The DOI matches its Crossref record.
Critical Roles for Rac1 and Rac2 GTPases in B Cell Development and Signaling
Abstract
The Rac1 guanosine triphosphatase (GTPase) has been implicated in multiple cellular functions, including actin dynamics, proliferation, apoptosis, adhesion, and migration resulting from signaling by multiple receptors, including the B cell antigen receptor (BCR). We used conditional gene targeting to generate mice with specific Rac1 deficiency in the B cell lineage. In the absence of both Rac1 and the highly related Rac2, B cell development was almost completely blocked. Both GTPases were required to transduce BCR signals leading to proliferation, survival and up-regulation of BAFF-R, a receptor for BAFF, a key survival molecule required for B cell development and maintenance.
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In the citing paper
“These 2 studies provide evidence for the requirement of Rac2 during T-and B-cell maturation.”
From Dominant activating RAC2 mutation with lymphopenia, immunodeficiency, and cytoskeletal defects (2019) · cites this paper as [39]
In the citing paper
“In Rac1/Rac2-deficient CD19 cells, bone marrow B-cell development appeared preserved across genotypes.”
From Dominant activating RAC2 mutation with lymphopenia, immunodeficiency, and cytoskeletal defects (2019) · cites this paper as [39]
In the citing paper
“This is apparent in Rac2 2/2 Rac1 flox/flox mice crossed with CD2-or CD19-driven Cre recombinase mice lacking both Rac1 and Rac2 in their T 38 or B cells, 39 respectively.”
From Dominant activating RAC2 mutation with lymphopenia, immunodeficiency, and cytoskeletal defects (2019) · cites this paper as [39]
In the citing paper
“However, Rac1/Rac2-deficient mice exhibited drastically reduced splenic and circulating mature B cells.”
From Dominant activating RAC2 mutation with lymphopenia, immunodeficiency, and cytoskeletal defects (2019) · cites this paper as [39]
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Research works printed but not linked: 25
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Dominant activating RAC2 mutation with lymphopenia, immunodeficiency, and cytoskeletal defects
Hsu, A. P., Donkó, A., Arrington, M. E., Swamydas, M., Fink, D., Das, A., Escobedo, O., Bonagura, V., Szabolcs, P., Steinberg, H. N., et al. (2019) · Blood · doi:10.1182/blood-2018-11-886028 · Cited by 92
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Piechulek, T., Rehlen, T., Walliser, C., Vatter, P., Moepps, B., & Gierschik, P. (2005) · Journal of Biological Chemistry · doi:10.1074/jbc.m509396200 · Cited by 80
Walliser, C., Retlich, M., Harris, R., Everett, K. L., Josephs, M. B., Vatter, P., Esposito, D., Driscoll, P. C., Katan, M., Gierschik, P., et al. (2008) · Journal of Biological Chemistry · doi:10.1074/jbc.m803316200 · Cited by 56
Metadata
- Authors
- Walmsley, M. J., Ooi, S. K. T., Reynolds, L. F., Smith, S. H., Ruf, S., Mathiot, A., Vanes, L., Williams, D. A., Cancro, M. P., & Tybulewicz, V. L. J.
- Affiliations
- Division of Immune Cell Biology, National Institute for Medical Research, The Ridgeway, Mill Hill, London, NW7 1AA, UK.
- Venue
- Science
- Published
- 2003-10-17
- Volume
- 302
- Issue
- 5644
- Pages
- 459-462
- ISSN
- 0036-8075
- 1095-9203
- Cited by
- 238
- References
- 0
- Language
- en
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