3qis - Revision history

OCA at 11:46, 14 March 2024

2024-03-14T11:46:52Z

←Older revision		Revision as of 11:46, 14 March 2024
Line 3:		Line 3:
	<StructureSection load='3qis' size='340' side='right'caption='[[3qis]], [[Resolution\|resolution]] 2.30Å' scene=''>		<StructureSection load='3qis' size='340' side='right'caption='[[3qis]], [[Resolution\|resolution]] 2.30Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[3qis]] is a 2 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=3QIS OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=3QIS FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[3qis]] 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=3QIS OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=3QIS FirstGlance]. <br>
-	</td></tr><tr id='~~gene~~'><td class="sblockLbl"><b>[[~~Gene~~\|~~Gene~~:]]</b></td><td class="sblockDat"~~>INPP5F, OCRL, OCRL1 ([https://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&~~id~~=9606 HUMAN])</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]] 2.3Å</td></tr>
-	~~<tr id='activity'><td class~~="~~sblockLbl~~">~~<b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[https://en.wikipedia.org/wiki/Phosphoinositide_5~~-~~phosphatase Phosphoinositide 5-phosphatase]~~, ~~with EC number~~ [~~https://www~~.~~brenda-enzymes.info/php/result_flat.php4?ecno=~~3~~.1.3.36 3.1.3.36] </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=3qis FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3qis OCA], [https://pdbe.org/3qis PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=3qis RCSB], [https://www.ebi.ac.uk/pdbsum/3qis PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=3qis 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=3qis FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3qis OCA], [https://pdbe.org/3qis PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=3qis RCSB], [https://www.ebi.ac.uk/pdbsum/3qis PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=3qis ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
-	[[https://www.uniprot.org/uniprot/OCRL_HUMAN OCRL_HUMAN]] Defects in OCRL are the cause of Lowe oculocerebrorenal syndrome (OCRL) [MIM:[https://omim.org/entry/309000 309000]]. It is an X-linked multisystem disorder affecting eyes, nervous system, and kidney. It is characterized by hydrophthalmia, cataract, mental retardation, vitamin D-resistant rickets, aminoaciduria, and reduced ammonia production by the kidney. Ocular abnormalities include cataract, glaucoma, microphthalmos, and decreased visual acuity. Developmental delay, hypotonia, behavior abnormalities, and areflexia are also present. Renal tubular involvement is characterized by impaired reabsorption of bicarbonate, amino acids, and phosphate. Musculoskeletal abnormalities such as joint hypermobility, dislocated hips, and fractures may develop as consequences of renal tubular acidosis and hypophosphatemia. Cataract is the only significant manifestation in carriers and is detected by slit-lamp examination.<ref>PMID:20133602</ref> <ref>PMID:21233288</ref> <ref>PMID:9199559</ref> <ref>PMID:9682219</ref> <ref>PMID:9632163</ref> <ref>PMID:9788721</ref> <ref>PMID:10923037</ref> <ref>PMID:10767176</ref> <ref>PMID:19168822</ref> <ref>PMID:21031565</ref> Defects in OCRL are the cause of Dent disease type 2 (DD2) [MIM:[https://omim.org/entry/300555 300555]]. DD2 is a renal disease belonging to the 'Dent disease complex', a group of disorders characterized by proximal renal tubular defect, hypercalciuria, nephrocalcinosis, and renal insufficiency. The spectrum of phenotypic features is remarkably similar in the various disorders, except for differences in the severity of bone deformities and renal impairment. Characteristic abnormalities include low-molecular-weight proteinuria and other features of Fanconi syndrome, such as glycosuria, aminoaciduria, and phosphaturia, but typically do not include proximal renal tubular acidosis. Progressive renal failure is common, as are nephrocalcinosis and kidney stones.<ref>PMID:21031565</ref> <ref>PMID:15627218</ref> <ref>PMID:17384968</ref>	+	[https://www.uniprot.org/uniprot/OCRL_HUMAN OCRL_HUMAN] Defects in OCRL are the cause of Lowe oculocerebrorenal syndrome (OCRL) [MIM:[https://omim.org/entry/309000 309000]. It is an X-linked multisystem disorder affecting eyes, nervous system, and kidney. It is characterized by hydrophthalmia, cataract, mental retardation, vitamin D-resistant rickets, aminoaciduria, and reduced ammonia production by the kidney. Ocular abnormalities include cataract, glaucoma, microphthalmos, and decreased visual acuity. Developmental delay, hypotonia, behavior abnormalities, and areflexia are also present. Renal tubular involvement is characterized by impaired reabsorption of bicarbonate, amino acids, and phosphate. Musculoskeletal abnormalities such as joint hypermobility, dislocated hips, and fractures may develop as consequences of renal tubular acidosis and hypophosphatemia. Cataract is the only significant manifestation in carriers and is detected by slit-lamp examination.<ref>PMID:20133602</ref> <ref>PMID:21233288</ref> <ref>PMID:9199559</ref> <ref>PMID:9682219</ref> <ref>PMID:9632163</ref> <ref>PMID:9788721</ref> <ref>PMID:10923037</ref> <ref>PMID:10767176</ref> <ref>PMID:19168822</ref> <ref>PMID:21031565</ref> Defects in OCRL are the cause of Dent disease type 2 (DD2) [MIM:[https://omim.org/entry/300555 300555]. DD2 is a renal disease belonging to the 'Dent disease complex', a group of disorders characterized by proximal renal tubular defect, hypercalciuria, nephrocalcinosis, and renal insufficiency. The spectrum of phenotypic features is remarkably similar in the various disorders, except for differences in the severity of bone deformities and renal impairment. Characteristic abnormalities include low-molecular-weight proteinuria and other features of Fanconi syndrome, such as glycosuria, aminoaciduria, and phosphaturia, but typically do not include proximal renal tubular acidosis. Progressive renal failure is common, as are nephrocalcinosis and kidney stones.<ref>PMID:21031565</ref> <ref>PMID:15627218</ref> <ref>PMID:17384968</ref>
	== Function ==		== Function ==
-	[[https://www.uniprot.org/uniprot/OCRL_HUMAN OCRL_HUMAN]] Converts phosphatidylinositol 4,5-bisphosphate to phosphatidylinositol 4-phosphate. Also converts inositol 1,4,5-trisphosphate to inositol 1,4-bisphosphate and inositol 1,3,4,5-tetrakisphosphate to inositol 1,3,4-trisphosphate. May function in lysosomal membrane trafficking by regulating the specific pool of phosphatidylinositol 4,5-bisphosphate that is associated with lysosomes. Involved in primary cilia assembly.<ref>PMID:22543976</ref> <ref>PMID:22228094</ref> [[https://www.uniprot.org/uniprot/SESQ1_HUMAN SESQ1_HUMAN]] Plays a role in endocytic trafficking. Required for receptor recycling from endosomes, both to the trans-Golgi network and the plasma membrane.<ref>PMID:21233288</ref>	+	[https://www.uniprot.org/uniprot/OCRL_HUMAN OCRL_HUMAN] Converts phosphatidylinositol 4,5-bisphosphate to phosphatidylinositol 4-phosphate. Also converts inositol 1,4,5-trisphosphate to inositol 1,4-bisphosphate and inositol 1,3,4,5-tetrakisphosphate to inositol 1,3,4-trisphosphate. May function in lysosomal membrane trafficking by regulating the specific pool of phosphatidylinositol 4,5-bisphosphate that is associated with lysosomes. Involved in primary cilia assembly.<ref>PMID:22543976</ref> <ref>PMID:22228094</ref>
-	~~<div style="background-color:#fffaf0;">~~	+
-	~~== Publication Abstract from PubMed ==~~	+
-	Lowe syndrome and type 2 Dent disease are caused by defects in the inositol 5-phosphatase OCRL. Most missense mutations in the OCRL ASH-RhoGAP domain that are found in affected individuals abolish interactions with the endocytic adaptors APPL1 and Ses (both Ses1 and Ses2), which bind OCRL through a short phenylalanine and histidine (F&H) motif. Using X-ray crystallography, we have identified the F&H motif binding site on the RhoGAP domain of OCRL. Missense mutations associated with disease affected F&H binding indirectly by destabilizing the RhoGAP fold. By contrast, a disease-associated mutation that does not perturb F&H binding and ASH-RhoGAP stability disrupted the interaction of OCRL with Rab5. The F&H binding site of OCRL is conserved even in species that do not have an identified homolog for APPL or Ses. Our study predicts the existence of other OCRL binding partners and shows that the perturbation of OCRL interactions has a crucial role in disease.	+
-		+
-	Recognition of the F&H motif by the Lowe syndrome protein OCRL.,Pirruccello M, Swan LE, Folta-Stogniew E, De Camilli P Nat Struct Mol Biol. 2011 Jun 12. doi: 10.1038/nsmb.2071. PMID:21666675<ref>PMID:21666675</ref>	+
-		+
-	~~From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>~~	+
-	~~</div>~~	+
-	~~<div class="pdbe-citations 3qis" style="background-color:#fffaf0;"></div~~>	+

