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Relevant bibliographies by topics / COQ4

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Journal articles

Academic literature on the topic 'COQ4'

Author: Grafiati

Published: 10 March 2023

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Journal articles on the topic "COQ4"

1

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

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2

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

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3

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 lig

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4

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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5

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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6

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

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7

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

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8

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,

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9

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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10

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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