3hrn

From Proteopedia

(Difference between revisions)
Jump to: navigation, search
Line 1: Line 1:
==crystal structure of a C-terminal coiled coil domain of Transient receptor potential (TRP) channel subfamily P member 2 (TRPP2, polycystic kidney disease 2)==
==crystal structure of a C-terminal coiled coil domain of Transient receptor potential (TRP) channel subfamily P member 2 (TRPP2, polycystic kidney disease 2)==
-
<StructureSection load='3hrn' size='340' side='right' caption='[[3hrn]], [[Resolution|resolution]] 1.90&Aring;' scene=''>
+
<StructureSection load='3hrn' size='340' side='right'caption='[[3hrn]], [[Resolution|resolution]] 1.90&Aring;' scene=''>
== Structural highlights ==
== Structural highlights ==
-
<table><tr><td colspan='2'>[[3hrn]] is a 1 chain structure with sequence from [http://en.wikipedia.org/wiki/Human Human]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3HRN OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3HRN FirstGlance]. <br>
+
<table><tr><td colspan='2'>[[3hrn]] is a 1 chain structure with sequence from [https://en.wikipedia.org/wiki/Human Human]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3HRN OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=3HRN FirstGlance]. <br>
-
</td></tr><tr id='related'><td class="sblockLbl"><b>[[Related_structure|Related:]]</b></td><td class="sblockDat">[[3hro|3hro]]</td></tr>
+
</td></tr><tr id='related'><td class="sblockLbl"><b>[[Related_structure|Related:]]</b></td><td class="sblockDat"><div style='overflow: auto; max-height: 3em;'>[[3hro|3hro]]</div></td></tr>
-
<tr id='gene'><td class="sblockLbl"><b>[[Gene|Gene:]]</b></td><td class="sblockDat">PKD2 ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN])</td></tr>
+
<tr id='gene'><td class="sblockLbl"><b>[[Gene|Gene:]]</b></td><td class="sblockDat">PKD2 ([https://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN])</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=3hrn FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3hrn OCA], [http://pdbe.org/3hrn PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=3hrn RCSB], [http://www.ebi.ac.uk/pdbsum/3hrn PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=3hrn 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=3hrn FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3hrn OCA], [https://pdbe.org/3hrn PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=3hrn RCSB], [https://www.ebi.ac.uk/pdbsum/3hrn PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=3hrn ProSAT]</span></td></tr>
</table>
</table>
== Disease ==
== Disease ==
-
[[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>
+
[[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 ==
== Function ==
-
[[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.
+
[[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.
== Evolutionary Conservation ==
== Evolutionary Conservation ==
[[Image:Consurf_key_small.gif|200px|right]]
[[Image:Consurf_key_small.gif|200px|right]]
Check<jmol>
Check<jmol>
<jmolCheckbox>
<jmolCheckbox>
-
<scriptWhenChecked>select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/hr/3hrn_consurf.spt"</scriptWhenChecked>
+
<scriptWhenChecked>; select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/hr/3hrn_consurf.spt"</scriptWhenChecked>
<scriptWhenUnchecked>script /wiki/extensions/Proteopedia/spt/initialview01.spt</scriptWhenUnchecked>
<scriptWhenUnchecked>script /wiki/extensions/Proteopedia/spt/initialview01.spt</scriptWhenUnchecked>
<text>to colour the structure by Evolutionary Conservation</text>
<text>to colour the structure by Evolutionary Conservation</text>
Line 36: Line 36:
</StructureSection>
</StructureSection>
[[Category: Human]]
[[Category: Human]]
 +
[[Category: Large Structures]]
[[Category: Buraei, Z]]
[[Category: Buraei, Z]]
[[Category: Chen, X Z]]
[[Category: Chen, X Z]]

Revision as of 11:55, 30 March 2022

crystal structure of a C-terminal coiled coil domain of Transient receptor potential (TRP) channel subfamily P member 2 (TRPP2, polycystic kidney disease 2)

PDB ID 3hrn

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/3hrn"
Personal tools