	==See Also==		==See Also==
Line 29:		Line 19:
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
-	[[Category: ~~Human~~]]	+	[[Category: Homo sapiens]]
	[[Category: Large Structures]]		[[Category: Large Structures]]
-	[[Category: ~~Phosphoinositide 5-phosphatase]]~~	+	[[Category: De Camilli P]]
-	~~[[Category:~~ Camilli, P De]]	+	[[Category: Folta-Stogniew E]]
-	[[Category: Folta-Stogniew, E]]	+	[[Category: Pirruccello M]]
-	[[Category: Pirruccello, M]]	+	[[Category: Swan LE]]
-	[[Category: Swan~~, L E]]~~	+
-	~~[[Category: Appl1]]~~	+
-	~~[[Category: Dent disease]]~~	+
-	~~[[Category: Endocytic pathway]]~~	+
-	~~[[Category: Golgi complex]]~~	+
-	~~[[Category: Hydrolase-protein binding complex]]~~	+
-	~~[[Category: Rab gtpase]]~~	+
-	~~[[Category: Rac1]]~~	+
-	~~[[Category: Ses2~~]]	+

OCA at 06:10, 8 June 2022

2022-06-08T06:10:28Z

←Older revision		Revision as of 06:10, 8 June 2022
Line 1:		Line 1:

