5bqe - Revision history

OCA at 11:16, 10 January 2024

2024-01-10T11:16:56Z

←Older revision		Revision as of 11:16, 10 January 2024
Line 4:		Line 4:
	== Structural highlights ==		== Structural highlights ==
	<table><tr><td colspan='2'>[[5bqe]] is a 3 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=5BQE OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=5BQE FirstGlance]. <br>		<table><tr><td colspan='2'>[[5bqe]] is a 3 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=5BQE OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=5BQE FirstGlance]. <br>
-	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=CL:CHLORIDE+ION'>CL</scene>, <scene name='pdbligand=MLY:N-DIMETHYL-LYSINE'>MLY</scene>, <scene name='pdbligand=NAG:N-ACETYL-D-GLUCOSAMINE'>NAG</scene>, <scene name='pdbligand=PG0:2-(2-METHOXYETHOXY)ETHANOL'>PG0</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]] 2.3Å</td></tr>
		+	<tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=CL:CHLORIDE+ION'>CL</scene>, <scene name='pdbligand=MLY:N-DIMETHYL-LYSINE'>MLY</scene>, <scene name='pdbligand=NAG:N-ACETYL-D-GLUCOSAMINE'>NAG</scene>, <scene name='pdbligand=PG0:2-(2-METHOXYETHOXY)ETHANOL'>PG0</scene></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=5bqe FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5bqe OCA], [https://pdbe.org/5bqe PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=5bqe RCSB], [https://www.ebi.ac.uk/pdbsum/5bqe PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=5bqe 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=5bqe FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5bqe OCA], [https://pdbe.org/5bqe PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=5bqe RCSB], [https://www.ebi.ac.uk/pdbsum/5bqe PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=5bqe ProSAT]</span></td></tr>
	</table>		</table>

