ArticleOncogene2003
Differential interaction and activation of Rho family GTPases by p210bcr-abl and p190bcr-abl.
Article in Oncogene, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 69 citations in OpenAlex.
- Article
- The differential role of the lipid raft-associated protein flotillin 2 for progression of myeloid leukemia.Blood advances · 2022Article
- Article
- Characterization of p190-Bcr-Abl chronic myeloid leukemia reveals specific signaling pathways and therapeutic targets.Leukemia · 2021Article
- Article
- Structural and functional dissection of the DH and PH domains of oncogenic Bcr-Abl tyrosine kinase.Nature communications · 2017Article
- Differential signaling through p190 and p210 BCR-ABL fusion proteins revealed by interactome and phosphoproteome analysis.Leukemia · 2017Article
- Genetic analysis of Ikaros target genes and tumor suppressor function in BCR-ABL1The Journal of experimental medicine · 2017Article
- The Philadelphia chromosome in leukemogenesis.Chinese journal of cancer · 2016Review
- Article
- Homoharringtonine contributes to imatinib sensitivity by blocking the EphB4/RhoA pathway in chronic myeloid leukemia cell lines.Medical oncology (Northwood, London, England) · 2014Article
- Vav family exchange factors: an integrated regulatory and functional view.Small GTPases · 2014Review
- Rho GTPases modulate malignant transformation of tumor cells.Small GTPases · 2014Review
- Article
- Vav3 collaborates with p190-BCR-ABL in lymphoid progenitor leukemogenesis, proliferation, and survival.Blood · 2012Article
- Article
- p185(BCR/ABL) has a lower sensitivity than p210(BCR/ABL) to the allosteric inhibitor GNF-2 in Philadelphia chromosome-positive acute lymphatic leukemia.Haematologica · 2012Article
- Article
- The diverse roles of Rac signaling in tumorigenesis.Cell cycle (Georgetown, Tex.) · 2011Review
- Tyrosine residues at the carboxyl terminus of Vav1 play an important role in regulation of its biological activity.The Journal of biological chemistry · 2010Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The p210(bcr-abl) and p190(bcr-abl) fusion proteins, respectively responsible for chronic myelogenous leukemia and acute lymphoblastic leukemia, present deregulated tyrosine kinase activity and abnormal localization. The Dbl homology domain of Bcr, activating Rho GTPases, is present in p210(bcr-abl), but absent in p190(bcr-abl). We investigated the interaction of Bcr-Abl chimeras and Rho proteins by coimmunoprecipitation, pull-down experiments and GEF activity measurement. RhoA, Rac1 and Cdc42 interact in vivo with p210(bcr-abl) only. Moreover, the three types of GTPases are activated in vitro and in vivo by p210(bcr-abl). Nevertheless, Rac1 and Cdc42, but not RhoA, are activated by p190(bcr-abl) in vitro and in vivo. Part of this GEF activity of p190(bcr-abl) is probably attributable to p95(vav), which is complexed with both p190(bcr-abl) and p210(bcr-abl) in an activated form. p160(bcr), also in complex with Bcr-Abl, presents no GEF activity in p190(bcr-abl)-expressing cells. These results suggest that differential activation of Rho proteins should play a major role in Bcr-Abl-induced leukemogenesis.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.