	==Recognition of the F&H motif by the Lowe Syndrome protein OCRL==		==Recognition of the F&H motif by the Lowe Syndrome protein OCRL==
-	<StructureSection load='3qis' size='340' side='right' caption='[[3qis]], [[Resolution\|resolution]] 2.30Å' scene=''>	+	<StructureSection load='3qis' size='340' side='right'caption='[[3qis]], [[Resolution\|resolution]] 2.30Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[3qis]] 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=3QIS OCA]. For a <b>guided tour on the structure components</b> use [~~http~~://~~oca~~.~~weizmann.ac.il/oca-docs~~/fgij/fg.htm?mol=3QIS FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[3qis]] is a 2 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=3QIS OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=3QIS FirstGlance]. <br>
-	</td></tr><tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">INPP5F, OCRL, OCRL1 ([~~http~~://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN])</td></tr>	+	</td></tr><tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">INPP5F, OCRL, OCRL1 ([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/Phosphoinositide_5-phosphatase Phosphoinositide 5-phosphatase], with EC number [~~http~~://www.brenda-enzymes.info/php/result_flat.php4?ecno=3.1.3.36 3.1.3.36] </span></td></tr>	+	<tr id='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[https://en.wikipedia.org/wiki/Phosphoinositide_5-phosphatase Phosphoinositide 5-phosphatase], with EC number [https://www.brenda-enzymes.info/php/result_flat.php4?ecno=3.1.3.36 3.1.3.36] </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=3qis FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3qis OCA], [~~http~~://pdbe.org/3qis PDBe], [~~http~~://www.rcsb.org/pdb/explore.do?structureId=3qis RCSB], [~~http~~://www.ebi.ac.uk/pdbsum/3qis PDBsum], [~~http~~://prosat.h-its.org/prosat/prosatexe?pdbcode=3qis 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=3qis FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3qis OCA], [https://pdbe.org/3qis PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=3qis RCSB], [https://www.ebi.ac.uk/pdbsum/3qis PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=3qis ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
-	[[~~http~~://www.uniprot.org/uniprot/OCRL_HUMAN OCRL_HUMAN]] Defects in OCRL are the cause of Lowe oculocerebrorenal syndrome (OCRL) [MIM:[~~http~~://omim.org/entry/309000 309000]]. It is an X-linked multisystem disorder affecting eyes, nervous system, and kidney. It is characterized by hydrophthalmia, cataract, mental retardation, vitamin D-resistant rickets, aminoaciduria, and reduced ammonia production by the kidney. Ocular abnormalities include cataract, glaucoma, microphthalmos, and decreased visual acuity. Developmental delay, hypotonia, behavior abnormalities, and areflexia are also present. Renal tubular involvement is characterized by impaired reabsorption of bicarbonate, amino acids, and phosphate. Musculoskeletal abnormalities such as joint hypermobility, dislocated hips, and fractures may develop as consequences of renal tubular acidosis and hypophosphatemia. Cataract is the only significant manifestation in carriers and is detected by slit-lamp examination.<ref>PMID:20133602</ref> <ref>PMID:21233288</ref> <ref>PMID:9199559</ref> <ref>PMID:9682219</ref> <ref>PMID:9632163</ref> <ref>PMID:9788721</ref> <ref>PMID:10923037</ref> <ref>PMID:10767176</ref> <ref>PMID:19168822</ref> <ref>PMID:21031565</ref> Defects in OCRL are the cause of Dent disease type 2 (DD2) [MIM:[~~http~~://omim.org/entry/300555 300555]]. DD2 is a renal disease belonging to the 'Dent disease complex', a group of disorders characterized by proximal renal tubular defect, hypercalciuria, nephrocalcinosis, and renal insufficiency. The spectrum of phenotypic features is remarkably similar in the various disorders, except for differences in the severity of bone deformities and renal impairment. Characteristic abnormalities include low-molecular-weight proteinuria and other features of Fanconi syndrome, such as glycosuria, aminoaciduria, and phosphaturia, but typically do not include proximal renal tubular acidosis. Progressive renal failure is common, as are nephrocalcinosis and kidney stones.