OCA at 06:03, 7 June 2023

2023-06-07T06:03:52Z

←Older revision		Revision as of 06:03, 7 June 2023
Line 3:		Line 3:
	<StructureSection load='5bqe' size='340' side='right'caption='[[5bqe]], [[Resolution\|resolution]] 2.30Å' scene=''>		<StructureSection load='5bqe' size='340' side='right'caption='[[5bqe]], [[Resolution\|resolution]] 2.30Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[5bqe]] is a 3 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=5BQE OCA]. For a <b>guided tour on the structure components</b> use [~~http~~://~~oca~~.~~weizmann.ac.il/oca-docs~~/fgij/fg.htm?mol=5BQE FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[5bqe]] is a 3 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=5BQE OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=5BQE FirstGlance]. <br>
-	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=CL:CHLORIDE+ION'>CL</scene>, <scene name='pdbligand=~~NAG~~:N-~~ACETYL~~-~~D-GLUCOSAMINE~~'>~~NAG~~</scene>, <scene name='pdbligand=~~PG0~~:2-(2-~~METHOXYETHOXY)ETHANOL~~'>~~PG0~~</scene>~~</td></tr>~~	+	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=CL:CHLORIDE+ION'>CL</scene>, <scene name='pdbligand=MLY:N-DIMETHYL-LYSINE'>MLY</scene>, <scene name='pdbligand=NAG:N-ACETYL-D-GLUCOSAMINE'>NAG</scene>, <scene name='pdbligand=PG0:2-(2-METHOXYETHOXY)ETHANOL'>PG0</scene></td></tr>
-	~~<tr id='NonStdRes'><td class="sblockLbl"><b>[[Non-Standard_Residue\|NonStd Res:]]</b></td><td class="sblockDat">~~<scene name='pdbligand=~~MLY~~:N-~~DIMETHYL~~-~~LYSINE~~'>~~MLY~~</scene>~~</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=5bqe FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5bqe OCA], [https://pdbe.org/5bqe PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=5bqe RCSB], [https://www.ebi.ac.uk/pdbsum/5bqe PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=5bqe ProSAT]</span></td></tr>
-	~~<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[5bqc\|5bqc]], [[5bpu\|5bpu]], [[5bq8\|5bq8]], [[5bqb\|5bqb]], [[5bpb\|5bpb]], [[5bpq\|5bpq]]~~</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=5bqe FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5bqe OCA], [~~http~~://pdbe.org/5bqe PDBe], [~~http~~://www.rcsb.org/pdb/explore.do?structureId=5bqe RCSB], [~~http~~://www.ebi.ac.uk/pdbsum/5bqe PDBsum], [~~http~~://prosat.h-its.org/prosat/prosatexe?pdbcode=5bqe ProSAT]</span></td></tr>	+
	</table>		</table>
	== Disease ==		== Disease ==
-	[~~[http~~://www.uniprot.org/uniprot/NDP_HUMAN NDP_HUMAN]] Retinopathy of prematurity;Familial exudative vitreoretinopathy;Coats disease;Persistent hyperplastic primary vitreous;Norrie disease. The disease is caused by mutations affecting the gene represented in this entry. The disease is caused by mutations affecting the gene represented in this entry. [[http://www.uniprot.org/uniprot/FZD4_HUMAN FZD4_HUMAN]] Retinopathy of prematurity;Familial exudative vitreoretinopathy;Persistent hyperplastic primary vitreous. The disease is caused by mutations affecting the gene represented in this entry.	+	[https://www.uniprot.org/uniprot/NDP_HUMAN NDP_HUMAN] Retinopathy of prematurity;Familial exudative vitreoretinopathy;Coats disease;Persistent hyperplastic primary vitreous;Norrie disease. The disease is caused by mutations affecting the gene represented in this entry. The disease is caused by mutations affecting the gene represented in this entry.
	== Function ==		== Function ==
-	[~~[http~~://www.uniprot.org/uniprot/NDP_HUMAN NDP_HUMAN]] Activates the canonical Wnt signaling pathway through FZD4 and LRP5 coreceptor. Plays a central role in retinal vascularization by acting as a ligand for FZD4 that signals via stabilizing beta-catenin (CTNNB1) and activating LEF/TCF-mediated transcriptional programs. Acts in concert with TSPAN12 to activate FZD4 independently of the Wnt-dependent activation of FZD4, suggesting the existence of a Wnt-independent signaling that also promote accumulation the beta-catenin (CTNNB1). May be involved in a pathway that regulates neural cell differentiation and proliferation. Possible role in neuroectodermal cell-cell interaction. [[http://www.uniprot.org/uniprot/FZD4_HUMAN FZD4_HUMAN]] Receptor for Wnt proteins. Most of frizzled receptors are coupled to the beta-catenin (CTNNB1) canonical signaling pathway, which leads to the activation of disheveled proteins, inhibition of GSK-3 kinase, nuclear accumulation of beta-catenin (CTNNB1) and activation of Wnt target genes. Plays a critical role in retinal vascularization by acting as a receptor for Wnt proteins and norrin (NDP). In retina, it can be both activated by Wnt protein-binding, but also by a Wnt-independent signaling via binding of norrin (NDP), promoting in both cases beta-catenin (CTNNB1) accumulation and stimulation of LEF/TCF-mediated transcriptional programs. A second signaling pathway involving PKC and calcium fluxes has been seen for some family members, but it is not yet clear if it represents a distinct pathway or if it can be integrated in the canonical pathway, as PKC seems to be required for Wnt-mediated inactivation of GSK-3 kinase. Both pathways seem to involve interactions with G-proteins. May be involved in transduction and intercellular transmission of polarity information during tissue morphogenesis and/or in differentiated tissues.	+	[https://www.uniprot.org/uniprot/NDP_HUMAN NDP_HUMAN] Activates the canonical Wnt signaling pathway through FZD4 and LRP5 coreceptor. Plays a central role in retinal vascularization by acting as a ligand for FZD4 that signals via stabilizing beta-catenin (CTNNB1) and activating LEF/TCF-mediated transcriptional programs. Acts in concert with TSPAN12 to activate FZD4 independently of the Wnt-dependent activation of FZD4, suggesting the existence of a Wnt-independent signaling that also promote accumulation the beta-catenin (CTNNB1). May be involved in a pathway that regulates neural cell differentiation and proliferation. Possible role in neuroectodermal cell-cell interaction.
	<div style="background-color:#fffaf0;">		<div style="background-color:#fffaf0;">
	== Publication Abstract from PubMed ==		== Publication Abstract from PubMed ==
Line 26:		Line 24:
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
		+	[[Category: Homo sapiens]]
	[[Category: Large Structures]]		[[Category: Large Structures]]
-	[[Category: Chang, T H]]	+	[[Category: Chang T-H]]
-	[[Category: Harlos, K]]	+	[[Category: Harlos K]]
-	[[Category: Hsieh, F L]]	+	[[Category: Hsieh F-L]]
-	[[Category: Jones~~, E Y]]~~	+	[[Category: Jones EY]]
-	~~[[Category: G protein coupled receptor]]~~	+
-	~~[[Category: Glycoprotein]]~~	+
-	~~[[Category: Norrie disease protein]]~~	+
-	~~[[Category: Signaling protein]]~~	+
-	~~[[Category: Wnt signalling pathway~~]]	+

