Role of Cytochrome <i>c</i> in Apoptosis: Increased Sensitivity to Tumor Necrosis Factor Alpha Is Associated with Respiratory Defects but Not with Lack of Cytochrome <i>c</i> Release

Vempati, Uma D.; Díaz, Francisca; Barrientos, Antoni; Narisawa, Sonoko; Mian, A. Mohsin; Millán, José Luis; Boise, Lawrence H.; Moraes, Carlos T.

doi:10.1128/mcb.00287-06

Cited by 54 publications

(56 citation statements)

References 48 publications

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“…Caspase 8 can induce a loss of mitochondrial membrane potential, which promotes releasing of cytochrome-C (83,122). The cytochrome-C is important to trigger apoptosis process in the target cell by downstream activation of caspase 3 (83,128) (Figure 4).…”

Section: Fas-fasl Intercellular Linkage-mediated Pathwaymentioning

confidence: 99%

Cell Death Mechanisms Induced by Cytotoxic Lymphocytes

et al. 2009

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One of the functions of the immune system is to recognize and destroy abnormal or infected cells to maintain homeostasis. This is accomplished by cytotoxic lymphocytes. Cytotoxicity is a highly organized multifactor process. Here, we reviewed the apoptosis pathways induced by the two main cytotoxic lymphocyte subsets, natural killer (NK) cells and CD8 + T cells. In base to recent experimental evidence, we reviewed NK receptors involved in recognition of target-cell, as well as lytic molecules such as perforin, granzymes-A and -B, and granulysin. In addition, we reviewed the Fas-FasL intercellular linkage mediated pathway, and briefly the cross-linking of tumor necrosis factor (TNF) and TNF receptor pathway. We discussed three models of possible molecular interaction between lytic molecules from effector cytotoxic cells and target-cell membrane to induction of apoptosis. Cellular & Molecular Immunology. 2009;6(1):15-25.

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Section: Fas-fasl Intercellular Linkage-mediated Pathwaymentioning

confidence: 99%

Cell Death Mechanisms Induced by Cytotoxic Lymphocytes

et al. 2009

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“…Recently, Vempati et al (21) were able to produce a Cc knockout mutant in mouse fibroblasts. Intriguingly, this mutant was resistant to pro-apoptotic agents acting through both intrinsic and extrinsic pathways.…”

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confidence: 99%

Structural and Functional Analysis of Novel Human Cytochrome c Targets in Apoptosis

Martínez-Fábregas

Dı́az-Moreno

González‐Arzola

et al. 2014

Molecular & Cellular Proteomics

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Since the first description of apoptosis four decades ago, great efforts have been made to elucidate, both in vivo and in vitro, the molecular mechanisms involved in its regulation. Although the role of cytochrome c during apoptosis is well established, relatively little is known about its participation in signaling pathways in vivo due to its essential role during respiration. To obtain a better understanding of the role of cytochrome c in the onset of apoptosis, we used a proteomic approach based on affinity chromatography with cytochrome c as bait in this study. In this approach, novel cytochrome c interaction partners were identified whose in vivo interaction and cellular localization were facilitated through bimolecular fluorescence complementation. Modeling of the complex interface between cytochrome c and its counterparts indicated the involvement of the surface surrounding the heme crevice of cytochrome c, in agreement with the vast majority of known redox adducts of cytochrome c. However, in contrast to the high turnover rate of the mitochondrial cytochrome c redox adducts, those occurring under apoptosis led to the formation of stable nucleo-cytoplasmic ensembles, as inferred mainly from surface plasmon resonance and nuclear magnetic resonance measurements, which permitted us to corroborate the formation of such complexes in vitro. The results obtained suggest that human cytochrome c interacts with pro-survival, anti-apoptotic proteins following its release into the cytoplasm. Thus, cytochrome c may interfere with cell survival pathways and unlock apoptosis in order to prevent the spatial and temporal coexistence of antagonist signals. Molecular & Cellular

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“…14 Our analysis did not detect pathogenic mutations in this gene, even in the 15 patients who were analyzed by direct sequencing. COX18 mutations might be very rare or associated with other phenotypes than those that we studied.…”

Section: Resultsmentioning

confidence: 56%

Mutation analysis of COX18 in 29 patients with isolated cytochrome c oxidase deficiency

2009

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Isolated cytochrome c oxidase (COX) deficiency (MIM#220110) is a relatively common biochemical finding in pediatric patients with mitochondrial disorder. It has been associated with different clinical phenotypes ranging from isolated myopathy to severe multisystem disorder. It is a genetically heterogeneous trait, and the most frequent genetic defects affect SURF1 and SCO2, two genes required for COX assembly. However, a significant proportion of patients lacks mutation in these genes and in other known genes that require COX biogenesis. COX18 is a novel COX assembly gene required for membrane insertion of the Cterminal portion of COX subunit II. We have studied 29 pediatric patients with isolated COX deficiency in the skeletal muscle associated with different clinical phenotypes. Mutations in SURF1, SCO2, SCO1, COX10, COX15 and in mitochondrial DNA, had been ruled out earlier. The COX18 gene was analyzed using a PCR-single-stranded conformation polymorphism (PCR-SSCP) protocol, and in 15 patients, the analysis was repeated by direct sequencing. No pathogenic mutations were detected in our cohort of patients indicating that COX18 mutations may be very rare or associated with other phenotypes than isolated COX deficiency in infancy.

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Role of Cytochrome c in Apoptosis: Increased Sensitivity to Tumor Necrosis Factor Alpha Is Associated with Respiratory Defects but Not with Lack of Cytochrome c Release

Cited by 54 publications

References 48 publications

Cell Death Mechanisms Induced by Cytotoxic Lymphocytes

Cell Death Mechanisms Induced by Cytotoxic Lymphocytes

Structural and Functional Analysis of Novel Human Cytochrome c Targets in Apoptosis

Mutation analysis of COX18 in 29 patients with isolated cytochrome c oxidase deficiency

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