvenile polyps usually occur in a number of Mendelian disorders. Sometimes, these polyps occur without associated features as in JPS; here, polyps tend to occur in the large bowel and are associated with an increased risk of colon and other gastrointestinal cancers.<ref>PMID:11381269</ref> <ref>PMID:11536076</ref> <ref>PMID:12417513</ref> <ref>PMID:12136244</ref> <ref>PMID:12630959</ref> Defects in BMPR1A are a cause of Cowden disease (CD) [MIM:[https://omim.org/entry/158350 158350]]. CD is an autosomal dominant cancer syndrome characterized by multiple hamartomas and by a high risk for breast, thyroid and endometrial cancers.<ref>PMID:11381269</ref> <ref>PMID:11536076</ref> Defects in BMPR1A are the cause of hereditary mixed polyposis syndrome 2 (HMPS2) [MIM:[https://omim.org/entry/610069 610069]]. Hereditary mixed polyposis syndrome (HMPS) is characterized by atypical juvenile polyps, colonic adenomas, and colorectal carcinomas.<ref>PMID:11381269</ref> Note=A microdeletion of chromosome 10q23 involving BMPR1A and PTEN is a cause of chromosome 10q23 deletion syndrome, which shows overlapping features of the following three disorders: Bannayan-Zonana syndrome, Cowden disease and juvenile polyposis syndrome.<ref>PMID:11381269</ref>	+	[https://www.uniprot.org/uniprot/BMR1A_HUMAN BMR1A_HUMAN] Defects in BMPR1A are a cause of juvenile polyposis syndrome (JPS) [MIM:[https://omim.org/entry/174900 174900]; also known as juvenile intestinal polyposis (JIP). JPS is an autosomal dominant gastrointestinal hamartomatous polyposis syndrome in which patients are at risk for developing gastrointestinal cancers. The lesions are typified by a smooth histological appearance, predominant stroma, cystic spaces and lack of a smooth muscle core. Multiple juvenile polyps usually occur in a number of Mendelian disorders. Sometimes, these polyps occur without associated features as in JPS; here, polyps tend to occur in the large bowel and are associated with an increased risk of colon and other gastrointestinal cancers.<ref>PMID:11381269</ref> <ref>PMID:11536076</ref> <ref>PMID:12417513</ref> <ref>PMID:12136244</ref> <ref>PMID:12630959</ref> Defects in BMPR1A are a cause of Cowden disease (CD) [MIM:[https://omim.org/entry/158350 158350]. CD is an autosomal dominant cancer syndrome characterized by multiple hamartomas and by a high risk for breast, thyroid and endometrial cancers.<ref>PMID:11381269</ref> <ref>PMID:11536076</ref> Defects in BMPR1A are the cause of hereditary mixed polyposis syndrome 2 (HMPS2) [MIM:[https://omim.org/entry/610069 610069]. Hereditary mixed polyposis syndrome (HMPS) is characterized by atypical juvenile polyps, colonic adenomas, and colorectal carcinomas.<ref>PMID:11381269</ref> Note=A microdeletion of chromosome 10q23 involving BMPR1A and PTEN is a cause of chromosome 10q23 deletion syndrome, which shows overlapping features of the following three disorders: Bannayan-Zonana syndrome, Cowden disease and juvenile polyposis syndrome.<ref>PMID:11381269</ref>
	== Function ==		== Function ==
-	[[https://www.uniprot.org/uniprot/BMR1A_HUMAN BMR1A_HUMAN]] On ligand binding, forms a receptor complex consisting of two type II and two type I transmembrane serine/threonine kinases. Type II receptors phosphorylate and activate type I receptors which autophosphorylate, then bind and activate SMAD transcriptional regulators. Receptor for BMP-2 and BMP-4.	+	[https://www.uniprot.org/uniprot/BMR1A_HUMAN BMR1A_HUMAN] On ligand binding, forms a receptor complex consisting of two type II and two type I transmembrane serine/threonine kinases. Type II receptors phosphorylate and activate type I receptors which autophosphorylate, then bind and activate SMAD transcriptional regulators. Receptor for BMP-2 and BMP-4.
	<div style="background-color:#fffaf0;">		<div style="background-color:#fffaf0;">
	== Publication Abstract from PubMed ==		== Publication Abstract from PubMed ==
Line 30:		Line 28:
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
-	[[Category: ~~Human~~]]	+	[[Category: Homo sapiens]]
	[[Category: Large Structures]]		[[Category: Large Structures]]
-	~~[[Category: Receptor protein serine/threonine kinase]]~~	+	[[Category: Harth S]]
-	[[Category: Harth, S]]	+	[[Category: Mueller TD]]
-	[[Category: Mueller~~, T D~~]]	+	[[Category: Sebald W]]
-	[[Category: Sebald, W]]	+
-	~~[[Category: Antibody-antigen complex]]~~	+
-	~~[[Category: Bmp receptor extracellular domain]]~~	+
-	~~[[Category: Bone morphogenetic protein]]~~	+
-	~~[[Category: Immune system~~]]	+

