We apologize for Proteopedia being slow to respond. For the past two years, a new implementation of Proteopedia has been being built. Soon, it will replace this 18-year old system. All existing content will be moved to the new system at a date that will be announced here.

2y4q

From Proteopedia

(Difference between revisions)
Jump to: navigation, search
Current revision (08:08, 23 August 2023) (edit) (undo)
 
(4 intermediate revisions not shown.)
Line 1: Line 1:
-
{{STRUCTURE_2y4q| PDB=2y4q | SCENE= }}
 
-
===SOLUTION STRUCTURE OF THE EF-HAND DOMAIN OF HUMAN POLYCYSTIN 2===
 
-
==Disease==
+
==Solution structure of the EF-hand domain of Human Polycystin 2==
-
[[http://www.uniprot.org/uniprot/PKD2_HUMAN PKD2_HUMAN]] Defects in PKD2 are the cause of polycystic kidney disease 2 (PKD2) [MIM:[http://omim.org/entry/613095 613095]]. PKD2 is a disorder characterized by progressive formation and enlargement of cysts in both kidneys, typically leading to end-stage renal disease in adult life. Cysts also occurs in the liver and other organs. It represents approximately 15% of the cases of autosomal dominant polycystic kidney disease. PKD2 is clinically milder than PKD1 but it has a deleterious impact on overall life expectancy.<ref>PMID:9326320</ref><ref>PMID:10541293</ref><ref>PMID:10411676</ref><ref>PMID:10835625</ref><ref>PMID:11968093</ref><ref>PMID:12707387</ref><ref>PMID:14993477</ref><ref>PMID:15772804</ref><ref>PMID:21115670</ref>
+
<StructureSection load='2y4q' size='340' side='right'caption='[[2y4q]]' scene=''>
 +
== Structural highlights ==
 +
<table><tr><td colspan='2'>[[2y4q]] is a 1 chain structure with sequence from [https://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2Y4Q OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=2Y4Q FirstGlance]. <br>
 +
</td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models|Method:]]</b></td><td class="sblockDat" id="methodDat">Solution NMR</td></tr>
 +
<tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=CA:CALCIUM+ION'>CA</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=2y4q FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2y4q OCA], [https://pdbe.org/2y4q PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=2y4q RCSB], [https://www.ebi.ac.uk/pdbsum/2y4q PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=2y4q ProSAT]</span></td></tr>
 +
</table>
 +
== Disease ==
 +
[https://www.uniprot.org/uniprot/PKD2_HUMAN PKD2_HUMAN] Defects in PKD2 are the cause of polycystic kidney disease 2 (PKD2) [MIM:[https://omim.org/entry/613095 613095]. PKD2 is a disorder characterized by progressive formation and enlargement of cysts in both kidneys, typically leading to end-stage renal disease in adult life. Cysts also occurs in the liver and other organs. It represents approximately 15% of the cases of autosomal dominant polycystic kidney disease. PKD2 is clinically milder than PKD1 but it has a deleterious impact on overall life expectancy.<ref>PMID:9326320</ref> <ref>PMID:10541293</ref> <ref>PMID:10411676</ref> <ref>PMID:10835625</ref> <ref>PMID:11968093</ref> <ref>PMID:12707387</ref> <ref>PMID:14993477</ref> <ref>PMID:15772804</ref> <ref>PMID:21115670</ref>
 +
== Function ==
 +
[https://www.uniprot.org/uniprot/PKD2_HUMAN PKD2_HUMAN] Involved in fluid-flow mechanosensation by the primary cilium in renal epithelium (By similarity). PKD1 and PKD2 may function through a common signaling pathway that is necessary for normal tubulogenesis (By similarity). Acts as a regulator of cilium length, together with PKD1 (By similarity). The dynamic control of cilium length is essential in the regulation of mechanotransductive signaling. The cilium length response creates a negative feedback loop whereby fluid shear-mediated deflection of the primary cilium, which decreases intracellular cAMP, leads to cilium shortening and thus decreases flow-induced signaling (By similarity). Functions as a calcium permeable cation channel.
 +
<div style="background-color:#fffaf0;">
 +
== Publication Abstract from PubMed ==
 +
Autosomal dominant polycystic kidney disease (ADPKD) affects over 1:1000 of the worldwide population and is caused by mutations in two genes, PKD1 and PKD2. PKD2 encodes a 968-amino acid membrane spanning protein, Polycystin-2 (PC2), that is a member of the TRP ion channel family. The C-terminal cytoplasmic tail contains an EF-hand motif followed by a short coiled-coil domain. We have determined the structure of the EF-hand region of PC-2 using NMR spectroscopy. The use of different boundaries compared with those used in previous studies, have enabled us to determine a high resolution structure and show that the EF hand motif forms a standard calcium-binding pocket. The affinity of this pocket for calcium has been measured and mutants that both decrease and increase its affinity for the metal ion have been created.
-
==Function==
+
A high-resolution structure of the EF-hand domain of human polycystin-2.,Allen MD, Qamar S, Vadivelu MK, Sandford RN, Bycroft M Protein Sci. 2014 Jul 2. doi: 10.1002/pro.2513. PMID:24990821<ref>PMID:24990821</ref>
-
[[http://www.uniprot.org/uniprot/PKD2_HUMAN PKD2_HUMAN]] Involved in fluid-flow mechanosensation by the primary cilium in renal epithelium (By similarity). PKD1 and PKD2 may function through a common signaling pathway that is necessary for normal tubulogenesis (By similarity). Acts as a regulator of cilium length, together with PKD1 (By similarity). The dynamic control of cilium length is essential in the regulation of mechanotransductive signaling. The cilium length response creates a negative feedback loop whereby fluid shear-mediated deflection of the primary cilium, which decreases intracellular cAMP, leads to cilium shortening and thus decreases flow-induced signaling (By similarity). Functions as a calcium permeable cation channel.
+
-
==About this Structure==
+
From MEDLINE&reg;/PubMed&reg;, a database of the U.S. National Library of Medicine.<br>
-
[[2y4q]] is a 1 chain structure. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2Y4Q OCA].
+
</div>
-
 
+
<div class="pdbe-citations 2y4q" style="background-color:#fffaf0;"></div>
-
==Reference==
+
== References ==
-
<references group="xtra"/><references/>
+
<references/>
-
[[Category: Allen, M D.]]
+
__TOC__
-
[[Category: Qamar, S.]]
+
</StructureSection>
-
[[Category: Sandford, R N.]]
+
[[Category: Homo sapiens]]
-
[[Category: Transport protein]]
+
[[Category: Large Structures]]
 +
[[Category: Allen MD]]
 +
[[Category: Qamar S]]
 +
[[Category: Sandford RN]]

Current revision

Solution structure of the EF-hand domain of Human Polycystin 2

PDB ID 2y4q

Drag the structure with the mouse to rotate

Proteopedia Page Contributors and Editors (what is this?)

OCA

Retrieved from "http://52.214.119.220/wiki/index.php/2y4q"
Personal tools