ArticleMolecular biology reports2014
β3-chimaerin, a novel member of the chimaerin Rac-GAP family.
Article in Molecular biology reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- β2-Chimaerin Deficiency Favors Polyp Growth in the Colon of ApcMolecules (Basel, Switzerland) · 2025Article
- Oncogenic and immunological roles of RACGAP1 in pan-cancer and its potential value in nasopharyngeal carcinoma.Apoptosis : an international journal on programmed cell death · 2024Article
- Article
- Plexin-Bs enhance their GAP activity with a novel activation switch loop generating a cooperative enzyme.Cellular and molecular life sciences : CMLS · 2021Article
- Identification of a truncated β1-chimaerin variant that inactivates nuclear Rac1.The Journal of biological chemistry · 2020Article
- Regulators of Rho GTPases in the Nervous System: Molecular Implication in Axon Guidance and Neurological Disorders.International journal of molecular sciences · 2019Review
- Protein kinase C in cancer: The top five unanswered questions.Molecular carcinogenesis · 2017Review
- A new role of the Rac-GAP β2-chimaerin in cell adhesion reveals opposite functions in breast cancer initiation and tumor progression.Oncotarget · 2016Article
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Authors and funding
6 authors.
Funding
Abstract
Chimaerins are a family of diacylglycerol- and phorbol ester-regulated GTPase activating proteins (GAPs) for the small G-protein Rac. Extensive evidence indicates that these proteins play important roles in development, axon guidance, metabolism, cell motility, and T cell activation. Four isoforms have been reported to-date, which are products of CHN1 (α1- and α2-chimaerins) and CHN2 (β1- and β2-chimaerins) genes. Although these gene products are assumed to be generated by alternative splicing, bioinformatics analysis of the CHN2 gene revealed that β1- and β2-chimaerins are the products of alternative transcription start sites (TSSs) in different promoter regions. Furthermore, we found an additional TSS in CHN2 gene that leads to a novel product, which we named β3-chimaerin. Expression profile analysis revealed predominantly low levels for the β3-chimaerin transcript, with higher expression levels in epididymis, plasma blood leucocytes, spleen, thymus, as well as various areas of the brain. In addition to the prototypical SH2, C1, and Rac-GAP domains, β3-chimaerin has a unique N-terminal domain. Studies in cells established that β3-chimaerin has Rac-GAP activity and is responsive to phorbol esters. The enhanced responsiveness of β3-chimaerin for phorbol ester-induced translocation relative to β2-chimaerin suggests differential ligand accessibility to the C1 domain.
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