OCA at 07:02, 12 May 2022

OCA — Thu, 12 May 2022 07:02:03 GMT

←Older revision		Revision as of 07:02, 12 May 2022
Line 1:		Line 1:

	==Crystal structure of the neutralizing Fab fragment AbD1556 bound to the BMP type I receptor IA==		==Crystal structure of the neutralizing Fab fragment AbD1556 bound to the BMP type I receptor IA==
-	<StructureSection load='3nh7' size='340' side='right' caption='[[3nh7]], [[Resolution\|resolution]] 2.70Å' scene=''>	+	<StructureSection load='3nh7' size='340' side='right'caption='[[3nh7]], [[Resolution\|resolution]] 2.70Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[3nh7]] is a 12 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=3NH7 OCA]. For a <b>guided tour on the structure components</b> use [~~http~~://~~oca~~.~~weizmann.ac.il/oca-docs~~/fgij/fg.htm?mol=3NH7 FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[3nh7]] is a 12 chain structure with sequence from [https://en.wikipedia.org/wiki/Human Human]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3NH7 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=3NH7 FirstGlance]. <br>
-	</td></tr><tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1rew\|1rew]], [[2k3g\|2k3g]]</td></tr>	+	</td></tr><tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat"><div style='overflow: auto; max-height: 3em;'>[[1rew\|1rew]], [[2k3g\|2k3g]]</div></td></tr>
-	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">BMPR1A ([~~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">BMPR1A ([https://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN])</td></tr>
-	<tr id='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[~~http~~://en.wikipedia.org/wiki/Receptor_protein_serine/threonine_kinase Receptor protein serine/threonine kinase], with EC number [~~http~~://www.brenda-enzymes.info/php/result_flat.php4?ecno=2.7.11.30 2.7.11.30] </span></td></tr>	+	<tr id='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[https://en.wikipedia.org/wiki/Receptor_protein_serine/threonine_kinase Receptor protein serine/threonine kinase], with EC number [https://www.brenda-enzymes.info/php/result_flat.php4?ecno=2.7.11.30 2.7.11.30] </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=3nh7 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3nh7 OCA], [~~http~~://pdbe.org/3nh7 PDBe], [~~http~~://www.rcsb.org/pdb/explore.do?structureId=3nh7 RCSB], [~~http~~://www.ebi.ac.uk/pdbsum/3nh7 PDBsum], [~~http~~://prosat.h-its.org/prosat/prosatexe?pdbcode=3nh7 ProSAT]</span></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=3nh7 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3nh7 OCA], [https://pdbe.org/3nh7 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=3nh7 RCSB], [https://www.ebi.ac.uk/pdbsum/3nh7 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=3nh7 ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
-	[[~~http~~://www.uniprot.org/uniprot/BMR1A_HUMAN BMR1A_HUMAN]] Defects in BMPR1A are a cause of juvenile polyposis syndrome (JPS) [MIM:[~~http~~://omim.org/entry/174900 174900]]; also known as juvenile intestinal polyposis (JIP). JPS is an autosomal dominant gastrointestinal hamartomatous polyposis syndrome in which patients are at risk for developing gastrointestinal cancers. The lesions are typified by a smooth histological appearance, predominant stroma, cystic spaces and lack of a smooth muscle core. Multiple juvenile polyps usually occur in a number of Mendelian disorders. Sometimes, these polyps occur without associated features as in JPS; here, polyps tend to occur in the large bowel and are associated with an increased risk of colon and other gastrointestinal cancers.<ref>PMID:11381269</ref> <ref>PMID:11536076</ref> <ref>PMID:12417513</ref> <ref>PMID:12136244</ref> <ref>PMID:12630959</ref> Defects in BMPR1A are a cause of Cowden disease (CD) [MIM:[~~http~~://omim.org/entry/158350 158350]]. CD is an autosomal dominant cancer syndrome characterized by multiple hamartomas and by a high risk for breast, thyroid and endometrial cancers.