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1 thesis of two isoforms of the ND3 subunit of NADH dehydrogenase.
2 -cytochrome P450 reductase and mitochondrial NADH dehydrogenase.
3 ND1 and ND3) encoding additional subunits of NADH dehydrogenase.
4 ts defective in the energy-conserving type I NADH dehydrogenase.
5 rovides further evidence for the presence of NADH dehydrogenase.
6 ster, which encodes the proton-translocating NADH dehydrogenase.
7 itch from transcription of type I to type II NADH dehydrogenase.
8 and major Amb a 1 allergens, and as unique, NADH dehydrogenases.
10 ated from the heavy strand promoter 2 [i.e., NADH dehydrogenase 1 (ND1) by 11-fold, P < 0.005; cytoch
11 assessed by measuring the copy number of the NADH dehydrogenase 1 gene using quantitative real-time P
12 t on mtRNA expression and that expression of NADH dehydrogenase 1, 3, and 6 (ND-1, ND-3, ND-6) and AT
13 ins including the phosphate carrier protein, NADH dehydrogenase 1alpha subcomplexes 2 and 3, transloc
16 ochrome c oxidase-IV, ATP synthase-beta, and NADH dehydrogenase-3 decreased markedly in FPG, and thes
18 the hepatoma cytochrome c oxidase I, II, and NADH dehydrogenase 5, 6, the downstream targets of Tfam,
20 ng mitochondrial genes encoded in the mtDNA [NADH dehydrogenase 6 (ND6) and cytochrome c oxidase subu
21 region of the mtDNA that contained the gene NADH dehydrogenase 6 (ND6), which encodes an essential c
22 it 6 (ATP6) by 6.5-fold, P < 0.005); but not NADH dehydrogenase 6 (ND6)], which is initiated from the
25 Thus, aberration in mitochondrial complex I NADH dehydrogenase activity can profoundly enhance the a
26 a threefold reduction in total mitochondrial NADH dehydrogenase activity in cells cultivated with glu
27 cerevisiae (NDI1) can completely restore the NADH dehydrogenase activity in mutant human cells that l
28 detection of a 700 kDa subcomplex retaining NADH dehydrogenase activity indicates an arrest in the a
29 phenotype analyses suggest that the external NADH dehydrogenase activity of Ndh1p is important for op
30 contrary, no decrease in rotenone-sensitive NADH dehydrogenase activity, using a water-soluble ubiqu
33 metformin inhibits mitochondrial complex I (NADH dehydrogenase) activity and cellular respiration.
34 are consistent with a protective role of the NADH dehydrogenases against oxidative stress, thus, when
35 atory electron transport chain that included NADH dehydrogenase, alternative complex III and cytochro
36 s of rotenone (an inhibitor of mitochondrial NADH dehydrogenase and a naturally occurring toxicant) o
38 e pathogenic mtDNA point mutations affecting NADH dehydrogenase and COX genes as well as regulatory e
39 are decreased by about 90%, whereas that of NADH dehydrogenase and cytochrome c reductase are unchan
40 and acetic acid tolerance; overexpression of NADH dehydrogenase and methylmalonyl-CoA epimerase impro
43 , suggesting that the external mitochondrial NADH dehydrogenase and the malate-aspartate shuttle may
44 rrected by expression of one of two enzymes: NADH dehydrogenase and the NADH-dependent malate dehydro
45 not caspase 3, and significantly suppressed NADH dehydrogenases and cytochrome c oxidases, consisten
46 t low RSV doses (1-5 muM) directly stimulate NADH dehydrogenases and, more specifically, mitochondria
47 (ND2 and ND5) encode interacting subunits of NADH dehydrogenase, and amino residues that were inferre
48 uo genes not present in C. jejuni encode the NADH dehydrogenase, and in their place in the operon are
50 native oxidase activity and that alternative NADH dehydrogenases are also up-regulated in these plant
52 ochondrial genes, those encoding subunits of NADH-dehydrogenase as well as cytochrome c oxidase subun
53 ays (additional photosystem genes, duplicate NADH dehydrogenase, ATP synthases), whose functionality
54 ransport proteins from Arabidopsis thaliana, NADH dehydrogenase B14.7 like (B14.7 [encoded by At2g422
55 tered respiratory function, as inhibition of NADH dehydrogenase brought ROS levels back to wild-type
56 er, in permeabilized cells NDI1 (alternative NADH dehydrogenase) bypassed complex I inhibition, where
60 mutant lacking nuoG, a subunit of the type I NADH dehydrogenase complex, exhibits attenuated growth i
61 systems but up-regulation of the chloroplast NADH dehydrogenase complex, plastocyanin, and Ca(2+) sen
63 ely 40 subunits of the mammalian respiratory NADH dehydrogenase (Complex I) are encoded in mitochondr
64 nate, which suggests that rotenone-sensitive NADH dehydrogenase (complex I) is present in these mitoc
65 en observed in the level of the mRNA for the NADH dehydrogenase (complex I) ND6 subunit gene, which i
67 ha blocked electron transfer at three sites, NADH dehydrogenase (complex I), succinate dehydrogenase
68 inhibition of the respiratory chain enzymes NADH-dehydrogenase (complex I) and succinate dehydrogena
69 ulation of the chloroplast photosystem I and NADH dehydrogenase complexes and had been proposed to fa
70 hat functional variation in cytochrome b and NADH dehydrogenase could mechanistically contribute to l
71 n transport chain, a large membrane-embedded NADH dehydrogenase, couples electron transfer to the rel
72 c for each type of mitochondrial lesion: the NADH dehydrogenase-defective NCS2 mutant has high expres
73 e was just sufficient to support the maximum NADH dehydrogenase-dependent respiration rate, with no u
76 rity to the 18-kD Fe-S subunit of complex I (NADH dehydrogenase, EC 1.6.5.3) in the mitochondrial ele
77 le-genome scanning technique to identify the NADH dehydrogenase gamma subunit (nuoG) primer set that
