ArticleOncogene2010
F-actin-binding domain of c-Abl regulates localized phosphorylation of C3G: role of C3G in c-Abl-mediated cell death.
Article in Oncogene, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 44 citations in OpenAlex.
- Development and tissue specific expression of RAPGEF1 (C3G) transcripts having exons encoding disordered segments with predicted regulatory function.Molecular biology reports · 2024Article
- Crk proteins activate the Rap1 guanine nucleotide exchange factor C3G by segregated adaptor-dependent and -independent mechanisms.Cell communication and signaling : CCS · 2023Article
- Comparative genomics reveals molecular mechanisms underlying health and reproduction in cryptorchid mammals.BMC genomics · 2021Article
- Expression of a novel brain specific isoform of C3G is regulated during development.Scientific reports · 2020Article
- C3G contributes to platelet activation and aggregation by regulating major signaling pathways.Signal transduction and targeted therapy · 2020Article
- C3G, through its GEF activity, induces megakaryocytic differentiation and proplatelet formation.Cell communication and signaling : CCS · 2018Article
- Development and characterization of a novel monoclonal antibody that recognizes an epitope in the central protein interaction domain of RapGEF1 (C3G).Molecular biology reports · 2018Article
- C3G shows regulated nucleocytoplasmic exchange and represses histone modifications associated with euchromatin.Molecular biology of the cell · 2017Article
- Abelson kinase acts as a robust, multifunctional scaffold in regulating embryonic morphogenesis.Molecular biology of the cell · 2016Article
- Angiotensin II down-regulates nephrin-Akt signaling and induces podocyte injury: roleof c-Abl.Molecular biology of the cell · 2016Article
- C3G forms complexes with Bcr-Abl and p38α MAPK at the focal adhesions in chronic myeloid leukemia cells: implication in the regulation of leukemic cell adhesion.Cell communication and signaling : CCS · 2013Article
- Reciprocal Negative Regulation between the Guanine Nucleotide Exchange Factor C3G and β-Catenin.Genes & cancer · 2012Article
- Selective targeting of c-Abl via a cryptic mitochondrial targeting signal activated by cellular redox status in leukemic and breast cancer cells.Pharmaceutical research · 2012Article
- Regulation of adherens junction dynamics by phosphorylation switches.Journal of signal transduction · 2012Article
- Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The c-Abl tyrosine kinase maintains cellular homeostasis through its ability to regulate apoptosis and actin dynamics. In vivo, c-Abl activity is stringently regulated and mechanisms involved are not fully understood. Here, we identified the Rap1 guanine nucleotide exchange factor, C3G (RapGEF1), as a substrate and an effector of c-Abl-mediated functions. Ectopic expression of c-Abl in mammalian cell lines, known to induce apoptosis, resulted in phosphorylation of endogenous C3G on Y504 coincident with cell detachment and chromatin condensation. Phosphorylation of C3G coincided with restricted c-Abl activation in regions rich in actin, and was dependent on cellular F-actin dynamics. Unlike C3G or c-Abl, p-C3G was resistant to detergent extraction, suggesting its enhanced affinity for the cytoskeleton. Localized C3G phosphorylation and coincidence with cells undergoing cell death was dependent on F-actin-binding domain (FABD) of c-Abl. Activation of endogenous c-Abl by oxidative stress was associated with phosphorylation of cellular C3G on Y504. Inhibition of C3G expression and function using RNAi or dominant-negative approaches inhibited c-Abl-mediated cell death. These findings identify C3G as a novel target of c-Abl and also show that FABD of c-Abl is essential for regulation of its restricted activation to induce apoptosis.
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