3sqo: Difference between revisions

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~~[[Image:3sqo.jpg|left|200px]]~~

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~~The line below this paragraph, containing "STRUCTURE_3sqo", creates the "Structure Box" on the page.~~

~~You may change the PDB parameter (which sets the PDB file loaded into the applet)~~

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===PCSK9 J16 Fab complex===

==Disease==

[[http://www.uniprot.org/uniprot/PCSK9_HUMAN PCSK9_HUMAN]] Defects in PCSK9 are the cause of hypercholesterolemia autosomal dominant type 3 (HCHOLA3) [MIM:[http://omim.org/entry/603776 603776]]. A familial condition characterized by elevated circulating cholesterol contained in either low-density lipoproteins alone or also in very-low-density lipoproteins.<ref>PMID:12730697</ref>

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==Function==

~~The line below this paragraph, {{ABSTRACT_PUBMED_22019884}}, adds the Publication Abstract to the page~~

[[http://www.uniprot.org/uniprot/PCSK9_HUMAN PCSK9_HUMAN]] Crucial player in the regulation of plasma cholesterol homeostasis. Binds to low-density lipid receptor family members: low density lipoprotein receptor (LDLR), very low density lipoprotein receptor (VLDLR), apolipoprotein E receptor (LRP1/APOER) and apolipoprotein receptor 2 (LRP8/APOER2), and promotes their degradation in intracellular acidic compartments. Acts via a non-proteolytic mechanism to enhance the degradation of the hepatic LDLR through a clathrin LDLRAP1/ARH-mediated pathway. May prevent the recycling of LDLR from endosomes to the cell surface or direct it to lysosomes for degradation. Can induce ubiquitination of LDLR leading to its subsequent degradation. Inhibits intracellular degradation of APOB via the autophagosome/lysosome pathway in a LDLR-independent manner. Involved in the disposal of non-acetylated intermediates of BACE1 in the early secretory pathway. Inhibits epithelial Na(+) channel (ENaC)-mediated Na(+) absorption by reducing ENaC surface expression primarily by increasing its proteasomal degradation. Regulates neuronal apoptosis via modulation of LRP8/APOER2 levels and related anti-apoptotic signaling pathways.<ref>PMID:17461796</ref><ref>PMID:18197702</ref><ref>PMID:18660751</ref><ref>PMID:18039658</ref><ref>PMID:22074827</ref><ref>PMID:22580899</ref><ref>PMID:22493497</ref>

~~(as it appears on PubMed at~~ http://www.~~pubmed~~.~~gov~~), ~~where 22019884 is~~ the ~~PubMed ID number~~.

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~~{{ABSTRACT_PUBMED_22019884}}~~

==About this Structure==

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==Reference==

[[Category: Homo sapiens]]

[[Category: Strop, P.]]

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@@ Line 1: / Line 1: @@
-[[Image:3sqo.jpg|left|200px]]
-<!--
-The line below this paragraph, containing "STRUCTURE_3sqo", 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_3sqo|  PDB=3sqo  |  SCENE=  }}
 ===PCSK9 J16 Fab complex===
+{{ABSTRACT_PUBMED_22019884}}
+==Disease==
+[[http://www.uniprot.org/uniprot/PCSK9_HUMAN PCSK9_HUMAN]] Defects in PCSK9 are the cause of hypercholesterolemia autosomal dominant type 3 (HCHOLA3) [MIM:[http://omim.org/entry/603776 603776]]. A familial condition characterized by elevated circulating cholesterol contained in either low-density lipoproteins alone or also in very-low-density lipoproteins.<ref>PMID:12730697</ref>
-<!--
+==Function==
-The line below this paragraph, {{ABSTRACT_PUBMED_22019884}}, adds the Publication Abstract to the page
+[[http://www.uniprot.org/uniprot/PCSK9_HUMAN PCSK9_HUMAN]] Crucial player in the regulation of plasma cholesterol homeostasis. Binds to low-density lipid receptor family members: low density lipoprotein receptor (LDLR), very low density lipoprotein receptor (VLDLR), apolipoprotein E receptor (LRP1/APOER) and apolipoprotein receptor 2 (LRP8/APOER2), and promotes their degradation in intracellular acidic compartments. Acts via a non-proteolytic mechanism to enhance the degradation of the hepatic LDLR through a clathrin LDLRAP1/ARH-mediated pathway. May prevent the recycling of LDLR from endosomes to the cell surface or direct it to lysosomes for degradation. Can induce ubiquitination of LDLR leading to its subsequent degradation. Inhibits intracellular degradation of APOB via the autophagosome/lysosome pathway in a LDLR-independent manner. Involved in the disposal of non-acetylated intermediates of BACE1 in the early secretory pathway. Inhibits epithelial Na(+) channel (ENaC)-mediated Na(+) absorption by reducing ENaC surface expression primarily by increasing its proteasomal degradation. Regulates neuronal apoptosis via modulation of LRP8/APOER2 levels and related anti-apoptotic signaling pathways.<ref>PMID:17461796</ref><ref>PMID:18197702</ref><ref>PMID:18660751</ref><ref>PMID:18039658</ref><ref>PMID:22074827</ref><ref>PMID:22580899</ref><ref>PMID:22493497</ref>
-(as it appears on PubMed at http://www.pubmed.gov), where 22019884 is the PubMed ID number.
--->
-{{ABSTRACT_PUBMED_22019884}}
 ==About this Structure==
@@ Line 22: / Line 13: @@
 ==Reference==
-<ref group="xtra">PMID:022019884</ref><references group="xtra"/>
+<ref group="xtra">PMID:022019884</ref><references group="xtra"/><references/>
 [[Category: Homo sapiens]]
 [[Category: Strop, P.]]