79 We report the first molecular defect in an NADH-dehydrogenase gene presenting as isolated myopathy.
80 iochlorophyll biosynthesis, cbb3 oxidase and NADH dehydrogenase genes, as well as genes for autotroph
81 l DNA-encoded ND5 subunit of the respiratory NADH dehydrogenase has been isolated and characterized.
84 lcarbodiimide, an inhibitor of mitochondrial NADH dehydrogenase I (also called complex I), inhibits t
86 nic message with the putative nuoF (encoding NADH dehydrogenase I chain F), secF (encoding protein ex
88 -containing aconitase, serine deaminase, and NADH dehydrogenase I enzymes of S. Typhimurium under bas
89 energetically efficient proton-translocating NADH dehydrogenase I is used in preference to the non-pr
90 DH-quinone oxidoreductase (energy-conserving NADH dehydrogenase I) from various eukaryotic and prokar
92 port chain, including cytochrome bo oxidase, NADH dehydrogenase I, NADH dehydrogenase II, and succina
100 n preference to the non-proton translocating NADH dehydrogenase II during periods of rapid growth, by
101 ne that encodes the non-proton-translocating NADH dehydrogenase II of Escherichia coli is anaerobical
103 cytochrome bo oxidase, NADH dehydrogenase I, NADH dehydrogenase II, and succinate dehydrogenase.
104 ided additional evidence for the presence of NADH dehydrogenase in bloodstream forms of T. brucei.
105 ine, coding for ND5, a subunit of complex I (NADH dehydrogenase) in the electron transport chain.
107 terized the iron-sulfur protein required for NADH dehydrogenase (INDH) in the model plant Arabidopsis
108 where ndhF is the ND5 protein of chloroplast NADH dehydrogenase) indicate that Hesperomannia belongs
111 ent of intact mitochondria revealed that the NADH dehydrogenase is located in the inner membrane/matr
112 ncentrations of digitonin suggested that the NADH dehydrogenase is loosely bound to the inner mitocho
114 onella strain bearing mutations in complex I NADH dehydrogenases is refractory to the early NADPH oxi
117 y plays a role in the down-regulation of the NADH dehydrogenase-like complex-dependent plastoquinone
120 xidized PQ pool upon inactivation of type II NADH dehydrogenase may be related to the facts that the
121 lasmic mtDNA mutations affecting subunits of NADH dehydrogenase may play a synergistic role in the es
122 alternative NADH:ubiquinone oxidoreductases (NADH dehydrogenases) may protect against oxidative stres
127 ith no change in CcO activity, and inhibited NADH dehydrogenase (NADH-DH) activity (P<0.01) without a
128 the ATPase 6 subunit gene (ATP), ATC for the NADH dehydrogenase (ND) 2 subunit gene, and ATT for the
129 perfectly conserved regions upstream of two NADH dehydrogenase (ND) genes are transcribed and likely
130 ncoding subunit ND4 of the respiratory chain NADH dehydrogenase (ND), did not affect the synthesis, s
132 gene for subunit 1 of the respiratory chain NADH dehydrogenase (ND1), complete genes for cytochrome
134 both major clades of Erodium contain intact NADH dehydrogenase (ndh) genes, but the 11 ndh genes are
137 type 2 NADH:quinone oxidoreductase complex (NADH dehydrogenase [NDH]) from M. capsulatus Bath, along
141 nteny group of THRSP and its flanking genes [NADH dehydrogenase (NDUFC2) and glucosyltransferase (ALG
142 with the rotenone-insensitive single-subunit NADH dehydrogenase of Saccharomyces cerevisiae (NDI1), w
146 enol and the presence of subunits 7 and 8 of NADH dehydrogenase provided additional evidence for the
147 g human cell lines carrying a frame-shift at NADH dehydrogenase (respiratory complex I) subunit 5 gen
149 lipolytica carrying an internal alternative NADH dehydrogenase resulted in slower growth and strongl
150 itochondrial genes (cytochrome b (Cytb), the NADH dehydrogenase subunit 1 (ND1) and cytochrome oxidas
151 nding peptides allowed us to characterize an NADH dehydrogenase subunit 1 (ND1)-derived peptide as th
153 s allowed us to characterize a mitochondrial NADH dehydrogenase subunit 1-derived 9-mer peptide as th
154 transversion in the mitochondrially encoded NADH dehydrogenase subunit 2 (mt-ND2, human; mt-Nd2, mou
156 l function of the mtDNA mutations, we cloned NADH dehydrogenase subunit 2 (ND2) mutants based on prim
158 rial genes, namely, cytochrome b (CYT B) and NADH dehydrogenase subunit 2 (ND2), from 383 archived sp
159 europilin (ESDN), prostatic binding protein, NADH dehydrogenase subunit 2, and an unknown protein.