<ref>PMID:11381269</ref> <ref>PMID:11536076</ref> Defects in BMPR1A are the cause of hereditary mixed polyposis syndrome 2 (HMPS2) [MIM:[~~http~~://omim.org/entry/610069 610069]]. Hereditary mixed polyposis syndrome (HMPS) is characterized by atypical juvenile polyps, colonic adenomas, and colorectal carcinomas.<ref>PMID:11381269</ref> Note=A microdeletion of chromosome 10q23 involving BMPR1A and PTEN is a cause of chromosome 10q23 deletion syndrome, which shows overlapping features of the following three disorders: Bannayan-Zonana syndrome, Cowden disease and juvenile polyposis syndrome.<ref>PMID:11381269</ref>	+	[[https://www.uniprot.org/uniprot/BMR1A_HUMAN BMR1A_HUMAN]] Defects in BMPR1A are a cause of juvenile polyposis syndrome (JPS) [MIM:[https://omim.org/entry/174900 174900]]; also known as juvenile intestinal polyposis (JIP). JPS is an autosomal dominant gastrointestinal hamartomatous polyposis syndrome in which patients are at risk for developing gastrointestinal cancers. The lesions are typified by a smooth histological appearance, predominant stroma, cystic spaces and lack of a smooth muscle core. Multiple juvenile polyps usually occur in a number of Mendelian disorders. Sometimes, these polyps occur without associated features as in JPS; here, polyps tend to occur in the large bowel and are associated with an increased risk of colon and other gastrointestinal cancers.<ref>PMID:11381269</ref> <ref>PMID:11536076</ref> <ref>PMID:12417513</ref> <ref>PMID:12136244</ref> <ref>PMID:12630959</ref> Defects in BMPR1A are a cause of Cowden disease (CD) [MIM:[https://omim.org/entry/158350 158350]]. CD is an autosomal dominant cancer syndrome characterized by multiple hamartomas and by a high risk for breast, thyroid and endometrial cancers.<ref>PMID:11381269</ref> <ref>PMID:11536076</ref> Defects in BMPR1A are the cause of hereditary mixed polyposis syndrome 2 (HMPS2) [MIM:[https://omim.org/entry/610069 610069]]. Hereditary mixed polyposis syndrome (HMPS) is characterized by atypical juvenile polyps, colonic adenomas, and colorectal carcinomas.<ref>PMID:11381269</ref> Note=A microdeletion of chromosome 10q23 involving BMPR1A and PTEN is a cause of chromosome 10q23 deletion syndrome, which shows overlapping features of the following three disorders: Bannayan-Zonana syndrome, Cowden disease and juvenile polyposis syndrome.<ref>PMID:11381269</ref>
	== Function ==		== Function ==
-	[[~~http~~://www.uniprot.org/uniprot/BMR1A_HUMAN BMR1A_HUMAN]] On ligand binding, forms a receptor complex consisting of two type II and two type I transmembrane serine/threonine kinases. Type II receptors phosphorylate and activate type I receptors which autophosphorylate, then bind and activate SMAD transcriptional regulators. Receptor for BMP-2 and BMP-4.	+	[[https://www.uniprot.org/uniprot/BMR1A_HUMAN BMR1A_HUMAN]] On ligand binding, forms a receptor complex consisting of two type II and two type I transmembrane serine/threonine kinases. Type II receptors phosphorylate and activate type I receptors which autophosphorylate, then bind and activate SMAD transcriptional regulators. Receptor for BMP-2 and BMP-4.
	<div style="background-color:#fffaf0;">		<div style="background-color:#fffaf0;">
	== Publication Abstract from PubMed ==		== Publication Abstract from PubMed ==
Line 25:		Line 25:
	==See Also==		==See Also==
	*[[Antibody 3D structures\|Antibody 3D structures]]		*[[Antibody 3D structures\|Antibody 3D structures]]
		+	*[[3D structures of human antibody\|3D structures of human antibody]]
	== References ==		== References ==
	<references/>		<references/>
Line 30:		Line 31:
	</StructureSection>		</StructureSection>
	[[Category: Human]]		[[Category: Human]]
		+	[[Category: Large Structures]]
	[[Category: Receptor protein serine/threonine kinase]]		[[Category: Receptor protein serine/threonine kinase]]
	[[Category: Harth, S]]		[[Category: Harth, S]]

