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Hematopoietic Cell Regulation by Rac1 and Rac2 Guanosine Triphosphatases
Abstract
The Rho guanosine triphosphatases (GTPases) Rac1 and Rac2 are critical signaling regulators in mammalian cells. The deletion of both Rac1 and Rac2 murine alleles leads to a massive egress of hematopoietic stem/progenitor cells (HSC/Ps) into the blood from the marrow, whereas Rac1 –/– but not Rac2 –/– HSC/Ps fail to engraft in the bone marrow of irradiated recipient mice. In contrast, Rac2, but not Rac1, regulates superoxide production and directed migration in neutrophils, and in each cell type, the two GTPases play distinct roles in actin organization, cell survival, and proliferation. Thus, Rac1 and Rac2 regulate unique aspects of hematopoietic development and function.
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In the citing paper
“The Rac subfamily of Rho guanosine triphosphatases (GTPases) plays an essential role in regulating normal hematopoiesis (1).”
From Rac guanosine triphosphatases represent a potential target in AML (2008) · cites this paper as [1]
In the citing paper
“In hematopoietic cells, Rac proteins integrate signals from growth factor, chemokine, and adhesion receptors to mediate a variety of cellular responses, including cell growth and survival, gene transcription, adhesion, motility, and formation of the actin cytoskeleton (1).”
From Rac guanosine triphosphatases represent a potential target in AML (2008) · cites this paper as [1]
In the citing paper
“Rac subfamily members, Rac1 and Rac2, are essential for cortical filamentous-actin (F-actin) assembly and chemotaxis in hematopoietic stem/progenitor cells.4,5”
From Cross-talk between RhoH and Rac1 in regulation of actin cytoskeleton and chemotaxis of hematopoietic progenitor cells (2008) · cites this paper as [5]
In the citing paper
“Loss of Rac1 and Rac2 alleles leads to defective engraftment and massive mobilization of hematopoietic progenitor cells (HPCs), which is associated with loss of adhesion, chemotaxis, and cortical F-actin polymerization.5”
From Cross-talk between RhoH and Rac1 in regulation of actin cytoskeleton and chemotaxis of hematopoietic progenitor cells (2008) · cites this paper as [5]
In the citing paper
“Loss of Rac1 and Rac2 alleles leads to defective engraftment and massive mobilization of hematopoietic progenitor cells (HPCs), which is associated with loss of adhesion, chemotaxis, and cortical F-actin polymerization.5”
From Cross-talk between RhoH and Rac1 in regulation of actin cytoskeleton and chemotaxis of hematopoietic progenitor cells (2008) · cites this paper as [5]
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References 25 · Cited by 510
Research works printed but not linked: 3
- J. Moll, G. Sansig, E. Fattori, H. van der Putten, Oncogene6, 863 (1991).
- N. V. Shirsat, R. J. Pignolo, B. L. Kreider, G. Rovera, Oncogene5, 769 (1990).
- T. M. Dexter, T. D. Allen, L. G. Lajtha, J. Cell. Physiol.91, 335 (1976).
Metadata
- Authors
- Gu, Y., Filippi, M.-D., Cancelas, J. A., Siefring, J. E., Williams, E. P., Jasti, A. C., Harris, C. E., Lee, A. W., Prabhakar, R., Atkinson, S. J., Kwiatkowski, D. J., & Williams, D. A.
- Affiliations
- Brigham and Women's Hospital (US)
- Division of Experimental Hematology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229, USA.
- Corresponding author
- Gu, Yi
- Filippi, Marie-Dominique
- Williams, David A.
- ORCID
- Venue
- Science
- Published
- 2003-10-17
- Volume
- 302
- Issue
- 5644
- Pages
- 445-449
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- OpenAlex
- W2164396922
- Semantic Scholar
- 2db2d3f74540fdf8cc400a7b89dd8e5ca99a54b4
- Cited by
- 510
- References
- 25
- Citations by year
- 2026: 2 · 2025: 7 · 2024: 4 · 2023: 8 · 2022: 7 · 2021: 1 · 2020: 9 · 2019: 12 · 2018: 19 · 2017: 18 · 2016: 18 · 2015: 23 · 2014: 26 · 2013: 27 · 2012: 28
- FWCI
- 11.69
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Science (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK062757)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
- Health Sciences › Medicine › Hematology › Hematopoietic Stem Cell Transplantation
- Health Sciences › Medicine › Hematology › Acute Myeloid Leukemia Research
- Keywords
- Rac1, Rac2, Rho GTPases, hematopoietic stem cells, hematopoietic progenitor cells, engraftment, bone marrow, neutrophil superoxide production, neutrophil migration, actin organization, cell survival, cell proliferation, hematopoietic development
- MeSH terms
- RAC2 GTP-Binding Protein, Actins, Animals, Cell Adhesion, Cell Cycle, Cell Movement, Colony-Forming Units Assay, Fibronectins, Hematopoiesis, Hematopoietic Stem Cells, Neutrophils, Proto-Oncogene Proteins, Recombination, Genetic, Superoxides, Signal Transduction, Bone Marrow Transplantation, Mice, SCID, Mice, Inbred NOD, Apoptosis, Protein Serine-Threonine Kinases, Hematopoietic Stem Cell Transplantation, Stem Cell Factor, Hematopoietic Stem Cell Mobilization, Cyclin D1, rac GTP-Binding Proteins, rac1 GTP-Binding Protein, Mitogen-Activated Protein Kinases, Cell Size, Proto-Oncogene Proteins c-akt, Mice
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- This page
- CoChat. (2026). Citation check: Hematopoietic Cell Regulation by Rac1 and Rac2 Guanosine Triphosphatases. https://app.cochat.ai/papers/10.1126/science.1088485
- The paper
- Gu, Y., Filippi, M.-D., Cancelas, J. A., Siefring, J. E., Williams, E. P., Jasti, A. C., Harris, C. E., Lee, A. W., Prabhakar, R., Atkinson, S. J., Kwiatkowski, D. J., & Williams, D. A. (2003). Hematopoietic Cell Regulation by Rac1 and Rac2 Guanosine Triphosphatases. Science. https://doi.org/10.1126/science.1088485
