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Cytochrome c was upregulated in the primary Sjogren's syndrome patients, indicating the potential role of cytochrome c in the pathogenesis and development of primary Sjogren's syndrome.
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The caspase-8/Bid/cytochrome c axis links signals from death receptors to mitochondrial reactive oxygen species production.
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This work reveals a direct conformational link between the 40-57 Omega-loop of cytochrome c in which residue 41 resides and the dynamical properties of the axial ligand to the heme iron.
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The naturally occurring Y48H variant of cytochrome c in its oxidized heme state is more peroxidatic than either the Wild Type protein or the G41S variant that is also implicated in thrombocytopenia.
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ROCK activation phosphorylated Rac1b at Ser71 and increased reactive oxygen species (ROS) levels by facilitating the interaction between Rac1b and cytochrome c. Conversely, ROCK inactivation abolished their interaction, concomitant with ROS reduction.
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Data suggest that although HCCS mediates heme attachment to N-terminal cysteine in heme-attachment site (CXXXH) of cytochrome C variants, up to 50% of cytochrome C produced is modified in an oxygen-dependent manner, resulting in a mixed population of cytochrome c. [HCCS = holocytochrome c synthase]
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Data suggest that the stronger effect of K72A mutation on the peroxidase activity of human versus yeast cytochrome c results from relief of steric interactions between side chains at positions 72 and 81 (Ile in human vs Ala in yeast), which suppresses the dynamics of omega-loop D necessary for the intrinsic peroxidase activity of cytochrome c.
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These findings establish a framework for understanding the molecular basis of cytochrome c-mediated blocking of SET/TAF-Ibeta.
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Monitoring of serum cytochrome c might also serve as a sensitive apoptotic marker in vivo reflecting chemotherapy-induced cell death burden in patients with non-small cell lung cancer.
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G-Rh2 causes rapid and dramatic translocation of both Bak and Bax, which subsequently triggers mitochondrial cytochrome c release and consequent caspase activation.
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The mitochondrial metalloprotease OMA1 was activated in a Bax- and Bak-dependent fashion.
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In vitro ultrastructural changes of MCF-7 for metastasise bone cancer and induction of apoptosis via mitochondrial cytochrome C released by CaCO3/Dox nanocrystals
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a mechanism of multiple radical formations in the cytochrome c-phospholipid complexes under H2O2 treatment, consistent with the stabilization of the radical in the G41S mutant, which elicits a greater peroxidase activity from cytochrome c
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proposed that mutation of residue 41, and interaction with cardiolipin, increase peroxidase activity by altering the 40-57 Omega loop and its hydrogen bond network with the propionate of haem ring A; these changes enhance access of hydrogen peroxide and substrate to the haem
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Data indicate a novel missense mutation (Y48H) of the cytochrome c (CYCS) gene responsible for thrombocytopenia.
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results suggest the impact of residue 41 on the conformation of cytochrome c influences its ability to act in both of its physiological roles, electron transport and caspase activation
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structural characterization of cytochrome c in micelle
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Data indicate that the formation of cytochrome c-Apaf-1 apoptosome and the presence of Smac are absolutely required for PSAP-induced apoptosis.
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Spectroscopic analyses of HCCS alone and complexes of HCCS with site-directed variants of cytochrome c revealed the fundamental steps of heme attachment and maturation.
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The levels of cellular apoptosis-associated proteins such as Smac/DIABLO, Cyto C, and the activated fragment of caspase-3 increased in pancreatic cancer cells, but the expression of XIAP was significantly decreased after 24 h treatment with the combination of TRAIL and gemcitabine.