OCA at 13:23, 16 January 2019

OCA — Wed, 16 Jan 2019 13:23:51 GMT

←Older revision		Revision as of 13:23, 16 January 2019
Line 24:		Line 24:

	==See Also==		==See Also==
-	*[[3D structures ~~of antibody~~\|3D structures ~~of antibody~~]]	+	*[[Antibody 3D structures\|Antibody 3D structures]]
	== References ==		== References ==
	<references/>		<references/>

OCA at 18:30, 4 August 2016

OCA — Thu, 04 Aug 2016 18:30:58 GMT

←Older revision		Revision as of 18:30, 4 August 2016
Line 1:		Line 1:
		+
	==Crystal structure of the neutralizing Fab fragment AbD1556 bound to the BMP type I receptor IA==		==Crystal structure of the neutralizing Fab fragment AbD1556 bound to the BMP type I receptor IA==
	<StructureSection load='3nh7' size='340' side='right' caption='[[3nh7]], [[Resolution\|resolution]] 2.70Å' scene=''>		<StructureSection load='3nh7' size='340' side='right' caption='[[3nh7]], [[Resolution\|resolution]] 2.70Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[3nh7]] is a 12 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=3NH7 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3NH7 FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[3nh7]] is a 12 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=3NH7 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3NH7 FirstGlance]. <br>
	</td></tr><tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1rew\|1rew]], [[2k3g\|2k3g]]</td></tr>		</td></tr><tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1rew\|1rew]], [[2k3g\|2k3g]]</td></tr>
-	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">BMPR1A ([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">BMPR1A ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN])</td></tr>
	<tr id='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[http://en.wikipedia.org/wiki/Receptor_protein_serine/threonine_kinase Receptor protein serine/threonine kinase], with EC number [http://www.brenda-enzymes.info/php/result_flat.php4?ecno=2.7.11.30 2.7.11.30] </span></td></tr>		<tr id='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[http://en.wikipedia.org/wiki/Receptor_protein_serine/threonine_kinase Receptor protein serine/threonine kinase], with EC number [http://www.brenda-enzymes.info/php/result_flat.php4?ecno=2.7.11.30 2.7.11.30] </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=3nh7 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3nh7 OCA], [http://www.rcsb.org/pdb/explore.do?structureId=3nh7 RCSB], [http://www.ebi.ac.uk/pdbsum/3nh7 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=3nh7 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3nh7 OCA], [http://pdbe.org/3nh7 PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=3nh7 RCSB], [http://www.ebi.ac.uk/pdbsum/3nh7 PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=3nh7 ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
Line 20:		Line 21:
	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 3nh7" style="background-color:#fffaf0;"></div>

	==See Also==		==See Also==
-	*[[~~Antibody~~\|~~Antibody~~]]	+	*[[3D structures of antibody\|3D structures of antibody]]
	== References ==		== References ==
	<references/>		<references/>
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
-	[[Category: ~~Homo sapiens~~]]	+	[[Category: Human]]
	[[Category: Receptor protein serine/threonine kinase]]		[[Category: Receptor protein serine/threonine kinase]]
	[[Category: Harth, S]]		[[Category: Harth, S]]

