ArticleMolecular and cellular biology2004
Involvement of Rho family GTPases in p19Arf- and p53-mediated proliferation of primary mouse embryonic fibroblasts.
Article in Molecular and cellular biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 58 citations in OpenAlex.
- RhoGDI in RBL-2H3 cells acts as a negative regulator of Rho GTPase signaling to inhibit granule exocytosis.Journal of leukocyte biology · 2024Article
- PI3K Functions Downstream of Cdc42 to Drive Cancer phenotypes in a Melanoma Cell Line.Small GTPases · 2023 · on this mapArticle
- Effect of TDP43-CTFs35 on Brain Endothelial Cell Functions in Cerebral Ischemic Injury.Molecular neurobiology · 2022Article
- Involvement of caveolin-1 in skin diseases.Frontiers in immunology · 2022Review
- RhoA and Cdc42 in T cells: Are they targetable for T cell-mediated inflammatory diseases?Precision clinical medicine · 2021Article
- Graded RhoA GTPase Expression in Treg Cells Distinguishes Tumor Immunity From Autoimmunity.Frontiers in immunology · 2021Article
- Paracrine signalling of AGR2 stimulates RhoA function in fibroblasts and modulates cell elongation and migration.Cell adhesion & migration · 2019Article
- Expression of Rho Guanine Nucleotide Exchange Factor 39 (ARHGEF39) and Its Prognostic Significance in Hepatocellular Carcinoma.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
- Reduced Cell Division Control Protein 42 Activity Compromises Hematopoiesis-Supportive Function of Fanconi Anemia Mesenchymal Stromal Cells.Stem cells (Dayton, Ohio) · 2018Article
- YAP/TAZ-CDC42 signaling regulates vascular tip cell migration.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
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- RhoA orchestrates glycolysis for TH2 cell differentiation and allergic airway inflammation.The Journal of allergy and clinical immunology · 2016Article
- Activation of Dopamine D1 Receptors Regulates Dendritic Morphogenesis Through Rac1 and RhoA in Prefrontal Cortex Neurons.Molecular neurobiology · 2015Article
- Cell-Substrate Interactions Feedback to Direct Cell Migration along or against Morphological Polarization.PloS one · 2015Article
- Gene targeting RhoA reveals its essential role in coordinating mitochondrial function and thymocyte development.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
- Rho GTPases modulate malignant transformation of tumor cells.Small GTPases · 2014Review
- Luteolin inhibits migration of human glioblastoma U-87 MG and T98G cells through downregulation of Cdc42 expression and PI3K/AKT activity.Molecular biology reports · 2013Article
- Article
- BART inhibits pancreatic cancer cell invasion by Rac1 inactivation through direct binding to active Rac1.Neoplasia (New York, N.Y.) · 2012Article
- Article
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
The Rho family GTPases Rac1, RhoA, and Cdc42 function as molecular switches that transduce intracellular signals regulating gene expression and cell proliferation as well as cell migration. p19(Arf) and p53, on the other hand, are tumor suppressors that act both independently and sequentially to regulate cell proliferation. To investigate the functional interaction and cooperativeness of Rho GTPases with the p19(Arf)-p53 pathway, we examined the contribution of Rho GTPases to the gene transcription and cell proliferation unleashed by deletion of p19Arf or p53 in primary mouse embryo fibroblasts. We found that (i) p19(Arf) or p53 deficiency led to a significant increase in PI 3-kinase activity, which in turn upregulated RhoA and Rac1 activities; (ii) deletion of p19Arf or p53 led to an increase in cell growth rate that was in part dependent on RhoA, Rac1, and Cdc42 activities; (iii) p19(Arf) or p53 deficiency caused an enhancement of the growth-related transcription factor NF-kappa B and cyclin D1 activities that are partly dependent on RhoA or Cdc42 but not on Rac1; (iv) forced expression of the activating mutants of Rac1, RhoA, or Cdc42 caused a hyperproliferative phenotype of the p19Arf(-/-) and p53(-/-) cells and promoted transformation of both cells; (v) RhoA appeared to contribute to p53-regulated cell proliferation by modulating cell cycle machinery, while hyperactivation of RhoA further suppressed a p53-independent apoptotic signal; and (vi) multiple pathways regulated by RhoA, including that of Rho-kinase, were required for RhoA to fully promote the transformation of p53(-/-) cells. Taken together, these results provide strong evidence indicating that signals through the Rho family GTPases can both contribute to cell growth regulation by p19Arf and p53 and cooperate with p19Arf or p53 deficiency to promote primary cell transformation.
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