Bibliografías temáticas / COQ4

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Literatura académica sobre el tema "COQ4"

Autor: Grafiati

Publicado: 10 de marzo de 2023

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Artículos de revistas sobre el tema "COQ4"

Yen, Hsiu-Chuan, Bing-Shian Chen, Si-Ling Yang, et al. "Levels of Coenzyme Q10 and Several COQ Proteins in Human Astrocytoma Tissues Are Inversely Correlated with Malignancy." Biomolecules 12, no. 2 (2022): 336. http://dx.doi.org/10.3390/biom12020336.

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In a previous study, we reported the alterations of primary antioxidant enzymes and decreased citrate synthase (CS) activities in different grades of human astrocytoma tissues. Here, we further investigated coenzyme Q10 (CoQ10) levels and protein levels of polyprenyl diphosphate synthase subunit (PDSS2) and several COQ proteins required for CoQ10 biosynthesis in these tissues. We found that the level of endogenous CoQ10, but not of exogenous α-tocopherol, was higher in nontumor controls than in all grades of astrocytoma tissues. The levels of COQ3, COQ5, COQ6, COQ7, COQ8A, and COQ9, but not of COQ4, were lower in Grade IV astrocytoma tissues than in controls or low-grade (Grades I and II) astrocytomas, but PDSS2 levels were higher in astrocytoma tissues than in controls. Correlation analysis revealed that the levels of CoQ10 and COQ proteins were negatively correlated with malignancy degree and positively correlated with CS activity, whereas PDSS2 level was positively correlated with malignancy. Moreover, lower level of mitochondrial DNA-encoded cytochrome c oxidase subunit 2 was not only associated with a higher malignancy degree but also with lower level of all COQ proteins detected. The results revealed that mitochondrial abnormalities are associated with impaired CoQ10 maintenance in human astrocytoma progression.

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Gomes, Fernando, Erich B. Tahara, Cleverson Busso, Alicia J. Kowaltowski, and Mario H. Barros. "nde1 deletion improves mitochondrial DNA maintenance in Saccharomyces cerevisiae coenzyme Q mutants." Biochemical Journal 449, no. 3 (2013): 595–603. http://dx.doi.org/10.1042/bj20121432.

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Saccharomyces cerevisiae has three distinct inner mitochondrial membrane NADH dehydrogenases mediating the transfer of electrons from NADH to CoQ (coenzyme Q): Nde1p, Nde2p and Ndi1p. The active site of Ndi1p faces the matrix side, whereas the enzymatic activities of Nde1p and Nde2p are restricted to the intermembrane space side, where they are responsible for cytosolic NADH oxidation. In the present study we genetically manipulated yeast strains in order to alter the redox state of CoQ and NADH dehydrogenases to evaluate the consequences on mtDNA (mitochondrial DNA) maintenance. Interestingly, nde1 deletion was protective for mtDNA in strains defective in CoQ function. Additionally, the absence of functional Nde1p promoted a decrease in the rate of H2O2 release in isolated mitochondria from different yeast strains. On the other hand, overexpression of the predominant NADH dehydrogenase NDE1 elevated the rate of mtDNA loss and was toxic to coq10 and coq4 mutants. Increased CoQ synthesis through COQ8 overexpression also demonstrated that there is a correlation between CoQ respiratory function and mtDNA loss: supraphysiological CoQ levels were protective against mtDNA loss in the presence of oxidative imbalance generated by Nde1p excess or exogenous H2O2. Altogether, our results indicate that impairment in the oxidation of cytosolic NADH by Nde1p is deleterious towards mitochondrial biogenesis due to an increase in reactive oxygen species release.

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Chen, Fengxiang, and Lei Yang. "The Transition Metal and Non-metal co-Doping Graphene for Oxygen Reduction Reaction Electrocatalysis: a Density Functional Theory Study." Bulletin of Science and Practice 7, no. 2 (2021): 197–207. http://dx.doi.org/10.33619/2414-2948/63/18.

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Proton exchange membrane fuel cells (PEMFCs) are vital energy-conversion devices in a hydrogen-fueled economic. In this study, we performed density functional theory (DFT) calculations to study 4e− oxygen reduction reaction process on transition metal embedded in single and double vacancies (SV and DV) in a graphene. We calculated bonding energy and adsorption energy on CoX3 (X = B, C, N, Si, P and S) and CoX4 (X = B, C, N, Si, P and S) embedded in graphene. Our DFT results indicate that formation of CoX3 is unfeasible and the formation of CoX4 is feasible. In addition, the crucial role of ligand atoms near embedded metal atoms is revealed via the molecular orbital theory. Then the Gibbs free energy of CoX4 are calculated and the CoN4, CoS4, and CoP4 are predicted to be active for catalyzing ORR, and these also show ligand atoms’ coordination effect for catalytic activity of central metal. Furthermore, we observed that they have identical rate-determining step (RDS). This work can provide some references for transition atoms catalytic doped in carbon materials.

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Finsterer, Josef, and Sinda Zarrouk-Mahjoub. "Mitochondrial cardioencephalopathy due to a COQ4 mutation." Molecular Genetics and Metabolism Reports 13 (December 2017): 7–8. http://dx.doi.org/10.1016/j.ymgmr.2017.07.003.

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Marbois, Beth, Peter Gin, Kym F. Faull, et al. "Coq3 and Coq4 Define a Polypeptide Complex in Yeast Mitochondria for the Biosynthesis of Coenzyme Q." Journal of Biological Chemistry 280, no. 21 (2005): 20231–38. http://dx.doi.org/10.1074/jbc.m501315200.