OCA at 16:12, 18 December 2014

OCA — Thu, 18 Dec 2014 16:12:08 GMT

←Older revision		Revision as of 16:12, 18 December 2014
Line 1:		Line 1:
-	~~{{STRUCTURE_3nh7\| PDB=3nh7 \| SCENE= }}~~	+	==Crystal structure of the neutralizing Fab fragment AbD1556 bound to the BMP type I receptor IA==
-	===Crystal structure of the neutralizing Fab fragment AbD1556 bound to the BMP type I receptor IA===	+	<StructureSection load='3nh7' size='340' side='right' caption='[[3nh7]], [[Resolution\|resolution]] 2.70Å' scene=''>
-	~~{{ABSTRACT_PUBMED_20927405}}~~	+	== Structural highlights ==
		+	<table><tr><td colspan='2'>[[3nh7]] is a 12 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=3NH7 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3NH7 FirstGlance]. <br>
		+	</td></tr><tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1rew\|1rew]], [[2k3g\|2k3g]]</td></tr>
		+	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">BMPR1A ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 Homo sapiens])</td></tr>
		+	<tr id='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[http://en.wikipedia.org/wiki/Receptor_protein_serine/threonine_kinase Receptor protein serine/threonine kinase], with EC number [http://www.brenda-enzymes.info/php/result_flat.php4?ecno=2.7.11.30 2.7.11.30] </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=3nh7 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3nh7 OCA], [http://www.rcsb.org/pdb/explore.do?structureId=3nh7 RCSB], [http://www.ebi.ac.uk/pdbsum/3nh7 PDBsum]</span></td></tr>
		+	</table>
		+	== Disease ==
		+	[[http://www.uniprot.org/uniprot/BMR1A_HUMAN BMR1A_HUMAN]] Defects in BMPR1A are a cause of juvenile polyposis syndrome (JPS) [MIM:[http://omim.org/entry/174900 174900]]; also known as juvenile intestinal polyposis (JIP). JPS is an autosomal dominant gastrointestinal hamartomatous polyposis syndrome in which patients are at risk for developing gastrointestinal cancers. The lesions are typified by a smooth histological appearance, predominant stroma, cystic spaces and lack of a smooth muscle core. Multiple juvenile polyps usually occur in a number of Mendelian disorders. Sometimes, these polyps occur without associated features as in JPS; here, polyps tend to occur in the large bowel and are associated with an increased risk of colon and other gastrointestinal cancers.<ref>PMID:11381269</ref> <ref>PMID:11536076</ref> <ref>PMID:12417513</ref> <ref>PMID:12136244</ref> <ref>PMID:12630959</ref> Defects in BMPR1A are a cause of Cowden disease (CD) [MIM:[http://omim.org/entry/158350 158350]]. CD is an autosomal dominant cancer syndrome characterized by multiple hamartomas and by a high risk for breast, thyroid and endometrial cancers.<ref>PMID:11381269</ref> <ref>PMID:11536076</ref> Defects in BMPR1A are the cause of hereditary mixed polyposis syndrome 2 (HMPS2) [MIM:[http://omim.org/entry/610069 610069]]. Hereditary mixed polyposis syndrome (HMPS) is characterized by atypical juvenile polyps, colonic adenomas, and colorectal carcinomas.<ref>PMID:11381269</ref> Note=A microdeletion of chromosome 10q23 involving BMPR1A and PTEN is a cause of chromosome 10q23 deletion syndrome, which shows overlapping features of the following three disorders: Bannayan-Zonana syndrome, Cowden disease and juvenile polyposis syndrome.<ref>PMID:11381269</ref>
		+	== Function ==
		+	[[http://www.uniprot.org/uniprot/BMR1A_HUMAN BMR1A_HUMAN]] On ligand binding, forms a receptor complex consisting of two type II and two type I transmembrane serine/threonine kinases. Type II receptors phosphorylate and activate type I receptors which autophosphorylate, then bind and activate SMAD transcriptional regulators. Receptor for BMP-2 and BMP-4.
		+	<div style="background-color:#fffaf0;">
		+	== Publication Abstract from PubMed ==
		+	BACKGROUND: Members of the TGF-beta superfamily are characterized by a highly promiscuous ligand-receptor interaction as is readily apparent from the numeral discrepancy of only seven type I and five type II receptors available for more than 40 ligands. Structural and functional studies have been used to address the question of how specific signals can be deduced from a limited number of receptor combinations and to unravel the molecular mechanisms underlying the protein-protein recognition that allow such limited specificity. PRINCIPAL FINDINGS: In this study we have investigated how an antigen binding antibody fragment (Fab) raised against the extracellular domain of the BMP receptor type IA (BMPR-IA) recognizes the receptor's BMP-2 binding epitope and thereby neutralizes BMP-2 receptor activation. The crystal structure of the complex of the BMPR-IA ectodomain bound to the Fab AbD1556 revealed that the contact surface of BMPR-IA overlaps extensively with the contact surface for BMP-2 interaction. Although the structural epitopes of BMPR-IA to both binding partners coincides, the structures of BMPR-IA in the two complexes differ significantly. In contrast to the structural differences, alanine-scanning mutagenesis of BMPR-IA showed that the functional determinants for binding to the antibody and BMP-2 are almost identical. CONCLUSIONS: Comparing the structures of BMPR-IA bound to BMP-2 or bound to the Fab AbD1556 with the structure of unbound BMPR-IA shows that binding of BMPR-IA to its interaction partners follows a selection fit mechanism, possibly indicating that the ligand promiscuity of BMPR-IA is inherently encoded by structural adaptability. The functional and structural analysis of the BMPR-IA binding antibody AbD1556 mimicking the BMP-2 binding epitope may thus pave the way for the design of low-molecular weight synthetic receptor binders/inhibitors.

