5cl1: Difference between revisions
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''' | ==Complex structure of Norrin with human Frizzled 4== | ||
<StructureSection load='5cl1' size='340' side='right' caption='[[5cl1]], [[Resolution|resolution]] 3.80Å' scene=''> | |||
== Structural highlights == | |||
<table><tr><td colspan='2'>[[5cl1]] is a 4 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=5CL1 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=5CL1 FirstGlance]. <br> | |||
</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=NAG:N-ACETYL-D-GLUCOSAMINE'>NAG</scene></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=5cl1 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5cl1 OCA], [http://www.rcsb.org/pdb/explore.do?structureId=5cl1 RCSB], [http://www.ebi.ac.uk/pdbsum/5cl1 PDBsum]</span></td></tr> | |||
</table> | |||
[[ | == Disease == | ||
[[ | [[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/MALE_ECO57 MALE_ECO57]] Involved in the high-affinity maltose membrane transport system MalEFGK. Initial receptor for the active transport of and chemotaxis toward maltooligosaccharides (By similarity). [[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: Cheng, Z]] | [[Category: Cheng, Z]] | ||
[[Category: Ke, J]] | |||
[[Category: Shen, G]] | |||
[[Category: Wang, Z]] | [[Category: Wang, Z]] | ||
[[Category: | [[Category: Xu, H E]] | ||
[[Category: Xu, W]] | [[Category: Xu, W]] | ||
[[Category: | [[Category: Frizzled]] | ||
[[Category: Norrin]] | |||
[[Category: Signaling protein]] | |||
[[Category: Wnt]] | |||