OCA at 08:54, 11 March 2020

2020-03-11T08:54:20Z

←Older revision		Revision as of 08:54, 11 March 2020
Line 1:		Line 1:

	==Crystal structure of Norrin in complex with the cysteine-rich domain of Frizzled 4 -Methylated form==		==Crystal structure of Norrin in complex with the cysteine-rich domain of Frizzled 4 -Methylated form==
-	<StructureSection load='5bqe' size='340' side='right' caption='[[5bqe]], [[Resolution\|resolution]] 2.30Å' scene=''>	+	<StructureSection load='5bqe' size='340' side='right'caption='[[5bqe]], [[Resolution\|resolution]] 2.30Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
	<table><tr><td colspan='2'>[[5bqe]] is a 3 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=5BQE OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=5BQE FirstGlance]. <br>		<table><tr><td colspan='2'>[[5bqe]] is a 3 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=5BQE OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=5BQE FirstGlance]. <br>
Line 26:		Line 26:
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
		+	[[Category: Large Structures]]
	[[Category: Chang, T H]]		[[Category: Chang, T H]]
	[[Category: Harlos, K]]		[[Category: Harlos, K]]

OCA at 13:31, 4 May 2017

2017-05-04T13:31:12Z

←Older revision		Revision as of 13:31, 4 May 2017
Line 1:		Line 1:
		+
	==Crystal structure of Norrin in complex with the cysteine-rich domain of Frizzled 4 -Methylated form==		==Crystal structure of Norrin in complex with the cysteine-rich domain of Frizzled 4 -Methylated form==
	<StructureSection load='5bqe' size='340' side='right' caption='[[5bqe]], [[Resolution\|resolution]] 2.30Å' scene=''>		<StructureSection load='5bqe' size='340' side='right' caption='[[5bqe]], [[Resolution\|resolution]] 2.30Å' scene=''>
Line 6:		Line 7:
	<tr id='NonStdRes'><td class="sblockLbl"><b>[[Non-Standard_Residue\|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=MLY:N-DIMETHYL-LYSINE'>MLY</scene></td></tr>		<tr id='NonStdRes'><td class="sblockLbl"><b>[[Non-Standard_Residue\|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=MLY:N-DIMETHYL-LYSINE'>MLY</scene></td></tr>
	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[5bqc\|5bqc]], [[5bpu\|5bpu]], [[5bq8\|5bq8]], [[5bqb\|5bqb]], [[5bpb\|5bpb]], [[5bpq\|5bpq]]</td></tr>		<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[5bqc\|5bqc]], [[5bpu\|5bpu]], [[5bq8\|5bq8]], [[5bqb\|5bqb]], [[5bpb\|5bpb]], [[5bpq\|5bpq]]</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=5bqe FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5bqe OCA], [http://www.rcsb.org/pdb/explore.do?structureId=5bqe RCSB], [http://www.ebi.ac.uk/pdbsum/5bqe 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=5bqe FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5bqe OCA], [http://pdbe.org/5bqe PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=5bqe RCSB], [http://www.ebi.ac.uk/pdbsum/5bqe PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=5bqe 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 5bqe" style="background-color:#fffaf0;"></div>
	== References ==		== References ==
	<references/>		<references/>