-	~~==Disease==~~	+	A selection fit mechanism in BMP receptor IA as a possible source for BMP ligand-receptor promiscuity.,Harth S, Kotzsch A, Hu J, Sebald W, Mueller TD PLoS One. 2010 Sep 28;5(9). pii: e13049. PMID:20927405<ref>PMID:20927405</ref>
-	~~[[http://www.uniprot.org/uniprot/BMR1A_HUMAN BMR1A_HUMAN]] Defects~~ in ~~BMPR1A are~~ a cause of juvenile polyposis syndrome (JPS) [MIM:[http://omim.org/entry/174900 174900]]; also known as juvenile intestinal polyposis (JIP). JPS is an autosomal dominant gastrointestinal hamartomatous polyposis syndrome in which patients are at risk for ~~developing gastrointestinal cancers~~. ~~The lesions are typified by a smooth histological appearance~~, ~~predominant stroma~~, ~~cystic spaces and lack of a smooth muscle core. Multiple juvenile polyps usually occur in a number of Mendelian disorders. Sometimes~~, ~~these polyps occur without associated features as in JPS; here~~, ~~polyps tend to occur in the large bowel and are associated with an increased risk of colon and other gastrointestinal cancers~~.~~<ref>PMID:11381269</ref><ref>PMID:11536076</ref><ref>PMID:12417513</ref><ref>PMID:12136244</ref><ref>PMID:12630959</ref> Defects in BMPR1A are a cause of Cowden disease~~ (CD) ~~[MIM:[http://omim~~.org/entry/158350 158350]]. CD is an autosomal dominant cancer syndrome characterized by multiple hamartomas and by a high risk for breast, thyroid and endometrial cancers.<ref>PMID:11381269</ref><ref>PMID:11536076</ref> Defects in BMPR1A are the cause of hereditary mixed polyposis syndrome 2 (HMPS2) [MIM:[http:~~//omim~~.~~org/entry/610069 610069]]. Hereditary mixed polyposis syndrome (HMPS) is characterized by atypical juvenile polyps, colonic adenomas, and colorectal carcinomas.<ref>~~PMID:11381269</ref> Note=A microdeletion of chromosome 10q23 involving BMPR1A and PTEN is a cause of chromosome 10q23 deletion syndrome, which shows overlapping features of the following three disorders: Bannayan-Zonana syndrome, Cowden disease and juvenile polyposis syndrome.<ref>PMID:~~11381269~~</ref>	+

-	~~==Function==~~	+	From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>
-	~~[[http://www.uniprot.org/uniprot~~/~~BMR1A_HUMAN BMR1A_HUMAN]] On ligand binding~~, ~~forms~~ a ~~receptor complex consisting~~ of ~~two type II and two type I transmembrane serine/threonine kinases~~. ~~Type II receptors phosphorylate and activate type I receptors which autophosphorylate, then bind and activate SMAD transcriptional regulators~~. ~~Receptor for BMP-2 and BMP-4~~.	+	</div>
-		+
-	~~==About this Structure==~~	+
-	~~[[3nh7]] is a 12 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=3NH7 OCA].~~	+

	==See Also==		==See Also==
	*[[Antibody\|Antibody]]		*[[Antibody\|Antibody]]
-		+	== References ==
-	==~~Reference~~==	+	<references/>
-	~~<ref group="xtra">PMID:020927405</ref>~~<references ~~group="xtra"~~/><~~references~~/>	+	__TOC__
		+	</StructureSection>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
	[[Category: Receptor protein serine/threonine kinase]]		[[Category: Receptor protein serine/threonine kinase]]
-	[[Category: Harth, S.]]	+	[[Category: Harth, S]]
-	[[Category: Mueller, T D.]]	+	[[Category: Mueller, T D]]
-	[[Category: Sebald, W.]]	+	[[Category: Sebald, W]]
	[[Category: Antibody-antigen complex]]		[[Category: Antibody-antigen complex]]
	[[Category: Bmp receptor extracellular domain]]		[[Category: Bmp receptor extracellular domain]]
	[[Category: Bone morphogenetic protein]]		[[Category: Bone morphogenetic protein]]
	[[Category: Immune system]]		[[Category: Immune system]]