161 s (cardiac alpha-actin, cyclin G1, stathmin, NADH dehydrogenase subunit 2, titin and prostatic bindin
164 nce, containing part of the tRNA glycine and NADH dehydrogenase subunit 3 genes, is the target of our
165 scripts in a 24-hour time course showed that NADH dehydrogenase subunit 4 mRNA decreased by 2-fold as
166 id evolutionary rates, 16S rRNA (379 bp) and NADH dehydrogenase subunit 5 (NADH-5, 318 bp), from mult
167 the cytochrome c oxidase subunit I (COI) and NADH dehydrogenase subunit 5 (ND5) genes each include a
168 for cytochrome c oxidase subunit I (COI) and NADH dehydrogenase subunit 5 (ND5) of the sea anemone Me
170 within the mitochondrial DNA (mtDNA)-encoded NADH dehydrogenase subunit 6 (ND6) gene has been identif
171 g CO2/HCO3 (-)-uptake mutant DeltandhD3 (for NADH dehydrogenase subunit D3)/ndhD4 (for NADH dehydroge
172 or NADH dehydrogenase subunit D3)/ndhD4 (for NADH dehydrogenase subunit D4)/cmpA (for bicarbonate tra
173 creased mRNA levels from both mitochondrial (NADH dehydrogenase subunit IV) and nuclear [cytochrome c
174 anscripts nicotinamide adenine dinucleotide (NADH) dehydrogenase subunit 4 and cytochrome b were down
176 t low peptide concentrations, shortening the NADH-dehydrogenase subunit 1 gene 9-mer peptide or mutat
177 ng events in cytochrome oxidase subunit2 and NADH dehydrogenase subunit4 transcripts, encoding subuni
180 3.8-kb mtDNA deletion in the region encoding NADH dehydrogenase subunits 1 and 2 and cytochrome c oxi
182 f the mitochondrial genes encoding the seven NADH-dehydrogenase subunits showed a G-to-A transition a
183 sidered to be the minimal form of the type I NADH dehydrogenase, the first enzyme complex in the resp
185 fully reduced in the mutant without type II NADH dehydrogenase, thus causing regulatory inhibition.
186 in vitro, in the gene for the ND4 subunit of NADH dehydrogenase) to undergo transcomplementation of t
188 mical reduction of the plastoquinone pool by NADH dehydrogenases type-1 and type-2 (NDH-1 and NDH-2).
189 ncoding a nuclear DNA-encoded subunit of CI (NADH dehydrogenase ubiquinone Fe-S protein 4), typically
190 (ubiquinone) 1beta subcomplex subunit 8, and NADH dehydrogenase (ubiquinone) 1alpha subcomplex subuni
191 rogenase (ubiquinone) iron-sulfur protein 3, NADH dehydrogenase (ubiquinone) 1beta subcomplex subunit
192 e show that human fibroblasts mutant for the NADH dehydrogenase (ubiquinone) Fe-S protein 1 (NDUFS1)
193 ochondrial respiratory chain subunit Ndufs4 [NADH dehydrogenase (ubiquinone) Fe-S protein 4], delays
194 chondrial membranes, decreased levels of the NADH dehydrogenase (ubiquinone) iron-sulfur protein 3, N
197 he unexpected loss of respiratory complex I (NADH dehydrogenase), universally present in all 300+ oth
200 ochondrial proteins, including aconitase and NADH dehydrogenases, were oxidized and their activities
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