<ref>PMID:21031565</ref> <ref>PMID:15627218</ref> <ref>PMID:17384968</ref>	+	[[https://www.uniprot.org/uniprot/OCRL_HUMAN OCRL_HUMAN]] Defects in OCRL are the cause of Lowe oculocerebrorenal syndrome (OCRL) [MIM:[https://omim.org/entry/309000 309000]]. It is an X-linked multisystem disorder affecting eyes, nervous system, and kidney. It is characterized by hydrophthalmia, cataract, mental retardation, vitamin D-resistant rickets, aminoaciduria, and reduced ammonia production by the kidney. Ocular abnormalities include cataract, glaucoma, microphthalmos, and decreased visual acuity. Developmental delay, hypotonia, behavior abnormalities, and areflexia are also present. Renal tubular involvement is characterized by impaired reabsorption of bicarbonate, amino acids, and phosphate. Musculoskeletal abnormalities such as joint hypermobility, dislocated hips, and fractures may develop as consequences of renal tubular acidosis and hypophosphatemia. Cataract is the only significant manifestation in carriers and is detected by slit-lamp examination.<ref>PMID:20133602</ref> <ref>PMID:21233288</ref> <ref>PMID:9199559</ref> <ref>PMID:9682219</ref> <ref>PMID:9632163</ref> <ref>PMID:9788721</ref> <ref>PMID:10923037</ref> <ref>PMID:10767176</ref> <ref>PMID:19168822</ref> <ref>PMID:21031565</ref> Defects in OCRL are the cause of Dent disease type 2 (DD2) [MIM:[https://omim.org/entry/300555 300555]]. DD2 is a renal disease belonging to the 'Dent disease complex', a group of disorders characterized by proximal renal tubular defect, hypercalciuria, nephrocalcinosis, and renal insufficiency. The spectrum of phenotypic features is remarkably similar in the various disorders, except for differences in the severity of bone deformities and renal impairment. Characteristic abnormalities include low-molecular-weight proteinuria and other features of Fanconi syndrome, such as glycosuria, aminoaciduria, and phosphaturia, but typically do not include proximal renal tubular acidosis. Progressive renal failure is common, as are nephrocalcinosis and kidney stones.<ref>PMID:21031565</ref> <ref>PMID:15627218</ref> <ref>PMID:17384968</ref>
	== Function ==		== Function ==
-	[[~~http~~://www.uniprot.org/uniprot/OCRL_HUMAN OCRL_HUMAN]] Converts phosphatidylinositol 4,5-bisphosphate to phosphatidylinositol 4-phosphate. Also converts inositol 1,4,5-trisphosphate to inositol 1,4-bisphosphate and inositol 1,3,4,5-tetrakisphosphate to inositol 1,3,4-trisphosphate. May function in lysosomal membrane trafficking by regulating the specific pool of phosphatidylinositol 4,5-bisphosphate that is associated with lysosomes. Involved in primary cilia assembly.<ref>PMID:22543976</ref> <ref>PMID:22228094</ref> [[~~http~~://www.uniprot.org/uniprot/SESQ1_HUMAN SESQ1_HUMAN]] Plays a role in endocytic trafficking. Required for receptor recycling from endosomes, both to the trans-Golgi network and the plasma membrane.<ref>PMID:21233288</ref>	+	[[https://www.uniprot.org/uniprot/OCRL_HUMAN OCRL_HUMAN]] Converts phosphatidylinositol 4,5-bisphosphate to phosphatidylinositol 4-phosphate. Also converts inositol 1,4,5-trisphosphate to inositol 1,4-bisphosphate and inositol 1,3,4,5-tetrakisphosphate to inositol 1,3,4-trisphosphate. May function in lysosomal membrane trafficking by regulating the specific pool of phosphatidylinositol 4,5-bisphosphate that is associated with lysosomes. Involved in primary cilia assembly.<ref>PMID:22543976</ref> <ref>PMID:22228094</ref> [[https://www.uniprot.org/uniprot/SESQ1_HUMAN SESQ1_HUMAN]] Plays a role in endocytic trafficking. Required for receptor recycling from endosomes, both to the trans-Golgi network and the plasma membrane.<ref>PMID:21233288</ref>
	<div style="background-color:#fffaf0;">		<div style="background-color:#fffaf0;">
	== Publication Abstract from PubMed ==		== Publication Abstract from PubMed ==
Line 21:		Line 21:
	</div>		</div>
	<div class="pdbe-citations 3qis" style="background-color:#fffaf0;"></div>		<div class="pdbe-citations 3qis" style="background-color:#fffaf0;"></div>
		+
		+	==See Also==
		+	*[[Inositol polyphosphate 5-phosphatase OCRL\|Inositol polyphosphate 5-phosphatase OCRL]]
		+	*[[3D structures of inositol polyphosphate 5-phosphatase OCRL\|3D structures of inositol polyphosphate 5-phosphatase OCRL]]
	== References ==		== References ==
	<references/>		<references/>
Line 26:		Line 30:
	</StructureSection>		</StructureSection>
	[[Category: Human]]		[[Category: Human]]
		+	[[Category: Large Structures]]
	[[Category: Phosphoinositide 5-phosphatase]]		[[Category: Phosphoinositide 5-phosphatase]]
	[[Category: Camilli, P De]]		[[Category: Camilli, P De]]