OCA at 00:23, 25 March 2013

OCA — Mon, 25 Mar 2013 00:23:56 GMT

←Older revision		Revision as of 00:23, 25 March 2013
Line 1:		Line 1:
-	[[Image:3nh7.png\|left\|200px]]
-
	{{STRUCTURE_3nh7\| PDB=3nh7 \| SCENE= }}		{{STRUCTURE_3nh7\| PDB=3nh7 \| SCENE= }}
-
	===Crystal structure of the neutralizing Fab fragment AbD1556 bound to the BMP type I receptor IA===		===Crystal structure of the neutralizing Fab fragment AbD1556 bound to the BMP type I receptor IA===
		+	{{ABSTRACT_PUBMED_20927405}}

-	~~{{ABSTRACT_PUBMED_20927405}}~~	+	==Disease==
		+	[[http://www.uniprot.org/uniprot/BMR1A_HUMAN BMR1A_HUMAN]] Defects in BMPR1A are a cause of juvenile polyposis syndrome (JPS) [MIM:[http://omim.org/entry/174900 174900]]; also known as juvenile intestinal polyposis (JIP). JPS is an autosomal dominant gastrointestinal hamartomatous polyposis syndrome in which patients are at risk for developing gastrointestinal cancers. The lesions are typified by a smooth histological appearance, predominant stroma, cystic spaces and lack of a smooth muscle core. Multiple juvenile polyps usually occur in a number of Mendelian disorders. Sometimes, these polyps occur without associated features as in JPS; here, polyps tend to occur in the large bowel and are associated with an increased risk of colon and other gastrointestinal cancers.<ref>PMID:11381269</ref><ref>PMID:11536076</ref><ref>PMID:12417513</ref><ref>PMID:12136244</ref><ref>PMID:12630959</ref> Defects in BMPR1A are a cause of Cowden disease (CD) [MIM:[http://omim.org/entry/158350 158350]]. CD is an autosomal dominant cancer syndrome characterized by multiple hamartomas and by a high risk for breast, thyroid and endometrial cancers.<ref>PMID:11381269</ref><ref>PMID:11536076</ref> Defects in BMPR1A are the cause of hereditary mixed polyposis syndrome 2 (HMPS2) [MIM:[http://omim.org/entry/610069 610069]]. Hereditary mixed polyposis syndrome (HMPS) is characterized by atypical juvenile polyps, colonic adenomas, and colorectal carcinomas.<ref>PMID:11381269</ref> Note=A microdeletion of chromosome 10q23 involving BMPR1A and PTEN is a cause of chromosome 10q23 deletion syndrome, which shows overlapping features of the following three disorders: Bannayan-Zonana syndrome, Cowden disease and juvenile polyposis syndrome.<ref>PMID:11381269</ref>
		+
		+	==Function==
		+	[[http://www.uniprot.org/uniprot/BMR1A_HUMAN BMR1A_HUMAN]] On ligand binding, forms a receptor complex consisting of two type II and two type I transmembrane serine/threonine kinases. Type II receptors phosphorylate and activate type I receptors which autophosphorylate, then bind and activate SMAD transcriptional regulators. Receptor for BMP-2 and BMP-4.

	==About this Structure==		==About this Structure==
Line 14:		Line 16:

	==Reference==		==Reference==
-	<ref group="xtra">PMID:020927405</ref><references group="xtra"/>	+	<ref group="xtra">PMID:020927405</ref><references group="xtra"/><references/>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
	[[Category: Receptor protein serine/threonine kinase]]		[[Category: Receptor protein serine/threonine kinase]]

OCA at 07:51, 20 October 2012

OCA — Sat, 20 Oct 2012 07:51:27 GMT

←Older revision		Revision as of 07:51, 20 October 2012
Line 8:		Line 8:

	==About this Structure==		==About this Structure==
-	[[3nh7]] is a 12 chain structure ~~of [[Antibody]]~~ 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=3NH7 OCA].	+	[[3nh7]] is a 12 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=3NH7 OCA].

