5ic3: Difference between revisions

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'''Unreleased structure'''


The entry 5ic3 is ON HOLD  until Paper Publication
==CAL PDZ domain with peptide and inhibitor==
 
<StructureSection load='5ic3' size='340' side='right' caption='[[5ic3]], [[Resolution|resolution]] 1.70&Aring;' scene=''>
Authors: Zhao, Y., Madden, D.R.
== Structural highlights ==
 
<table><tr><td colspan='2'>[[5ic3]] is a 4 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=5IC3 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=5IC3 FirstGlance]. <br>
Description: CAL PDZ domain with peptide and inhibitor
</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=PQR:4-[METHYL(NITROSO)AMINO]BENZENE-1,2-DIOL'>PQR</scene></td></tr>
[[Category: Unreleased Structures]]
<tr id='related'><td class="sblockLbl"><b>[[Related_structure|Related:]]</b></td><td class="sblockDat">[[4jor|4jor]]</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=5ic3 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5ic3 OCA], [http://pdbe.org/5ic3 PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=5ic3 RCSB], [http://www.ebi.ac.uk/pdbsum/5ic3 PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=5ic3 ProSAT]</span></td></tr>
</table>
== Disease ==
[[http://www.uniprot.org/uniprot/GOPC_HUMAN GOPC_HUMAN]] Note=A chromosomal aberration involving GOPC is found in a glioblastoma multiforme sample. An intra-chromosomal deletion del(6)(q21q21) is responsible for the formation of GOPC-ROS1 chimeric protein which has a constitutive receptor tyrosine kinase activity.<ref>PMID:12661006</ref> 
== Function ==
[[http://www.uniprot.org/uniprot/GOPC_HUMAN GOPC_HUMAN]] Plays a role in intracellular protein trafficking and degradation. May regulate CFTR chloride currents and acid-induced ASIC3 currents by modulating cell surface expression of both channels. May also regulate the intracellular trafficking of the ADR1B receptor. May play a role in autophagy. Overexpression results in CFTR intracellular retention and degradation in the lysosomes.<ref>PMID:11707463</ref> <ref>PMID:14570915</ref> <ref>PMID:15358775</ref> 
== References ==
<references/>
__TOC__
</StructureSection>
[[Category: Madden, D R]]
[[Category: Zhao, Y]]
[[Category: Zhao, Y]]
[[Category: Madden, D.R]]
[[Category: Cal pdz]]
[[Category: Complex]]
[[Category: Inhibitor]]
[[Category: Peptide binding protein]]
[[Category: Peptide binding protein-inhibitor complex]]