"rac1 GTP-Binding Protein" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus,
MeSH (Medical Subject Headings). Descriptors are arranged in a hierarchical structure,
which enables searching at various levels of specificity.
A rac GTP-binding protein involved in regulating actin filaments at the plasma membrane. It controls the development of filopodia and lamellipodia in cells and thereby influences cellular motility and adhesion. It is also involved in activation of NADPH OXIDASES. This enzyme was formerly listed as EC 3.6.1.47.
| Descriptor ID |
D020830
|
| MeSH Number(s) |
D08.811.277.040.330.300.400.700.100.500 D12.644.360.525.700.100.100 D12.776.157.325.515.700.100.100 D12.776.476.525.700.100.100
|
| Concept/Terms |
rac1 GTP-Binding Protein- rac1 GTP-Binding Protein
- GTP-Binding Protein, rac1
- rac1 GTP Binding Protein
- rac1 Protein
- TC-25 GTP-Binding Protein
- GTP-Binding Protein, TC-25
- TC 25 GTP Binding Protein
- ras-Related C3 Botulinum Toxin Substrate 1
- ras Related C3 Botulinum Toxin Substrate 1
|
Below are MeSH descriptors whose meaning is more general than "rac1 GTP-Binding Protein".
Below are MeSH descriptors whose meaning is more specific than "rac1 GTP-Binding Protein".
This graph shows the total number of publications written about "rac1 GTP-Binding Protein" by people in this website by year, and whether "rac1 GTP-Binding Protein" was a major or minor topic of these publications.
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click here.
| Year | Major Topic | Minor Topic | Total |
|---|
| 2003 | 0 | 1 | 1 |
| 2005 | 0 | 1 | 1 |
| 2008 | 1 | 0 | 1 |
| 2009 | 1 | 0 | 1 |
| 2010 | 0 | 1 | 1 |
| 2013 | 1 | 0 | 1 |
| 2014 | 1 | 0 | 1 |
| 2016 | 1 | 0 | 1 |
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Below are the most recent publications written about "rac1 GTP-Binding Protein" by people in Profiles.
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Rac1-mediated cytoskeleton rearrangements induced by intersectin-1s deficiency promotes lung cancer cell proliferation, migration and metastasis. Mol Cancer. 2016 09 14; 15(1):59.
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A sequence variant in human KALRN impairs protein function and coincides with reduced cortical thickness. Nat Commun. 2014 Sep 16; 5:4858.
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Sphingomyelinase-like phosphodiesterase 3b expression levels determine podocyte injury phenotypes in glomerular disease. J Am Soc Nephrol. 2015 Jan; 26(1):133-47.
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Conditional deletion of FAK in mice endothelium disrupts lung vascular barrier function due to destabilization of RhoA and Rac1 activities. Am J Physiol Lung Cell Mol Physiol. 2013 Aug 15; 305(4):L291-300.
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Negative regulation of EGFR-Vav2 signaling axis by Cbl ubiquitin ligase controls EGF receptor-mediated epithelial cell adherens junction dynamics and cell migration. J Biol Chem. 2011 Jan 07; 286(1):620-33.
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Proteinuria: an enzymatic disease of the podocyte? Kidney Int. 2010 Apr; 77(7):571-80.
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Distinct roles for Rho versus Rac/Cdc42 GTPases downstream of Vav2 in regulating mammary epithelial acinar architecture. J Biol Chem. 2010 Jan 08; 285(2):1555-68.
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Tiam1 and Rac1 are required for platelet-activating factor-induced endothelial junctional disassembly and increase in vascular permeability. J Biol Chem. 2009 Feb 20; 284(8):5381-94.
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Use of a novel coinfection system reveals a role for Rac1, H-Ras, and CrkII phosphorylation in Helicobacter pylori-induced host cell actin cytoskeletal rearrangements. FEMS Immunol Med Microbiol. 2007 Jul; 50(2):190-205.
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Lysophosphatidylcholine increases endothelial permeability: role of PKCalpha and RhoA cross talk. Am J Physiol Lung Cell Mol Physiol. 2005 Aug; 289(2):L176-85.