Journal
ONCOGENE
Volume 33, Issue 31, Pages 4021-4035Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/onc.2013.362
Keywords
Rac1; RhoA; Cdc42; guanine nucleotide exchange factors; cancer; mouse models
Funding
- NIH
- AACR/Pancreatic Cancer Action Network
- Lustgarten Pancreatic Cancer Foundation
- [CA71341]
- [CA159821]
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The aberrant activity of Ras homologous (Rho) family small GTPases (20 human members) has been implicated in cancer and other human diseases. However, in contrast to the direct mutational activation of Ras found in cancer and developmental disorders, Rho GTPases are activated most commonly in disease by indirect mechanisms. One prevalent mechanism involves aberrant Rho activation via the deregulated expression and/or activity of Rho family guanine nucleotide exchange factors (RhoGEFs). RhoGEFs promote formation of the active GTP-bound state of Rho GTPases. The largest family of RhoGEFs is comprised of the Dbl family RhoGEFs with 70 human members. The multitude of RhoGEFs that activate a single Rho GTPase reflects the very specific role of each RhoGEF in controlling distinct signaling mechanisms involved in Rho activation. In this review, we summarize the role of Dbl RhoGEFs in development and disease, with a focus on Ect2 (epithelial cell transforming squence 2), Tiam1 (T-cell lymphoma invasion and metastasis 1), Vav and P-Rex1/2 (PtdIns(3,4,5) P3 (phosphatidylinositol (3,4,5)-triphosphate)-dependent Rac exchanger).
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