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Wang, Sining, Akash Jain, Noelle Alexa Novales, Audrey N. Nashner, Fiona Tran, and Catherine F. Clarke. "Predicting and Understanding the Pathology of Single Nucleotide Variants in Human COQ Genes." Antioxidants 11, no. 12 (2022): 2308. http://dx.doi.org/10.3390/antiox11122308.

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Coenzyme Q (CoQ) is a vital lipid that functions as an electron carrier in the mitochondrial electron transport chain and as a membrane-soluble antioxidant. Deficiencies in CoQ lead to metabolic diseases with a wide range of clinical manifestations. There are currently few treatments that can slow or stop disease progression. Primary CoQ10 deficiency can arise from mutations in any of the COQ genes responsible for CoQ biosynthesis. While many mutations in these genes have been identified, the clinical significance of most of them remains unclear. Here we analyzed the structural and functional impact of 429 human missense single nucleotide variants (SNVs) that give rise to amino acid substitutions in the conserved and functional regions of human genes encoding a high molecular weight complex known as the CoQ synthome (or Complex Q), consisting of the COQ3–COQ7 and COQ9 gene products. Using structures of COQ polypeptides, close homologs, and AlphaFold models, we identified 115 SNVs that are potentially pathogenic. Further biochemical characterizations in model organisms such as Saccharomyces cerevisiae are required to validate the pathogenicity of the identified SNVs. Collectively, our results will provide a resource for clinicians during patient diagnosis and guide therapeutic efforts toward combating primary CoQ10 deficiency.

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Basselin, Mireille, Shannon M. Hunt, Hiam Abdala-Valencia, and Edna S. Kaneshiro. "Ubiquinone Synthesis in Mitochondrial and Microsomal Subcellular Fractions of Pneumocystis spp.: Differential Sensitivities to Atovaquone." Eukaryotic Cell 4, no. 8 (2005): 1483–92. http://dx.doi.org/10.1128/ec.4.8.1483-1492.2005.

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ABSTRACT The lung pathogen Pneumocystis spp. is the causative agent of a type of pneumonia that can be fatal in people with defective immune systems, such as AIDS patients. Atovaquone, an analog of ubiquinone (coenzyme Q [CoQ]), inhibits mitochondrial electron transport and is effective in clearing mild to moderate cases of the infection. Purified rat-derived intact Pneumocystis carinii cells synthesize de novo four CoQ homologs, CoQ7, CoQ8, CoQ9, and CoQ10, as demonstrated by the incorporation of radiolabeled precursors of both the benzoquinone ring and the polyprenyl chain. A central step in CoQ biosynthesis is the condensation of p-hydroxybenzoic acid (PHBA) with a long-chain polyprenyl diphosphate molecule. In the present study, CoQ biosynthesis was evaluated by the incorporation of PHBA into completed CoQ molecules using P. carinii cell-free preparations. CoQ synthesis in whole-cell homogenates was not affected by the respiratory inhibitors antimycin A and dicyclohexylcarbodiimide but was diminished by atovaquone. Thus, atovaquone has inhibitory activity on both electron transport and CoQ synthesis in this pathogen. Furthermore, both the mitochondrial and microsomal fractions were shown to synthesize de novo all four P. carinii CoQ homologs. Interestingly, atovaquone inhibited microsomal CoQ synthesis, whereas it had no effect on mitochondrial CoQ synthesis. This is the first pathogenic eukaryotic microorganism in which biosynthesis of CoQ molecules from the initial PHBA:polyprenyl transferase reaction has been unambiguously shown to occur in two distinct compartments of the same cell.

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Spinazzi, Marco, Enrico Radaelli, Katrien Horré, et al. "PARL deficiency in mouse causes Complex III defects, coenzyme Q depletion, and Leigh-like syndrome." Proceedings of the National Academy of Sciences 116, no. 1 (2018): 277–86. http://dx.doi.org/10.1073/pnas.1811938116.

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The mitochondrial intramembrane rhomboid protease PARL has been implicated in diverse functions in vitro, but its physiological role in vivo remains unclear. Here we show that Parl ablation in mouse causes a necrotizing encephalomyelopathy similar to Leigh syndrome, a mitochondrial disease characterized by disrupted energy production. Mice with conditional PARL deficiency in the nervous system, but not in muscle, develop a similar phenotype as germline Parl KOs, demonstrating the vital role of PARL in neurological homeostasis. Genetic modification of two major PARL substrates, PINK1 and PGAM5, do not modify this severe neurological phenotype. Parl−/− brain mitochondria are affected by progressive ultrastructural changes and by defects in Complex III (CIII) activity, coenzyme Q (CoQ) biosynthesis, and mitochondrial calcium metabolism. PARL is necessary for the stable expression of TTC19, which is required for CIII activity, and of COQ4, which is essential in CoQ biosynthesis. Thus, PARL plays a previously overlooked constitutive role in the maintenance of the respiratory chain in the nervous system, and its deficiency causes progressive mitochondrial dysfunction and structural abnormalities leading to neuronal necrosis and Leigh-like syndrome.

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Sondheimer, Neal, Stacy Hewson, Jessie M. Cameron, et al. "Novel recessive mutations in COQ4 cause severe infantile cardiomyopathy and encephalopathy associated with CoQ 10 deficiency." Molecular Genetics and Metabolism Reports 12 (September 2017): 23–27. http://dx.doi.org/10.1016/j.ymgmr.2017.05.001.

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Caglayan, Ahmet Okay, Hakan Gumus, Erin Sandford, et al. "COQ4 Mutation Leads to Childhood-Onset Ataxia Improved by CoQ10 Administration." Cerebellum 18, no. 3 (2019): 665–69. http://dx.doi.org/10.1007/s12311-019-01011-x.

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