1cee: Difference between revisions

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~~[[Image:1cee.png|left|200px]]~~

===SOLUTION STRUCTURE OF CDC42 IN COMPLEX WITH THE GTPASE BINDING DOMAIN OF WASP===

==~~=SOLUTION STRUCTURE OF CDC42 IN COMPLEX WITH THE GTPASE BINDING DOMAIN OF WASP=~~==

==Disease==

[[http://www.uniprot.org/uniprot/WASP_HUMAN WASP_HUMAN]] Defects in WAS are the cause of Wiskott-Aldrich syndrome (WAS) [MIM:[http://omim.org/entry/301000 301000]]; also known as eczema-thrombocytopenia-immunodeficiency syndrome. WAS is an X-linked recessive immunodeficiency characterized by eczema, thrombocytopenia, recurrent infections, and bloody diarrhea. Death usually occurs before age 10.<ref>PMID:7753869</ref><ref>PMID:8528198</ref><ref>PMID:8528199</ref><ref>PMID:8682510</ref><ref>PMID:9126958</ref><ref>PMID:9098856</ref><ref>PMID:9683546</ref><ref>PMID:9713366</ref><ref>PMID:9445409</ref><ref>PMID:10447259</ref><ref>PMID:11793485</ref> Defects in WAS are the cause of thrombocytopenia type 1 (THC1) [MIM:[http://omim.org/entry/313900 313900]]. Thrombocytopenia is defined by a decrease in the number of platelets in circulating blood, resulting in the potential for increased bleeding and decreased ability for clotting.<ref>PMID:8528199</ref><ref>PMID:10447259</ref><ref>PMID:7795648</ref><ref>PMID:11167787</ref><ref>PMID:11877312</ref> Defects in WAS are a cause of neutropenia severe congenital X-linked (XLN) [MIM:[http://omim.org/entry/300299 300299]]. XLN is an immunodeficiency syndrome characterized by recurrent major bacterial infections, severe congenital neutropenia, and monocytopenia.<ref>PMID:11242115</ref>

~~{{ABSTRACT_PUBMED_10360578}}~~

==Function==

[[http://www.uniprot.org/uniprot/CDC42_HUMAN CDC42_HUMAN]] Plasma membrane-associated small GTPase which cycles between an active GTP-bound and an inactive GDP-bound state. In active state binds to a variety of effector proteins to regulate cellular responses. Involved in epithelial cell polarization processes. Regulates the bipolar attachment of spindle microtubules to kinetochores before chromosome congression in metaphase. Plays a role in the extension and maintenance of the formation of thin, actin-rich surface projections called filopodia. Mediates CDC42-dependent cell migration.<ref>PMID:14978216</ref><ref>PMID:15642749</ref><ref>PMID:17038317</ref> [[http://www.uniprot.org/uniprot/WASP_HUMAN WASP_HUMAN]] Effector protein for Rho-type GTPases. Regulates actin filament reorganization via its interaction with the Arp2/3 complex. Important for efficient actin polymerization. Possible regulator of lymphocyte and platelet function. Mediates actin filament reorganization and the formation of actin pedestals upon infection by pathogenic bacteria.<ref>PMID:12235133</ref><ref>PMID:16275905</ref><ref>PMID:18650809</ref>

==About this Structure==

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==Reference==

[[Category: Homo sapiens]]

[[Category: Abdul-Manan, N.]]

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@@ Line 1: / Line 1: @@
-[[Image:1cee.png|left|200px]]
 {{STRUCTURE_1cee|  PDB=1cee  |  SCENE=  }}
+===SOLUTION STRUCTURE OF CDC42 IN COMPLEX WITH THE GTPASE BINDING DOMAIN OF WASP===
+{{ABSTRACT_PUBMED_10360578}}
-===SOLUTION STRUCTURE OF CDC42 IN COMPLEX WITH THE GTPASE BINDING DOMAIN OF WASP===
+==Disease==
+[[http://www.uniprot.org/uniprot/WASP_HUMAN WASP_HUMAN]] Defects in WAS are the cause of Wiskott-Aldrich syndrome (WAS) [MIM:[http://omim.org/entry/301000 301000]]; also known as eczema-thrombocytopenia-immunodeficiency syndrome. WAS is an X-linked recessive immunodeficiency characterized by eczema, thrombocytopenia, recurrent infections, and bloody diarrhea. Death usually occurs before age 10.<ref>PMID:7753869</ref><ref>PMID:8528198</ref><ref>PMID:8528199</ref><ref>PMID:8682510</ref><ref>PMID:9126958</ref><ref>PMID:9098856</ref><ref>PMID:9683546</ref><ref>PMID:9713366</ref><ref>PMID:9445409</ref><ref>PMID:10447259</ref><ref>PMID:11793485</ref>  Defects in WAS are the cause of thrombocytopenia type 1 (THC1) [MIM:[http://omim.org/entry/313900 313900]]. Thrombocytopenia is defined by a decrease in the number of platelets in circulating blood, resulting in the potential for increased bleeding and decreased ability for clotting.<ref>PMID:8528199</ref><ref>PMID:10447259</ref><ref>PMID:7795648</ref><ref>PMID:11167787</ref><ref>PMID:11877312</ref>  Defects in WAS are a cause of neutropenia severe congenital X-linked (XLN) [MIM:[http://omim.org/entry/300299 300299]]. XLN is an immunodeficiency syndrome characterized by recurrent major bacterial infections, severe congenital neutropenia, and monocytopenia.<ref>PMID:11242115</ref>
-{{ABSTRACT_PUBMED_10360578}}
+==Function==
+[[http://www.uniprot.org/uniprot/CDC42_HUMAN CDC42_HUMAN]] Plasma membrane-associated small GTPase which cycles between an active GTP-bound and an inactive GDP-bound state. In active state binds to a variety of effector proteins to regulate cellular responses. Involved in epithelial cell polarization processes. Regulates the bipolar attachment of spindle microtubules to kinetochores before chromosome congression in metaphase. Plays a role in the extension and maintenance of the formation of thin, actin-rich surface projections called filopodia. Mediates CDC42-dependent cell migration.<ref>PMID:14978216</ref><ref>PMID:15642749</ref><ref>PMID:17038317</ref> [[http://www.uniprot.org/uniprot/WASP_HUMAN WASP_HUMAN]] Effector protein for Rho-type GTPases. Regulates actin filament reorganization via its interaction with the Arp2/3 complex. Important for efficient actin polymerization. Possible regulator of lymphocyte and platelet function. Mediates actin filament reorganization and the formation of actin pedestals upon infection by pathogenic bacteria.<ref>PMID:12235133</ref><ref>PMID:16275905</ref><ref>PMID:18650809</ref>
 ==About this Structure==
@@ Line 11: / Line 13: @@
 ==Reference==
-<ref group="xtra">PMID:010360578</ref><references group="xtra"/>
+<ref group="xtra">PMID:010360578</ref><references group="xtra"/><references/>
 [[Category: Homo sapiens]]
 [[Category: Abdul-Manan, N.]]