	==See Also==		==See Also==

OCA: Protected "3nh7" [edit=sysop:move=sysop]

OCA — Wed, 25 Jul 2012 17:41:25 GMT

Protected "3nh7" [edit=sysop:move=sysop]

←Older revision

Revision as of 17:41, 25 July 2012

OCA at 17:41, 25 July 2012

OCA — Wed, 25 Jul 2012 17:41:23 GMT

←Older revision		Revision as of 17:41, 25 July 2012
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-	~~{{Seed}}~~	+	[[Image:3nh7.png\|left\|200px]]
-	[[Image:3nh7.~~jpg~~\|left\|200px]]	+

-	<!--
-	The line below this paragraph, containing "STRUCTURE_3nh7", 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_3nh7\| PDB=3nh7 \| SCENE= }}		{{STRUCTURE_3nh7\| PDB=3nh7 \| SCENE= }}

	===Crystal structure of the neutralizing Fab fragment AbD1556 bound to the BMP type I receptor IA===		===Crystal structure of the neutralizing Fab fragment AbD1556 bound to the BMP type I receptor IA===

-
-	<!--
-	The line below this paragraph, {{ABSTRACT_PUBMED_20927405}}, adds the Publication Abstract to the page
-	(as it appears on PubMed at http://www.pubmed.gov), where 20927405 is the PubMed ID number.
-	-->
	{{ABSTRACT_PUBMED_20927405}}		{{ABSTRACT_PUBMED_20927405}}

	==About this Structure==		==About this Structure==
-	~~3NH7~~ is a 12 ~~chains~~ structure with ~~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=3NH7 OCA].	+	[[3nh7]] is a 12 chain structure of [[Antibody]] 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=3NH7 OCA].
		+
		+	==See Also==
		+	*[[Antibody\|Antibody]]

	==Reference==		==Reference==
-	<ref group="xtra">PMID:~~20927405~~</ref><references group="xtra"/>	+	<ref group="xtra">PMID:020927405</ref><references group="xtra"/>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
	[[Category: Receptor protein serine/threonine kinase]]		[[Category: Receptor protein serine/threonine kinase]]
Line 33:		Line 24:
	[[Category: Bone morphogenetic protein]]		[[Category: Bone morphogenetic protein]]
	[[Category: Immune system]]		[[Category: Immune system]]
-
-	''Page seeded by [http://oca.weizmann.ac.il/oca OCA ] on Wed Oct 27 12:13:16 2010''

OCA at 09:02, 27 October 2010

OCA — Wed, 27 Oct 2010 09:02:55 GMT

←Older revision		Revision as of 09:02, 27 October 2010
Line 1:		Line 1:
-	~~'''Unreleased structure'''~~	+	{{Seed}}
		+	[[Image:3nh7.jpg\|left\|200px]]

-	The ~~entry 3nh7~~ is ~~ON HOLD~~ ~~until Paper Publication~~	+	<!--
		+	The line below this paragraph, containing "STRUCTURE_3nh7", 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_3nh7\| PDB=3nh7 \| SCENE= }}

-	~~Authors: Mueller, T.D., Harth, S., Sebald, W.~~	+	===Crystal structure of the neutralizing Fab fragment AbD1556 bound to the BMP type I receptor IA===

-	Description: Crystal structure of the neutralizing Fab fragment AbD1556 bound to the BMP type I receptor IA

-	''Page seeded by [http://oca.weizmann.ac.il/oca OCA ] on Wed ~~Aug 18 11~~:22:14 2010''	+	<!--
		+	The line below this paragraph, {{ABSTRACT_PUBMED_20927405}}, adds the Publication Abstract to the page
		+	(as it appears on PubMed at http://www.pubmed.gov), where 20927405 is the PubMed ID number.
		+	-->
		+	{{ABSTRACT_PUBMED_20927405}}
		+
		+	==About this Structure==
		+	3NH7 is a 12 chains structure with 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=3NH7 OCA].
		+
		+	==Reference==
		+	<ref group="xtra">PMID:20927405</ref><references group="xtra"/>
		+	[[Category: Homo sapiens]]
		+	[[Category: Receptor protein serine/threonine kinase]]
		+	[[Category: Harth, S.]]
		+	[[Category: Mueller, T D.]]
		+	[[Category: Sebald, W.]]
		+	[[Category: Antibody-antigen complex]]
		+	[[Category: Bmp receptor extracellular domain]]
		+	[[Category: Bone morphogenetic protein]]
		+	[[Category: Immune system]]
		+
		+	''Page seeded by [http://oca.weizmann.ac.il/oca OCA ] on Wed Oct 27 12:13:16 2010''