OCA at 08:28, 22 July 2015

2015-07-22T08:28:54Z

←Older revision		Revision as of 08:28, 22 July 2015
Line 12:		Line 12:
	== Function ==		== Function ==
	[[http://www.uniprot.org/uniprot/NDP_HUMAN NDP_HUMAN]] Activates the canonical Wnt signaling pathway through FZD4 and LRP5 coreceptor. Plays a central role in retinal vascularization by acting as a ligand for FZD4 that signals via stabilizing beta-catenin (CTNNB1) and activating LEF/TCF-mediated transcriptional programs. Acts in concert with TSPAN12 to activate FZD4 independently of the Wnt-dependent activation of FZD4, suggesting the existence of a Wnt-independent signaling that also promote accumulation the beta-catenin (CTNNB1). May be involved in a pathway that regulates neural cell differentiation and proliferation. Possible role in neuroectodermal cell-cell interaction. [[http://www.uniprot.org/uniprot/FZD4_HUMAN FZD4_HUMAN]] Receptor for Wnt proteins. Most of frizzled receptors are coupled to the beta-catenin (CTNNB1) canonical signaling pathway, which leads to the activation of disheveled proteins, inhibition of GSK-3 kinase, nuclear accumulation of beta-catenin (CTNNB1) and activation of Wnt target genes. Plays a critical role in retinal vascularization by acting as a receptor for Wnt proteins and norrin (NDP). In retina, it can be both activated by Wnt protein-binding, but also by a Wnt-independent signaling via binding of norrin (NDP), promoting in both cases beta-catenin (CTNNB1) accumulation and stimulation of LEF/TCF-mediated transcriptional programs. A second signaling pathway involving PKC and calcium fluxes has been seen for some family members, but it is not yet clear if it represents a distinct pathway or if it can be integrated in the canonical pathway, as PKC seems to be required for Wnt-mediated inactivation of GSK-3 kinase. Both pathways seem to involve interactions with G-proteins. May be involved in transduction and intercellular transmission of polarity information during tissue morphogenesis and/or in differentiated tissues.		[[http://www.uniprot.org/uniprot/NDP_HUMAN NDP_HUMAN]] Activates the canonical Wnt signaling pathway through FZD4 and LRP5 coreceptor. Plays a central role in retinal vascularization by acting as a ligand for FZD4 that signals via stabilizing beta-catenin (CTNNB1) and activating LEF/TCF-mediated transcriptional programs. Acts in concert with TSPAN12 to activate FZD4 independently of the Wnt-dependent activation of FZD4, suggesting the existence of a Wnt-independent signaling that also promote accumulation the beta-catenin (CTNNB1). May be involved in a pathway that regulates neural cell differentiation and proliferation. Possible role in neuroectodermal cell-cell interaction. [[http://www.uniprot.org/uniprot/FZD4_HUMAN FZD4_HUMAN]] Receptor for Wnt proteins. Most of frizzled receptors are coupled to the beta-catenin (CTNNB1) canonical signaling pathway, which leads to the activation of disheveled proteins, inhibition of GSK-3 kinase, nuclear accumulation of beta-catenin (CTNNB1) and activation of Wnt target genes. Plays a critical role in retinal vascularization by acting as a receptor for Wnt proteins and norrin (NDP). In retina, it can be both activated by Wnt protein-binding, but also by a Wnt-independent signaling via binding of norrin (NDP), promoting in both cases beta-catenin (CTNNB1) accumulation and stimulation of LEF/TCF-mediated transcriptional programs. A second signaling pathway involving PKC and calcium fluxes has been seen for some family members, but it is not yet clear if it represents a distinct pathway or if it can be integrated in the canonical pathway, as PKC seems to be required for Wnt-mediated inactivation of GSK-3 kinase. Both pathways seem to involve interactions with G-proteins. May be involved in transduction and intercellular transmission of polarity information during tissue morphogenesis and/or in differentiated tissues.
		+	<div style="background-color:#fffaf0;">
		+	== Publication Abstract from PubMed ==
		+	Wnt signalling regulates multiple processes including angiogenesis, inflammation, and tumorigenesis. Norrin (Norrie Disease Protein) is a cystine-knot like growth factor. Although unrelated to Wnt, Norrin activates the Wnt/beta-catenin pathway. Signal complex formation involves Frizzled4 (Fz4), low-density lipoprotein receptor related protein 5/6 (Lrp5/6), Tetraspanin-12 and glycosaminoglycans (GAGs). Here, we report crystallographic and small-angle X-ray scattering analyses of Norrin in complex with Fz4 cysteine-rich domain (Fz4CRD), of this complex bound with GAG analogues, and of unliganded Norrin and Fz4CRD. Our structural, biophysical and cellular data, map Fz4 and putative Lrp5/6 binding sites to distinct patches on Norrin, and reveal a GAG binding site spanning Norrin and Fz4CRD. These results explain numerous disease-associated mutations. Comparison with the Xenopus Wnt8-mouse Fz8CRD complex reveals Norrin mimics Wnt for Frizzled recognition. The production and characterization of wild-type and mutant Norrins reported here open new avenues for the development of therapeutics to combat abnormal Norrin/Wnt signalling.
		+
		+	Structure and functional properties of Norrin mimic Wnt for signalling with Frizzled4, Lrp5/6, and proteoglycan.,Chang TH, Hsieh FL, Zebisch M, Harlos K, Elegheert J, Jones EY Elife. 2015 Jul 9;4. doi: 10.7554/eLife.06554. PMID:26158506<ref>PMID:26158506</ref>
		+
		+	From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>
		+	</div>
		+	== References ==
		+	<references/>
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>