OCA at 13:05, 4 August 2016

2016-08-04T13:05:12Z

←Older revision		Revision as of 13:05, 4 August 2016
Line 1:		Line 1:
		+
	==Recognition of the F&H motif by the Lowe Syndrome protein OCRL==		==Recognition of the F&H motif by the Lowe Syndrome protein OCRL==
	<StructureSection load='3qis' size='340' side='right' caption='[[3qis]], [[Resolution\|resolution]] 2.30Å' scene=''>		<StructureSection load='3qis' size='340' side='right' caption='[[3qis]], [[Resolution\|resolution]] 2.30Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[3qis]] 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=3QIS OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3QIS FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[3qis]] 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=3QIS OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3QIS FirstGlance]. <br>
-	</td></tr><tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">INPP5F, OCRL, OCRL1 ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 ~~Homo sapiens~~])</td></tr>	+	</td></tr><tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">INPP5F, OCRL, OCRL1 ([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/Phosphoinositide_5-phosphatase Phosphoinositide 5-phosphatase], with EC number [http://www.brenda-enzymes.info/php/result_flat.php4?ecno=3.1.3.36 3.1.3.36] </span></td></tr>		<tr id='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[http://en.wikipedia.org/wiki/Phosphoinositide_5-phosphatase Phosphoinositide 5-phosphatase], with EC number [http://www.brenda-enzymes.info/php/result_flat.php4?ecno=3.1.3.36 3.1.3.36] </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=3qis FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3qis OCA], [http://www.rcsb.org/pdb/explore.do?structureId=3qis RCSB], [http://www.ebi.ac.uk/pdbsum/3qis 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=3qis FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3qis OCA], [http://pdbe.org/3qis PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=3qis RCSB], [http://www.ebi.ac.uk/pdbsum/3qis PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=3qis ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
	[[http://www.uniprot.org/uniprot/OCRL_HUMAN OCRL_HUMAN]] Defects in OCRL are the cause of Lowe oculocerebrorenal syndrome (OCRL) [MIM:[http://omim.org/entry/309000 309000]]. It is an X-linked multisystem disorder affecting eyes, nervous system, and kidney. It is characterized by hydrophthalmia, cataract, mental retardation, vitamin D-resistant rickets, aminoaciduria, and reduced ammonia production by the kidney. Ocular abnormalities include cataract, glaucoma, microphthalmos, and decreased visual acuity. Developmental delay, hypotonia, behavior abnormalities, and areflexia are also present. Renal tubular involvement is characterized by impaired reabsorption of bicarbonate, amino acids, and phosphate. Musculoskeletal abnormalities such as joint hypermobility, dislocated hips, and fractures may develop as consequences of renal tubular acidosis and hypophosphatemia. Cataract is the only significant manifestation in carriers and is detected by slit-lamp examination.<ref>PMID:20133602</ref> <ref>PMID:21233288</ref> <ref>PMID:9199559</ref> <ref>PMID:9682219</ref> <ref>PMID:9632163</ref> <ref>PMID:9788721</ref> <ref>PMID:10923037</ref> <ref>PMID:10767176</ref> <ref>PMID:19168822</ref> <ref>PMID:21031565</ref> Defects in OCRL are the cause of Dent disease type 2 (DD2) [MIM:[http://omim.org/entry/300555 300555]]. DD2 is a renal disease belonging to the 'Dent disease complex', a group of disorders characterized by proximal renal tubular defect, hypercalciuria, nephrocalcinosis, and renal insufficiency. The spectrum of phenotypic features is remarkably similar in the various disorders, except for differences in the severity of bone deformities and renal impairment. Characteristic abnormalities include low-molecular-weight proteinuria and other features of Fanconi syndrome, such as glycosuria, aminoaciduria, and phosphaturia, but typically do not include proximal renal tubular acidosis. Progressive renal failure is common, as are nephrocalcinosis and kidney stones.<ref>PMID:21031565</ref> <ref>PMID:15627218</ref> <ref>PMID:17384968</ref>		[[http://www.uniprot.org/uniprot/OCRL_HUMAN OCRL_HUMAN]] Defects in OCRL are the cause of Lowe oculocerebrorenal syndrome (OCRL) [MIM:[http://omim.org/entry/309000 309000]]. It is an X-linked multisystem disorder affecting eyes, nervous system, and kidney. It is characterized by hydrophthalmia, cataract, mental retardation, vitamin D-resistant rickets, aminoaciduria, and reduced ammonia production by the kidney. Ocular abnormalities include cataract, glaucoma, microphthalmos, and decreased visual acuity. Developmental delay, hypotonia, behavior abnormalities, and areflexia are also present. Renal tubular involvement is characterized by impaired reabsorption of bicarbonate, amino acids, and phosphate. Musculoskeletal abnormalities such as joint hypermobility, dislocated hips, and fractures may develop as consequences of renal tubular acidosis and hypophosphatemia. Cataract is the only significant manifestation in carriers and is detected by slit-lamp examination.<ref>PMID:20133602</ref> <ref>PMID:21233288</ref> <ref>PMID:9199559</ref> <ref>PMID:9682219</ref> <ref>PMID:9632163</ref> <ref>PMID:9788721</ref> <ref>PMID:10923037</ref> <ref>PMID:10767176</ref> <ref>PMID:19168822</ref> <ref>PMID:21031565</ref> Defects in OCRL are the cause of Dent disease type 2 (DD2) [MIM:[http://omim.org/entry/300555 300555]]. DD2 is a renal disease belonging to the 'Dent disease complex', a group of disorders characterized by proximal renal tubular defect, hypercalciuria, nephrocalcinosis, and renal insufficiency. The spectrum of phenotypic features is remarkably similar in the various disorders, except for differences in the severity of bone deformities and renal impairment. Characteristic abnormalities include low-molecular-weight proteinuria and other features of Fanconi syndrome, such as glycosuria, aminoaciduria, and phosphaturia, but typically do not include proximal renal tubular acidosis. Progressive renal failure is common, as are nephrocalcinosis and kidney stones.<ref>PMID:21031565</ref> <ref>PMID:15627218</ref> <ref>PMID:17384968</ref>
	== Function ==		== Function ==
-	[[http://www.uniprot.org/uniprot/OCRL_HUMAN OCRL_HUMAN]] Converts phosphatidylinositol 4,5-bisphosphate to phosphatidylinositol 4-phosphate. Also converts inositol 1,4,5-trisphosphate to inositol 1,4-bisphosphate and inositol 1,3,4,5-tetrakisphosphate to inositol 1,3,4-trisphosphate. May function in lysosomal membrane trafficking by regulating the specific pool of phosphatidylinositol 4,5-bisphosphate that is associated with lysosomes. Involved in primary cilia assembly.<ref>PMID:22543976</ref> <ref>PMID:22228094</ref>	+	[[http://www.uniprot.org/uniprot/OCRL_HUMAN OCRL_HUMAN]] Converts phosphatidylinositol 4,5-bisphosphate to phosphatidylinositol 4-phosphate. Also converts inositol 1,4,5-trisphosphate to inositol 1,4-bisphosphate and inositol 1,3,4,5-tetrakisphosphate to inositol 1,3,4-trisphosphate. May function in lysosomal membrane trafficking by regulating the specific pool of phosphatidylinositol 4,5-bisphosphate that is associated with lysosomes. Involved in primary cilia assembly.<ref>PMID:22543976</ref> <ref>PMID:22228094</ref> [[http://www.uniprot.org/uniprot/SESQ1_HUMAN SESQ1_HUMAN]] Plays a role in endocytic trafficking. Required for receptor recycling from endosomes, both to the trans-Golgi network and the plasma membrane.<ref>PMID:21233288</ref>
	<div style="background-color:#fffaf0;">		<div style="background-color:#fffaf0;">
	== Publication Abstract from PubMed ==		== Publication Abstract from PubMed ==
Line 19:		Line 20:
	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 3qis" style="background-color:#fffaf0;"></div>
	== References ==		== References ==
	<references/>		<references/>
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
-	[[Category: ~~Homo sapiens~~]]	+	[[Category: Human]]
	[[Category: Phosphoinositide 5-phosphatase]]		[[Category: Phosphoinositide 5-phosphatase]]
	[[Category: Camilli, P De]]		[[Category: Camilli, P De]]

