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- W2155133898 abstract "The GTPase Ras is a molecular switch engaged downstream of G-protein coupled receptors and receptor tyrosine kinases that controls multiple cell fate-determining signalling pathways. Ras signalling is frequently deregulated in cancer underlying associated changes in cell phenotype. Although Ca2+ signalling pathways control some overlapping functions with Ras, and altered Ca2+ signalling pathways are emerging as important players in oncogenic transformation, how Ca2+ signalling is remodelled during transformation and whether it has a causal role remains unclear. We have investigated Ca2+ signalling in two human colorectal cancer cell lines and their isogenic derivatives in which the mutated K-Ras allele (G13D) has been deleted by homologous recombination. We show that agonist-induced Ca2+ release from intracellular stores is enhanced by loss of K-RasG13D through an increase in the ER store content and a modification of IP3R subtype abundance. Consistently, uptake of Ca2+ into mitochondria and sensitivity to apoptosis was enhanced as a result of K-RasG13D loss. These results suggest that suppression of Ca2+ signalling is a common response to naturally occurring levels of K-RasG13D that contributes to a survival advantage during oncogenic transformation." @default.
- W2155133898 created "2016-06-24" @default.
- W2155133898 creator A5004459131 @default.
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- W2155133898 date "2014-01-01" @default.
- W2155133898 modified "2023-09-24" @default.
- W2155133898 title "Oncogenic K-Ras suppresses IP3-dependent Ca2+ release through remodeling of IP3Rs isoform composition and ER luminal Ca2+ levels in colorectal cancer cell lines" @default.
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- W2155133898 doi "https://doi.org/10.1242/jcs.141408" @default.
- W2155133898 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/24522186" @default.
- W2155133898 hasPublicationYear "2014" @default.
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