OCA at 12:28, 1 July 2015

2015-07-01T12:28:17Z

←Older revision		Revision as of 12:28, 1 July 2015
Line 1:		Line 1:
-	'''~~Unreleased structure~~'''	+	==Crystal structure of Norrin in complex with the cysteine-rich domain of Frizzled 4 -Methylated form==
-		+	<StructureSection load='5bqe' size='340' side='right' caption='[[5bqe]], [[Resolution\|resolution]] 2.30Å' scene=''>
-	~~The entry~~ 5bqe is ~~ON HOLD until Paper Publication~~	+	== Structural highlights ==
-		+	<table><tr><td colspan='2'>[[5bqe]] is a 3 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=5BQE OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=5BQE FirstGlance]. <br>
-	~~Authors~~: ~~Chang~~, T.-H., ~~Hsieh, F~~.-L.~~, Harlos, K~~., ~~Jones~~, E.Y.	+	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=CL:CHLORIDE+ION'>CL</scene>, <scene name='pdbligand=NAG:N-ACETYL-D-GLUCOSAMINE'>NAG</scene>, <scene name='pdbligand=PG0:2-(2-METHOXYETHOXY)ETHANOL'>PG0</scene></td></tr>
-		+	<tr id='NonStdRes'><td class="sblockLbl"><b>[[Non-Standard_Residue\|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=MLY:N-DIMETHYL-LYSINE'>MLY</scene></td></tr>
-	~~Description:~~	+	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[5bqc\|5bqc]], [[5bpu\|5bpu]], [[5bq8\|5bq8]], [[5bqb\|5bqb]], [[5bpb\|5bpb]], [[5bpq\|5bpq]]</td></tr>
-	[[~~Category~~: ~~Unreleased Structures~~]]	+	<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=5bqe FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5bqe OCA], [http://www.rcsb.org/pdb/explore.do?structureId=5bqe RCSB], [http://www.ebi.ac.uk/pdbsum/5bqe PDBsum]</span></td></tr>
-	[[~~Category~~: ~~Hsieh~~, F.-L]]	+	</table>
		+	== Disease ==
		+	[[http://www.uniprot.org/uniprot/NDP_HUMAN NDP_HUMAN]] Retinopathy of prematurity;Familial exudative vitreoretinopathy;Coats disease;Persistent hyperplastic primary vitreous;Norrie disease. The disease is caused by mutations affecting the gene represented in this entry. The disease is caused by mutations affecting the gene represented in this entry. [[http://www.uniprot.org/uniprot/FZD4_HUMAN FZD4_HUMAN]] Retinopathy of prematurity;Familial exudative vitreoretinopathy;Persistent hyperplastic primary vitreous. The disease is caused by mutations affecting the gene represented in this entry.
		+	== Function ==
		+	[[http://www.uniprot.org/uniprot/NDP_HUMAN NDP_HUMAN]] Activates the canonical Wnt signaling pathway through FZD4 and LRP5 coreceptor. Plays a central role in retinal vascularization by acting as a ligand for FZD4 that signals via stabilizing beta-catenin (CTNNB1) and activating LEF/TCF-mediated transcriptional programs. Acts in concert with TSPAN12 to activate FZD4 independently of the Wnt-dependent activation of FZD4, suggesting the existence of a Wnt-independent signaling that also promote accumulation the beta-catenin (CTNNB1). May be involved in a pathway that regulates neural cell differentiation and proliferation. Possible role in neuroectodermal cell-cell interaction. [[http://www.uniprot.org/uniprot/FZD4_HUMAN FZD4_HUMAN]] Receptor for Wnt proteins. Most of frizzled receptors are coupled to the beta-catenin (CTNNB1) canonical signaling pathway, which leads to the activation of disheveled proteins, inhibition of GSK-3 kinase, nuclear accumulation of beta-catenin (CTNNB1) and activation of Wnt target genes. Plays a critical role in retinal vascularization by acting as a receptor for Wnt proteins and norrin (NDP). In retina, it can be both activated by Wnt protein-binding, but also by a Wnt-independent signaling via binding of norrin (NDP), promoting in both cases beta-catenin (CTNNB1) accumulation and stimulation of LEF/TCF-mediated transcriptional programs. A second signaling pathway involving PKC and calcium fluxes has been seen for some family members, but it is not yet clear if it represents a distinct pathway or if it can be integrated in the canonical pathway, as PKC seems to be required for Wnt-mediated inactivation of GSK-3 kinase. Both pathways seem to involve interactions with G-proteins. May be involved in transduction and intercellular transmission of polarity information during tissue morphogenesis and/or in differentiated tissues.
		+	__TOC__
		+	</StructureSection>
		+	[[Category: Chang, T H]]
	[[Category: Harlos, K]]		[[Category: Harlos, K]]
-	[[Category: Jones, E.Y]]	+	[[Category: Hsieh, F L]]
-	[[Category: ~~Chang, T.-H~~]]	+	[[Category: Jones, E Y]]
		+	[[Category: G protein coupled receptor]]
		+	[[Category: Glycoprotein]]
		+	[[Category: Norrie disease protein]]
		+	[[Category: Signaling protein]]
		+	[[Category: Wnt signalling pathway]]