OCA at 11:01, 19 December 2014

2014-12-19T11:01:34Z

←Older revision		Revision as of 11:01, 19 December 2014
Line 1:		Line 1:
-	~~{{STRUCTURE_3qis\| PDB=3qis \| SCENE= }}~~	+	==Recognition of the F&H motif by the Lowe Syndrome protein OCRL==
-	===Recognition of the F&H motif by the Lowe Syndrome protein OCRL===	+	<StructureSection load='3qis' size='340' side='right' caption='[[3qis]], [[Resolution\|resolution]] 2.30Å' scene=''>
-	~~{{ABSTRACT_PUBMED_21666675}}~~	+	== Structural highlights ==
		+	<table><tr><td colspan='2'>[[3qis]] 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=3QIS OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3QIS FirstGlance]. <br>
		+	</td></tr><tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">INPP5F, OCRL, OCRL1 ([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/Phosphoinositide_5-phosphatase Phosphoinositide 5-phosphatase], with EC number [http://www.brenda-enzymes.info/php/result_flat.php4?ecno=3.1.3.36 3.1.3.36] </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=3qis FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3qis OCA], [http://www.rcsb.org/pdb/explore.do?structureId=3qis RCSB], [http://www.ebi.ac.uk/pdbsum/3qis PDBsum]</span></td></tr>
		+	</table>
		+	== Disease ==
		+	[[http://www.uniprot.org/uniprot/OCRL_HUMAN OCRL_HUMAN]] Defects in OCRL are the cause of Lowe oculocerebrorenal syndrome (OCRL) [MIM:[http://omim.org/entry/309000 309000]]. It is an X-linked multisystem disorder affecting eyes, nervous system, and kidney. It is characterized by hydrophthalmia, cataract, mental retardation, vitamin D-resistant rickets, aminoaciduria, and reduced ammonia production by the kidney. Ocular abnormalities include cataract, glaucoma, microphthalmos, and decreased visual acuity. Developmental delay, hypotonia, behavior abnormalities, and areflexia are also present. Renal tubular involvement is characterized by impaired reabsorption of bicarbonate, amino acids, and phosphate. Musculoskeletal abnormalities such as joint hypermobility, dislocated hips, and fractures may develop as consequences of renal tubular acidosis and hypophosphatemia. Cataract is the only significant manifestation in carriers and is detected by slit-lamp examination.<ref>PMID:20133602</ref> <ref>PMID:21233288</ref> <ref>PMID:9199559</ref> <ref>PMID:9682219</ref> <ref>PMID:9632163</ref> <ref>PMID:9788721</ref> <ref>PMID:10923037</ref> <ref>PMID:10767176</ref> <ref>PMID:19168822</ref> <ref>PMID:21031565</ref> Defects in OCRL are the cause of Dent disease type 2 (DD2) [MIM:[http://omim.org/entry/300555 300555]]. DD2 is a renal disease belonging to the 'Dent disease complex', a group of disorders characterized by proximal renal tubular defect, hypercalciuria, nephrocalcinosis, and renal insufficiency. The spectrum of phenotypic features is remarkably similar in the various disorders, except for differences in the severity of bone deformities and renal impairment. Characteristic abnormalities include low-molecular-weight proteinuria and other features of Fanconi syndrome, such as glycosuria, aminoaciduria, and phosphaturia, but typically do not include proximal renal tubular acidosis. Progressive renal failure is common, as are nephrocalcinosis and kidney stones.<ref>PMID:21031565</ref> <ref>PMID:15627218</ref> <ref>PMID:17384968</ref>
		+	== Function ==
		+	[[http://www.uniprot.org/uniprot/OCRL_HUMAN OCRL_HUMAN]] Converts phosphatidylinositol 4,5-bisphosphate to phosphatidylinositol 4-phosphate. Also converts inositol 1,4,5-trisphosphate to inositol 1,4-bisphosphate and inositol 1,3,4,5-tetrakisphosphate to inositol 1,3,4-trisphosphate. May function in lysosomal membrane trafficking by regulating the specific pool of phosphatidylinositol 4,5-bisphosphate that is associated with lysosomes. Involved in primary cilia assembly.<ref>PMID:22543976</ref> <ref>PMID:22228094</ref>
		+	<div style="background-color:#fffaf0;">
		+	== Publication Abstract from PubMed ==
		+	Lowe syndrome and type 2 Dent disease are caused by defects in the inositol 5-phosphatase OCRL. Most missense mutations in the OCRL ASH-RhoGAP domain that are found in affected individuals abolish interactions with the endocytic adaptors APPL1 and Ses (both Ses1 and Ses2), which bind OCRL through a short phenylalanine and histidine (F&H) motif. Using X-ray crystallography, we have identified the F&H motif binding site on the RhoGAP domain of OCRL. Missense mutations associated with disease affected F&H binding indirectly by destabilizing the RhoGAP fold. By contrast, a disease-associated mutation that does not perturb F&H binding and ASH-RhoGAP stability disrupted the interaction of OCRL with Rab5. The F&H binding site of OCRL is conserved even in species that do not have an identified homolog for APPL or Ses. Our study predicts the existence of other OCRL binding partners and shows that the perturbation of OCRL interactions has a crucial role in disease.

-	~~==Disease==~~	+	Recognition of the F&H motif by the Lowe syndrome protein OCRL.,Pirruccello M, Swan LE, Folta-Stogniew E, De Camilli P Nat Struct Mol Biol. 2011 Jun 12. doi: 10.1038/nsmb.2071. PMID:21666675<ref>PMID:21666675</ref>
-	~~[[http://www.uniprot.org/uniprot/OCRL_HUMAN OCRL_HUMAN]] Defects in OCRL are~~ the ~~cause of~~ Lowe ~~oculocerebrorenal~~ syndrome (OCRL~~) [MIM:[http://omim~~.~~org/entry/309000 309000]]. It is an X-linked multisystem disorder affecting eyes~~, ~~nervous system~~, ~~and kidney. It is characterized by hydrophthalmia~~, ~~cataract, mental retardation, vitamin D~~-~~resistant rickets~~, ~~aminoaciduria, and reduced ammonia production by the kidney~~. ~~Ocular abnormalities include cataract, glaucoma, microphthalmos, and decreased visual acuity~~. Developmental delay, hypotonia, behavior abnormalities, and areflexia are also present. Renal tubular involvement is characterized by impaired reabsorption of bicarbonate, amino acids, and phosphate. Musculoskeletal abnormalities such as joint hypermobility, dislocated hips, and fractures may develop as consequences of renal tubular acidosis and hypophosphatemia. Cataract is the only significant manifestation in carriers and is detected by slit-lamp examination.<ref>PMID:20133602</ref><ref>PMID:21233288</ref><ref>PMID:9199559</ref><ref>PMID:9682219</ref><ref>PMID:9632163</ref><ref>PMID:9788721</ref><ref>PMID:10923037</ref><ref>PMID:10767176</ref><ref>PMID:19168822</ref><ref>PMID:21031565</ref> Defects in OCRL are the cause of Dent disease type 2 (DD2) [MIM:[http://omim.~~org~~/~~entry/300555 300555]]~~. ~~DD2 is a renal disease belonging to the 'Dent disease complex', a group of disorders characterized by proximal renal tubular defect, hypercalciuria, nephrocalcinosis, and renal insufficiency~~. The spectrum of phenotypic features is remarkably similar in the various disorders, except for differences in the severity of bone deformities and renal impairment. Characteristic abnormalities include low-molecular-weight proteinuria and other features of Fanconi syndrome, such as glycosuria, aminoaciduria, and phosphaturia, but typically do not include proximal renal tubular acidosis. Progressive renal failure is common, as are nephrocalcinosis and kidney stones.<ref>PMID:~~21031565</ref><ref>PMID:15627218</ref>~~<ref>PMID:~~17384968~~</ref>	+

