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1 tween complex II and complex III, presumably coenzyme Q.
2 tion of several substrates, such as heme and coenzyme Q.
3 oxidizes H(2)S while concomitantly reducing coenzyme Q.
4 and transferring the energy to mitochondrial coenzyme Q.
5 electron transport, including Vitamin K and Coenzyme Q.
6 which was accompanied by a lower content of coenzyme Q.
7 es electrons from acyl-CoA dehydrogenases to coenzyme Q.
8 diate, as well as the final product (13)C(6)-coenzyme Q.
11 ADH-ferricyanide reductase activity and NADH-coenzyme Q(0) reductase activity of plasma membranes and
24 functions as an oxidoreductase that reduces coenzyme Q(10) (CoQ) (also known as ubiquinone-10), whic
25 fying diseases displaying chronic low plasma Coenzyme Q(10) (CoQ) values may be important to prevent
27 study demonstrates that delivery of oxidized Coenzyme Q(10) (ubidecarenone) to increase mitochondrial
28 chondrial antioxidants alpha-lipoic acid and coenzyme Q(10) also suppresses Bak expression in the coc
33 ured skin fibroblasts from the patient had a coenzyme Q(10) biosynthetic rate of 11% of normal contro
36 c acid, a-tocopherol, all-trans-retinol, and coenzyme Q(10) in the tested samples was determined thro
37 id, alpha-tocopherol, all-trans-retinol, and coenzyme Q(10) in the tested samples was determined thro
41 n and a consequent increase in the levels of coenzyme Q(10), an endogenous lipophilic antioxidant.
42 SP1 is mediated by ubiquinone (also known as coenzyme Q(10), CoQ(10)): the reduced form, ubiquinol, t
43 ial in animal models of PD include creatine, coenzyme Q(10), Ginkgo biloba, nicotinamide, and acetyl-
45 toxicity was seen with the parent ubiquinone coenzyme Q(10.) Inhibition of cancer cell growth by Mito
48 he Caenorhabditis elegans clk-1 mutants lack coenzyme Q(9) and instead accumulate the biosynthetic in
49 s indicated that both codon reassignment and coenzyme Q(9) likely had single origins with multiple lo
51 n to 4-hydroxybenzoic acid as a precursor of coenzyme Q, a redox lipid essential to the function of t
52 d that individuals with mutations in COQ6, a coenzyme Q (also called CoQ(10), CoQ, or ubiquinone) bio
54 , alpha tocopherol, ebselen, or idebenone (a coenzyme Q analogue); or the MPT blockers, cyclosporin A
55 s of Complex III, cyanide, oligomycin A, and coenzyme Q analogues decreased 4HPR-induced hydroperoxid
59 pet mutant C92 was found to be deficient in coenzyme Q and to have low mitochondrial NADH-cytochrome
60 reaction in the biosynthesis of ubiquinone (coenzyme Q) and menaquinone (vitamin K2), essential isop
61 sue concentrations of the essential cofactor coenzyme Q are decreased by statins, and this could be h
62 role, H(2)S transfers its reducing power to coenzyme Q as it is oxidized by sulfide quinone oxidored
64 e of electron leakage is located proximal to coenzyme Q at the electron transfer flavoprotein that sh
68 ne that supports both complex I assembly and coenzyme Q biosynthesis and is disrupted in a previously
69 compensatory mechanisms, including enhanced coenzyme Q biosynthesis and the mitochondrial unfolded p
70 and enables autophosphorylation but inhibits coenzyme Q biosynthesis in vivo, demonstrating functiona
72 a nonfermentable carbon source and restored coenzyme Q biosynthesis, although at lower levels than t
73 ntrol of several metabolic processes such as coenzyme Q biosynthesis, assuring an appropriate energy
74 patient fibroblasts also exhibited defective coenzyme Q biosynthesis, substantiating a second functio
77 role in bacterial ubiquinone (also known as coenzyme Q) biosynthesis or microbial biodegradation of
79 rnesylated analogues of intermediates in the coenzyme Q biosynthetic pathway as substrates showed tha
80 Coq9p may either catalyze a reaction in the coenzyme Q biosynthetic pathway or have a regulatory rol
83 product, the mitochondrial electron carrier coenzyme Q, both in cultured cancer cells and tumors.
86 NDUF-2.1 to coordinate electron transfer to coenzyme Q by destabilizing the Q-binding pocket, causin
87 amination and ultimately its conversion into coenzyme Q by the other proteins constituting the coenzy
91 d its human homolog ALDH3A1 to mitochondrial coenzyme Q (CoQ) biosynthesis, an essential pathway disr
92 t electron transfer chain defects, disrupted coenzyme Q (CoQ) biosynthesis, and metabolic rewiring.
93 d by defects in Complex III (CIII) activity, coenzyme Q (CoQ) biosynthesis, and mitochondrial calcium
94 mitochondrial matrix octapeptidase Oct1p and coenzyme Q (CoQ) biosynthesis-a pathway essential for mi
98 roton leak in Fmr1 KO mitochondria caused by coenzyme Q (CoQ) deficiency and an open cyclosporine-sen
99 t the relative amounts of the ubiquinones or coenzyme Q (CoQ) homologues, CoQ9 and CoQ10, are related
100 6.99.2] functions to maintain membrane-bound coenzyme Q (CoQ) in its reduced antioxidant state, there
109 Previously we showed that deficiency of coenzyme Q (CoQ) is necessary and sufficient for IR in a
113 ality because its concentration reflects the coenzyme Q (CoQ) pool redox state, a central redox coupl
117 erated) have a programmed deficit in cardiac coenzyme Q (CoQ) that was associated with accelerated ca
121 ond its role in mitochondrial bioenergetics, Coenzyme Q (CoQ, ubiquinone) serves as a key membrane-em
122 erting lanostane to ergostane triterpenoids, coenzymes Q (COQ) for antroquinonol biosynthesis in myce
123 d ADI), NADPH/NADP(+) and/or reduced form of coenzyme Q (CoQH(2))/CoQ redox potentials (NDI1, AOX, Lb
125 the mevalonate-cholesterol pathway, such as coenzyme Q, driven by increased activity of the transcri
126 mouse heart mitochondria, a model system of coenzyme Q excess and relatively decreased mPTP open pro
128 deletion in COQ7 leading to a deficiency in coenzyme Q had a much more severe thermosensitivity phen
133 rpose of this study was to determine whether coenzyme Q is an independent predictor of prognosis in h
143 th the terminal stages of CI assembly and in coenzyme Q metabolism, and that pathogenic RTN4IP1 varia
144 es the electrons one at a time from FMN to a coenzyme Q molecule bound in the vicinity of the junctio
145 a substrate of the CYP2U1 enzyme, as well as coenzyme Q, neopterin, and IFN-a levels as putative biom
150 siae homologue, is essential for ubiquinone (coenzyme Q or Q) synthesis and therefore respiration.
151 RQ is structurally similar to ubiquinone (coenzyme Q or Q), a polyprenylated benzoquinone used in
154 sess the retinal consequences of stimulating coenzyme Q oxidation and respiration without ATP generat
155 es the importance to outer retinal health of coenzyme Q oxidation in the RPE and identifies a metabol
167 Q, but even in patients with a low baseline coenzyme Q, rosuvastatin treatment was not associated wi
168 tients in the lowest compared to the highest coenzyme Q tertile in a univariate analysis (hazard rati
176 n which the intra-mitochondrial synthesis of coenzyme Q (ubiquinone, Q) and Q levels are profoundly d
180 such as COQ3, required for the synthesis of coenzyme Q, were reduced in their ability to accumulate