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- W2000009969 abstract "Depletion of mitochondrial DNA (mtDNA) or treatment with mitochondrial poison CCCP initiates mitochondrial stress signaling, which operates through altered Ca 2+ homeostasis . In C2C12 rhabdomyoblasts and A549 human lung carcinoma cells mitochondrial stress signaling activates calcineurin and a number of Ca 2+ responsive factors including ATF, NFAT , CEBP/δ and CREB. Additionally, PKC and MAP kinase are also activated. A number of nuclear gene targets including those involved in Ca 2+ storage/release (RyR1, calreticulin , calsequestrin), glucose metabolism (hexokinase, pyruvate kinase , Glut4), oncogenesis (TGFβ1, cathepsin L , IGFR1, melanoma antigen) and apoptosis (Bcl-2, Bid, Bad, p53) are upregulated. Mitochondrial stress in both C2C12 myoblasts and A549 cells induced morphological changes and invasive phenotypes. These cells also showed markedly increased resistance to etoposide-induced apoptosis that is a hallmark of highly invasive tumors. Our results describe a new mechanism of altered nuclear gene expression and phenotypic changes triggered by mitochondrial dysfunction and mtDNA damage." @default.
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- W2000009969 date "2005-07-01" @default.
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- W2000009969 title "Mitochondria-to-nucleus stress signaling in mammalian cells: Nature of nuclear gene targets, transcription regulation, and induced resistance to apoptosis" @default.
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- W2000009969 doi "https://doi.org/10.1016/j.gene.2005.03.028" @default.
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