-	~~==Function==~~	+	From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>
-	~~[[http:~~/~~/www.uniprot.org/uniprot/OCRL_HUMAN OCRL_HUMAN]] Converts phosphatidylinositol 4~~,~~5-bisphosphate to phosphatidylinositol 4-phosphate~~. ~~Also converts inositol 1,4,5-trisphosphate to inositol 1,4-bisphosphate and inositol 1,3,4,5-tetrakisphosphate to inositol 1,3,4-trisphosphate~~. ~~May function in lysosomal membrane trafficking by regulating the specific pool~~ of ~~phosphatidylinositol 4,5-bisphosphate that is associated with lysosomes. Involved in primary cilia assembly~~.<~~ref~~>~~PMID:22543976~~</~~ref~~>~~<ref>PMID:22228094</ref>~~	+	</div>
-		+	== References ==
-	==~~About this Structure==~~	+	<references/>
-	[[3qis]] 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=3QIS OCA].	+	__TOC__
-		+	</StructureSection>
-	~~==Reference~~==	+
-	~~<ref group="xtra">PMID:021666675</ref>~~<references ~~group="xtra"~~/><~~references~~/>	+
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
	[[Category: Phosphoinositide 5-phosphatase]]		[[Category: Phosphoinositide 5-phosphatase]]
-	[[Category: Camilli, P De.]]	+	[[Category: Camilli, P De]]
-	[[Category: Folta-Stogniew, E.]]	+	[[Category: Folta-Stogniew, E]]
-	[[Category: Pirruccello, M.]]	+	[[Category: Pirruccello, M]]
-	[[Category: Swan, L E.]]	+	[[Category: Swan, L E]]
	[[Category: Appl1]]		[[Category: Appl1]]
	[[Category: Dent disease]]		[[Category: Dent disease]]

OCA at 19:05, 24 March 2013

2013-03-24T19:05:13Z

←Older revision		Revision as of 19:05, 24 March 2013
Line 1:		Line 1:
-	[[Image:3qis.png\|left\|200px]]
-
-	<!--
-	The line below this paragraph, containing "STRUCTURE_3qis", 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_3qis\| PDB=3qis \| SCENE= }}		{{STRUCTURE_3qis\| PDB=3qis \| SCENE= }}
-
	===Recognition of the F&H motif by the Lowe Syndrome protein OCRL===		===Recognition of the F&H motif by the Lowe Syndrome protein OCRL===
		+	{{ABSTRACT_PUBMED_21666675}}

		+	==Disease==
		+	[[http://www.uniprot.org/uniprot/OCRL_HUMAN OCRL_HUMAN]] Defects in OCRL are the cause of Lowe oculocerebrorenal syndrome (OCRL) [MIM:[http://omim.org/entry/309000 309000]]. It is an X-linked multisystem disorder affecting eyes, nervous system, and kidney. It is characterized by hydrophthalmia, cataract, mental retardation, vitamin D-resistant rickets, aminoaciduria, and reduced ammonia production by the kidney. Ocular abnormalities include cataract, glaucoma, microphthalmos, and decreased visual acuity. Developmental delay, hypotonia, behavior abnormalities, and areflexia are also present. Renal tubular involvement is characterized by impaired reabsorption of bicarbonate, amino acids, and phosphate. Musculoskeletal abnormalities such as joint hypermobility, dislocated hips, and fractures may develop as consequences of renal tubular acidosis and hypophosphatemia. Cataract is the only significant manifestation in carriers and is detected by slit-lamp examination.<ref>PMID:20133602</ref><ref>PMID:21233288</ref><ref>PMID:9199559</ref><ref>PMID:9682219</ref><ref>PMID:9632163</ref><ref>PMID:9788721</ref><ref>PMID:10923037</ref><ref>PMID:10767176</ref><ref>PMID:19168822</ref><ref>PMID:21031565</ref> Defects in OCRL are the cause of Dent disease type 2 (DD2) [MIM:[http://omim.org/entry/300555 300555]]. DD2 is a renal disease belonging to the 'Dent disease complex', a group of disorders characterized by proximal renal tubular defect, hypercalciuria, nephrocalcinosis, and renal insufficiency. The spectrum of phenotypic features is remarkably similar in the various disorders, except for differences in the severity of bone deformities and renal impairment. Characteristic abnormalities include low-molecular-weight proteinuria and other features of Fanconi syndrome, such as glycosuria, aminoaciduria, and phosphaturia, but typically do not include proximal renal tubular acidosis. Progressive renal failure is common, as are nephrocalcinosis and kidney stones.<ref>PMID:21031565</ref><ref>PMID:15627218</ref><ref>PMID:17384968</ref>

