Rac GTPase interacts with GAPs and target proteins through multiple effector sites.
Open accessAbstract
Rac, a small GTPase in the ras superfamily, regulates at least two biological processes in animal cells: (i) the polymerization of actin and the assembly of integrin complexes to produce lamellipodia and ruffles; and (ii) the activity of an NADPH oxidase in phagocytic cells. NADPH oxidase activation is mediated through a rac effector protein, p67phox, and using chimeras made between rac and the closely related GTPase, rho, we have identified two distinct effector sites in rac, one N-terminal and one C-terminal, both of which are required for activation of p67phox. The same two effector sites are essential for rac-induced actin polymerization in fibroblasts. p65PAK, a ubiquitous serine/threonine kinase, interacts with rac at both the N- and C-terminal effector sites, but the GTPase-activating protein, bcr interacts with rac at a different region. This makes p65PAK, but not bcr, a candidate effector of rac-induced lamellipodium formation.
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Rac2 is only expressed in hematopoietic and endothelial cells, whereas Rac1 and Rac3 are ubiquitously expressed in mammalian systems.
“Rac2 is only expressed in hematopoietic and endothelial cells whereas Rac1 and Rac3 are ubiquitously expressed in mammalian systems [3], [4], [5].”
From Rac2 Controls Tumor Growth, Metastasis and M1-M2 Macrophage Differentiation In Vivo (2014) · cites this paper as [5]
The Introduction discusses rac activity in phagocytic cells, and the Methods identify a human rac1 construct, but neither passage describes where the Rac isoforms are expressed. Searches for Rac2, Rac3, and tissue distribution found no passage supporting the claimed restricted or ubiquitous expression patterns. Page numbers were not available in our copy. (LLM, conf=0.76)
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Activated Ras interacts with the Ral guanine nucleotide dissociation stimulator.
Hofer, F., Fields, S., Schneider, C., & Martin, G. S. (1994) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.91.23.11089 · Cited by 287 · see citing works
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Research works printed but not linked: 2
- Hofer,F., Fields,S., Schneider,C. and Martin,G.S. (1994) Proc. Natl Acad. Sci. USA, 91, 11089-11093.
- Ramer,S.W. and Davis,R.W. (1993) Proc. Natl Acad. Sci. USA, 90, 452-456.
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Roberts, A. W., Kim, C., Zhen, L., Lowe, J. B., Kapur, R., Petryniak, B., Spaetti, A., Pollock, J. D., Borneo, J. B., Bradford, G. B., et al. (1999) · Immunity · doi:10.1016/s1074-7613(00)80019-9 · Cited by 556 · see citing works
Rac2 Controls Tumor Growth, Metastasis and M1-M2 Macrophage Differentiation In Vivo
Joshi, S., Singh, A. R., Zulcic, M., Bao, L., Messer, K., Ideker, T., Dutkowski, J., & Durden, D. L. (2014) · PLoS ONE · doi:10.1371/journal.pone.0095893 · Cited by 128 · see citing works
“Rac2 is only expressed in hematopoietic and endothelial cells whereas Rac1 and Rac3 are ubiquitously expressed in mammalian systems [3,4,5].”
BackgroundAlbertinazzi, C., Gilardelli, D., Paris, S., Longhi, R., & de Curtis, I. (1998) · The Journal of Cell Biology · doi:10.1083/jcb.142.3.815 · Cited by 93 · see citing works
Bioinformatics analysis of microarray data to reveal the pathogenesis of brain ischemia
He, J., Gao, Y., Wu, G., Lei, X., Zhang, Y., Pan, W., & Yu, H. (2018) · Molecular Medicine Reports · doi:10.3892/mmr.2018.9000 · Cited by 11 · see citing works
- Authors
- Diekmann, D., Nobes, C. D., Burbelo, P. D., Abo, A., & Hall, A.
- Affiliations
- MRC Laboratory for Molecular Cell Biology (GB)
- Venue
- The EMBO Journal
- Published
- 1995-11-01
- Volume
- 14
- Issue
- 21
- Pages
- 5297-5305
- ISSN
- 0261-4189 (ISSN-L)
- 1460-2075
- PMC
- PMC394639
- OpenAlex
- W139895096
- Cited by
- 123
- References
- 1
- Citations by year
- 2025: 1 · 2024: 2 · 2023: 2 · 2021: 2 · 2019: 1 · 2018: 1 · 2017: 2 · 2015: 1 · 2014: 4 · 2013: 3 · 2012: 2
- FWCI
- 5.71
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- The EMBO Journal (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Wellcome Trust
- Medical Research Council
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Cellular transport and secretion
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Cellular Mechanics and Interactions
- Keywords
- Rac GTPase, GTPase-activating protein, p67phox, NADPH oxidase, BCR, actin polymerization, lamellipodia, Rho GTPases, chimeras, fibroblasts, cell motility
- MeSH terms
- Actins, Animals, Binding Sites, NADH, NADPH Oxidoreductases, Proteins, Recombinant Fusion Proteins, 3T3 Cells, Protein Serine-Threonine Kinases, GTP-Binding Proteins, NADPH Oxidases, GTPase-Activating Proteins, ras GTPase-Activating Proteins, rac GTP-Binding Proteins, Mice
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