3nx0: Difference between revisions

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~~[[Image:3nx0.png|left|200px]]~~

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~~The line below this paragraph, containing "STRUCTURE_3nx0", 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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===Hinge-loop mutation can be used to control 3D domain swapping and amyloidogenesis of human cystatin C===

==Disease==

[[http://www.uniprot.org/uniprot/CYTC_HUMAN CYTC_HUMAN]] Defects in CST3 are the cause of amyloidosis type 6 (AMYL6) [MIM:[http://omim.org/entry/105150 105150]]; also known as hereditary cerebral hemorrhage with amyloidosis (HCHWA), cerebral amyloid angiopathy (CAA) or cerebroarterial amyloidosis Icelandic type. AMYL6 is a hereditary generalized amyloidosis due to cystatin C amyloid deposition. Cystatin C amyloid accumulates in the walls of arteries, arterioles, and sometimes capillaries and veins of the brain, and in various organs including lymphoid tissue, spleen, salivary glands, and seminal vesicles. Amyloid deposition in the cerebral vessels results in cerebral amyloid angiopathy, cerebral hemorrhage and premature stroke. Cystatin C levels in the cerebrospinal fluid are abnormally low.<ref>PMID:2541223</ref><ref>PMID:1352269</ref> Genetic variations in CST3 are associated with age-related macular degeneration type 11 (ARMD11) [MIM:[http://omim.org/entry/611953 611953]]. ARMD is a multifactorial eye disease and the most common cause of irreversible vision loss in the developed world. In most patients, the disease is manifest as ophthalmoscopically visible yellowish accumulations of protein and lipid that lie beneath the retinal pigment epithelium and within an elastin-containing structure known as Bruch membrane.<ref>PMID:11815350</ref>

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==Function==

~~The line below this paragraph, {{ABSTRACT_PUBMED_21074623}}, adds the Publication Abstract to the page~~

[[http://www.uniprot.org/uniprot/CYTC_HUMAN CYTC_HUMAN]] As an inhibitor of cysteine proteinases, this protein is thought to serve an important physiological role as a local regulator of this enzyme activity.

~~(as it appears on PubMed at~~ http://www.~~pubmed~~.~~gov)~~, ~~where 21074623~~ is ~~the PubMed ID number~~.

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~~{{ABSTRACT_PUBMED_21074623}}~~

==About this Structure==

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==Reference==

[[Category: Homo sapiens]]

[[Category: Jankowska, E.]]

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[[Category: Orlikowska, M.]]

[[Category: Szymanska, A.]]

[[Category: 3d domain swapping]]

[[Category: Amyloid]]

[[Category: Cysteine protease inhibitor]]

[[Category: Hydrolase inhibitor]]

[[Category: Protein aggregation]]

[[Category: Protein engineering]]

[[Category: Protein oligomerization]]

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@@ Line 1: / Line 1: @@
-[[Image:3nx0.png|left|200px]]
-<!--
-The line below this paragraph, containing "STRUCTURE_3nx0", 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_3nx0|  PDB=3nx0  |  SCENE=  }}
 ===Hinge-loop mutation can be used to control 3D domain swapping and amyloidogenesis of human cystatin C===
+{{ABSTRACT_PUBMED_21074623}}
+==Disease==
+[[http://www.uniprot.org/uniprot/CYTC_HUMAN CYTC_HUMAN]] Defects in CST3 are the cause of amyloidosis type 6 (AMYL6) [MIM:[http://omim.org/entry/105150 105150]]; also known as hereditary cerebral hemorrhage with amyloidosis (HCHWA), cerebral amyloid angiopathy (CAA) or cerebroarterial amyloidosis Icelandic type. AMYL6 is a hereditary generalized amyloidosis due to cystatin C amyloid deposition. Cystatin C amyloid accumulates in the walls of arteries, arterioles, and sometimes capillaries and veins of the brain, and in various organs including lymphoid tissue, spleen, salivary glands, and seminal vesicles. Amyloid deposition in the cerebral vessels results in cerebral amyloid angiopathy, cerebral hemorrhage and premature stroke. Cystatin C levels in the cerebrospinal fluid are abnormally low.<ref>PMID:2541223</ref><ref>PMID:1352269</ref>  Genetic variations in CST3 are associated with age-related macular degeneration type 11 (ARMD11) [MIM:[http://omim.org/entry/611953 611953]]. ARMD is a multifactorial eye disease and the most common cause of irreversible vision loss in the developed world. In most patients, the disease is manifest as ophthalmoscopically visible yellowish accumulations of protein and lipid that lie beneath the retinal pigment epithelium and within an elastin-containing structure known as Bruch membrane.<ref>PMID:11815350</ref>
-<!--
+==Function==
-The line below this paragraph, {{ABSTRACT_PUBMED_21074623}}, adds the Publication Abstract to the page
+[[http://www.uniprot.org/uniprot/CYTC_HUMAN CYTC_HUMAN]] As an inhibitor of cysteine proteinases, this protein is thought to serve an important physiological role as a local regulator of this enzyme activity.
-(as it appears on PubMed at http://www.pubmed.gov), where 21074623 is the PubMed ID number.
--->
-{{ABSTRACT_PUBMED_21074623}}
 ==About this Structure==
@@ Line 22: / Line 13: @@
 ==Reference==
-<ref group="xtra">PMID:21074623</ref><references group="xtra"/>
+<ref group="xtra">PMID:021074623</ref><references group="xtra"/><references/>
 [[Category: Homo sapiens]]
 [[Category: Jankowska, E.]]
@@ Line 29: / Line 20: @@
 [[Category: Orlikowska, M.]]
 [[Category: Szymanska, A.]]
+[[Category: 3d domain swapping]]
+[[Category: Amyloid]]
+[[Category: Cysteine protease inhibitor]]
+[[Category: Hydrolase inhibitor]]
+[[Category: Protein aggregation]]
+[[Category: Protein engineering]]
+[[Category: Protein oligomerization]]