OCA at 12:53, 10 June 2015

2015-06-10T12:53:22Z

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	'''Unreleased structure'''		'''Unreleased structure'''

-	The entry 5bqe is ON HOLD	+	The entry 5bqe is ON HOLD until Paper Publication

	Authors: Chang, T.-H., Hsieh, F.-L., Harlos, K., Jones, E.Y.		Authors: Chang, T.-H., Hsieh, F.-L., Harlos, K., Jones, E.Y.

OCA: Protected "5bqe" [edit=sysop:move=sysop]

2015-06-03T11:48:49Z

Protected "5bqe" [edit=sysop:move=sysop]

←Older revision

Revision as of 11:48, 3 June 2015

OCA: New page: '''Unreleased structure''' The entry 5bqe is ON HOLD Authors: Chang, T.-H., Hsieh, F.-L., Harlos, K., Jones, E.Y. Description: Category: Unreleased Structures [[Category: Hsieh, F...

2015-06-03T11:48:47Z

New page: '''Unreleased structure''' The entry 5bqe is ON HOLD Authors: Chang, T.-H., Hsieh, F.-L., Harlos, K., Jones, E.Y. Description: Category: Unreleased Structures [[Category: Hsieh, F...

New page

'''Unreleased structure'''

The entry 5bqe is ON HOLD

Authors: Chang, T.-H., Hsieh, F.-L., Harlos, K., Jones, E.Y.

Description:
[[Category: Unreleased Structures]]
[[Category: Hsieh, F.-L]]
[[Category: Harlos, K]]
[[Category: Jones, E.Y]]
[[Category: Chang, T.-H]]