-	~~<!--~~	+	==Function==
-	~~The line below this paragraph, {{ABSTRACT_PUBMED_21666675}}, adds the Publication Abstract to the page~~	+	[[http://www.uniprot.org/uniprot/OCRL_HUMAN OCRL_HUMAN]] Converts phosphatidylinositol 4,5-bisphosphate to phosphatidylinositol 4-phosphate. Also converts inositol 1,4,5-trisphosphate to inositol 1,4-bisphosphate and inositol 1,3,4,5-tetrakisphosphate to inositol 1,3,4-trisphosphate. May function in lysosomal membrane trafficking by regulating the specific pool of phosphatidylinositol 4,5-bisphosphate that is associated with lysosomes. Involved in primary cilia assembly.<ref>PMID:22543976</ref><ref>PMID:22228094</ref>
-	~~(as it appears on PubMed at~~ http://www.~~pubmed~~.~~gov)~~, ~~where 21666675 is the PubMed ID number~~.	+
-	-->	+
-	~~{{ABSTRACT_PUBMED_21666675}}~~	+

	==About this Structure==		==About this Structure==
Line 22:		Line 13:

	==Reference==		==Reference==
-	<ref group="xtra">PMID:021666675</ref><references group="xtra"/>	+	<ref group="xtra">PMID:021666675</ref><references group="xtra"/><references/>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
	[[Category: Phosphoinositide 5-phosphatase]]		[[Category: Phosphoinositide 5-phosphatase]]

OCA at 05:21, 29 June 2011

2011-06-29T05:21:58Z

←Older revision		Revision as of 05:21, 29 June 2011
Line 1:		Line 1:
-	[[Image:3qis.~~jpg~~\|left\|200px]]	+	[[Image:3qis.png\|left\|200px]]

	<!--		<!--
Line 11:		Line 11:
	===Recognition of the F&H motif by the Lowe Syndrome protein OCRL===		===Recognition of the F&H motif by the Lowe Syndrome protein OCRL===

		+
		+	<!--
		+	The line below this paragraph, {{ABSTRACT_PUBMED_21666675}}, adds the Publication Abstract to the page
		+	(as it appears on PubMed at http://www.pubmed.gov), where 21666675 is the PubMed ID number.
		+	-->
		+	{{ABSTRACT_PUBMED_21666675}}

	==About this Structure==		==About this Structure==
	[[3qis]] 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=3QIS OCA].		[[3qis]] 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=3QIS OCA].
		+
		+	==Reference==
		+	<ref group="xtra">PMID:021666675</ref><references group="xtra"/>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
	[[Category: Phosphoinositide 5-phosphatase]]		[[Category: Phosphoinositide 5-phosphatase]]

OCA at 06:32, 15 June 2011

2011-06-15T06:32:49Z

←Older revision		Revision as of 06:32, 15 June 2011
Line 1:		Line 1:
-	~~'''Unreleased structure'''~~	+	[[Image:3qis.jpg\|left\|200px]]

-	The ~~entry 3qis~~ is ~~ON HOLD~~ ~~until Paper Publication~~	+	<!--
		+	The line below this paragraph, containing "STRUCTURE_3qis", 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_3qis\| PDB=3qis \| SCENE= }}

-	~~Authors: Pirruccello, M., Swan, L.E., Folta-Stogniew, E., De Camilli, P.~~	+	===Recognition of the F&H motif by the Lowe Syndrome protein OCRL===

-	~~Description~~: ~~Recognition of the F&H motif by the Lowe Syndrome~~ protein ~~OCRL~~	+
		+	==About this Structure==
		+	[[3qis]] 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=3QIS OCA].
		+	[[Category: Homo sapiens]]
		+	[[Category: Phosphoinositide 5-phosphatase]]
		+	[[Category: Camilli, P De.]]
		+	[[Category: Folta-Stogniew, E.]]
		+	[[Category: Pirruccello, M.]]
		+	[[Category: Swan, L E.]]
		+	[[Category: Appl1]]
		+	[[Category: Dent disease]]
		+	[[Category: Endocytic pathway]]
		+	[[Category: Golgi complex]]
		+	[[Category: Hydrolase-protein binding complex]]
		+	[[Category: Rab gtpase]]
		+	[[Category: Rac1]]
		+	[[Category: Ses2]]

OCA at 06:39, 2 March 2011

2011-03-02T06:39:30Z

←Older revision		Revision as of 06:39, 2 March 2011
Line 1:		Line 1:
	'''Unreleased structure'''		'''Unreleased structure'''

-	The entry 3qis is ON HOLD	+	The entry 3qis is ON HOLD until Paper Publication

	Authors: Pirruccello, M., Swan, L.E., Folta-Stogniew, E., De Camilli, P.		Authors: Pirruccello, M., Swan, L.E., Folta-Stogniew, E., De Camilli, P.

	Description: Recognition of the F&H motif by the Lowe Syndrome protein OCRL		Description: Recognition of the F&H motif by the Lowe Syndrome protein OCRL

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

2011-02-02T06:13:44Z

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

←Older revision

Revision as of 06:13, 2 February 2011

OCA: New page: '''Unreleased structure''' The entry 3qis is ON HOLD Authors: Pirruccello, M., Swan, L.E., Folta-Stogniew, E., De Camilli, P. Description: Recognition of the F&H motif by the Lowe Synd...

2011-02-02T06:13:43Z

New page: '''Unreleased structure''' The entry 3qis is ON HOLD Authors: Pirruccello, M., Swan, L.E., Folta-Stogniew, E., De Camilli, P. Description: Recognition of the F&H motif by the Lowe Synd...

New page

'''Unreleased structure'''

The entry 3qis is ON HOLD

Authors: Pirruccello, M., Swan, L.E., Folta-Stogniew, E., De Camilli, P.

Description: Recognition of the F&H motif by the Lowe Syndrome protein OCRL