2kld: Difference between revisions

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~~[[Image:2kld.png|left|200px]]~~

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===Solution Structure of the Calcium Binding Domain of the C-terminal Cytosolic Domain of Polycystin-2===

==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>

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==Function==

~~The line below this paragraph, {{ABSTRACT_PUBMED_19636966}}, adds the Publication Abstract to the page~~

[[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.

~~(as it appears on PubMed at~~ http://www.~~pubmed~~.~~gov~~), ~~where 19636966~~ is the ~~PubMed ID number~~.

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~~{{ABSTRACT_PUBMED_19636966}}~~

==About this Structure==

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==Reference==

[[Category: Homo sapiens]]

[[Category: Kalbitzer, H R.]]

~~[[Category: Calcium]]~~

[[Category: Calcium binding domain]]

~~[[Category: Coiled coil]]~~

[[Category: Cytosolic]]

[[Category: Disease mutation]]

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[[Category: Phosphoprotein]]

[[Category: Pkd2]]

~~[[Category: Polymorphism]]~~

[[Category: Transmembrane]]

[[Category: Transport]]

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@@ Line 1: / Line 1: @@
-[[Image:2kld.png|left|200px]]
-<!--
-The line below this paragraph, containing "STRUCTURE_2kld", creates the "Structure Box" on the page.
-You may change the PDB parameter (which sets the PDB file loaded into the applet)
-or the SCENE parameter (which sets the initial scene displayed when the page is loaded),
-or leave the SCENE parameter empty for the default display.
--->
 {{STRUCTURE_2kld|  PDB=2kld  |  SCENE=  }}
 ===Solution Structure of the Calcium Binding Domain of the C-terminal Cytosolic Domain of Polycystin-2===
+{{ABSTRACT_PUBMED_19636966}}
+==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>
-<!--
+==Function==
-The line below this paragraph, {{ABSTRACT_PUBMED_19636966}}, adds the Publication Abstract to the page
+[[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.
-(as it appears on PubMed at http://www.pubmed.gov), where 19636966 is the PubMed ID number.
--->
-{{ABSTRACT_PUBMED_19636966}}
 ==About this Structure==
@@ Line 22: / Line 13: @@
 ==Reference==
-<ref group="xtra">PMID:019636966</ref><ref group="xtra">PMID:019546223</ref><references group="xtra"/>
+<ref group="xtra">PMID:019636966</ref><ref group="xtra">PMID:019546223</ref><references group="xtra"/><references/>
 [[Category: Homo sapiens]]
 [[Category: Kalbitzer, H R.]]
-[[Category: Calcium]]
 [[Category: Calcium binding domain]]
-[[Category: Coiled coil]]
 [[Category: Cytosolic]]
 [[Category: Disease mutation]]
@@ Line 39: / Line 28: @@
 [[Category: Phosphoprotein]]
 [[Category: Pkd2]]
-[[Category: Polymorphism]]
 [[Category: Transmembrane]]
 [[Category: Transport]]