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Michal Harel (talk | contribs) New page: <StructureSection load='2h7v' size='340' side='right' caption='Caption for this structure' scene=''> == Function == The small G-protein '''Rac''' or '''Ras-related C3 botulinum toxin sub... |
Michal Harel (talk | contribs) No edit summary |
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<StructureSection load='2h7v' size='340' side='right' caption='Human Rac1 (grey) complex with YpkA (pink) and GDP (PDB code [[2h7v]])' scene=''> | |||
<StructureSection load='2h7v' size='340' side='right' caption=' | |||
== Function == | == Function == | ||
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== Disease == | == Disease == | ||
Mutations in Rac2 are associated with neutrophil immunodeficiency syndrome. | Mutations in Rac2 are associated with neutrophil immunodeficiency syndrome. | ||
== Structural highlights == | == Structural highlights == | ||
The interactions between Rac1 and YpkA are via switch I and switch II of Rac1 and a helical portion of the protein kinase YpkA<ref>PMID:16959567</ref>. | |||
</StructureSection> | </StructureSection> | ||
Revision as of 14:16, 12 February 2017
FunctionThe small G-protein Rac or Ras-related C3 botulinum toxin substrate. Ras1 is involved in the regulation of cytoskeletal organization, cell adhesion, migration and morphological changes[1]. Ras3 binds to a variety of effector proteins to regulate cellular responses like cell spreading and the formation of actin-based protrusions. DiseaseMutations in Rac2 are associated with neutrophil immunodeficiency syndrome. Structural highlightsThe interactions between Rac1 and YpkA are via switch I and switch II of Rac1 and a helical portion of the protein kinase YpkA[2].
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3D structures of Rac3D structures of Rac
Updated on 12-February-2017
ReferencesReferences
- ↑ Asahara S, Shibutani Y, Teruyama K, Inoue HY, Kawada Y, Etoh H, Matsuda T, Kimura-Koyanagi M, Hashimoto N, Sakahara M, Fujimoto W, Takahashi H, Ueda S, Hosooka T, Satoh T, Inoue H, Matsumoto M, Aiba A, Kasuga M, Kido Y. Ras-related C3 botulinum toxin substrate 1 (RAC1) regulates glucose-stimulated insulin secretion via modulation of F-actin. Diabetologia. 2013 May;56(5):1088-97. doi: 10.1007/s00125-013-2849-5. Epub 2013, Feb 15. PMID:23412604 doi:http://dx.doi.org/10.1007/s00125-013-2849-5
- ↑ Prehna G, Ivanov MI, Bliska JB, Stebbins CE. Yersinia virulence depends on mimicry of host Rho-family nucleotide dissociation inhibitors. Cell. 2006 Sep 8;126(5):869-80. PMID:16959567 doi:10.1016/j.cell.2006.06.056