ArticleOncogene2003
CrkII induces serum response factor activation and cellular transformation through its function in Rho activation.
Article in Oncogene, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
8 citing papers in PubMed, 16 citations in OpenAlex.
- Review
- The adaptor protein CrkII regulates IGF-1-induced biological behaviors of pancreatic ductal adenocarcinoma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- Electroacupuncture inhibits apoptosis in annulus fibrosis cells through suppression of the mitochondria-dependent pathway in a rat model of cervical intervertebral disc degradation.Genetics and molecular biology · 2012Article
- Crk adaptor proteins act as key signaling integrators for breast tumorigenesis.Breast cancer research : BCR · 2012Article
- Proteins that bind the Src homology 3 domain of CrkI have distinct roles in Crk transformation.Oncogene · 2010Article
- CrkII transgene induces atypical mammary gland development and tumorigenesis.The American journal of pathology · 2010Article
- Involvement of adaptor protein Crk in malignant feature of human ovarian cancer cell line MCAS.Oncogene · 2006Article
- CrkII regulates focal adhesion kinase activation by making a complex with Crk-associated substrate, p130Cas.Proceedings of the National Academy of Sciences of the United States of America · 2004Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
CrkII belongs to the adaptor protein family that plays a crucial role in signal transduction. In order to better understand the biological functions of CrkII, we focused on the regulation of gene expression by CrkII. Various transcriptional control elements were examined for their activation by CrkII-expression, and we found that CrkII selectively activates the serum response element (SRE), a transcriptional control element of immediate-early genes. This SRE activation induced by CrkII-overexpression was mediated by the serum response factor (SRF) via Rho. Indeed, we confirmed that the amount of activated Rho was increased in the CrkII-expressing cells. Moreover, we showed that when overexpressed, CrkII induces the cellular transformation of NIH 3T3 cells and that a dominant negative mutant of Rho suppresses this transformation, strongly suggesting that activation of Rho is essential for the transforming activity by CrkII. Furthermore, we also found that CrkII and Galpha12, a member of the heterotrimeric G proteins, synergistically activates Rho as well as the SRF, and that an SH3 mutant of CrkII can inhibit the Galpha12-induced activation of SRF. These results strongly suggest that CrkII is involved in the activation of Rho and SRF by Galpha12. Our study provides strong evidence that Rho activation plays a crucial role in CrkII-mediated signals to induce gene expression and cellular transformation.
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Registered trials
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.