5bpb: Difference between revisions
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''' | ==Crystal structure of the cysteine-rich domain of human Frizzled 4 - Crystal Form I== | ||
<StructureSection load='5bpb' size='340' side='right' caption='[[5bpb]], [[Resolution|resolution]] 2.20Å' scene=''> | |||
== Structural highlights == | |||
<table><tr><td colspan='2'>[[5bpb]] is a 4 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=5BPB OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=5BPB 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=5bpb FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5bpb OCA], [http://www.rcsb.org/pdb/explore.do?structureId=5bpb RCSB], [http://www.ebi.ac.uk/pdbsum/5bpb PDBsum]</span></td></tr> | |||
</table> | |||
[[ | == Disease == | ||
[[Category: | [[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/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 | [[Category: Hsieh, F L]] | ||
[[Category: | [[Category: Jones, E Y]] | ||
[[Category: G protein coupled receptor]] | |||
[[Category: Glycoprotein]] | |||
[[Category: Receptor for norrin recognition]] | |||
[[Category: Signaling protein]] | |||
[[Category: Wnt signalling pathway]] | |||