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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.
9 itochondrial DNA: the matR gene found within NADH dehydrogenase 1 (nad1) intron 4.
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
14        Silencing of the phosphate carrier or NADH dehydrogenase 1alpha subcomplexes 2 or 3 in 3T3-L1
15  change from threonine to alanine within the NADH dehydrogenase 3 (ND3) of complex I.
16 ochrome c oxidase-IV, ATP synthase-beta, and NADH dehydrogenase-3 decreased markedly in FPG, and thes
17                        A novel mitochondrial NADH dehydrogenase 5 (ND5) m.12955A > G mutation was ide
18 the hepatoma cytochrome c oxidase I, II, and NADH dehydrogenase 5, 6, the downstream targets of Tfam,
19  of somatic truncating mutations occurred in NADH dehydrogenase 5.
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
23                                        Their NADH dehydrogenase activities were almost normal.
24                        Mutations that reduce NADH dehydrogenase activity (Ndh; type II) cause multipl
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
31               In terms of immunochemical and NADH dehydrogenase activity-staining analyses, all site-
32 n of a mouse A9 cell derivative defective in NADH dehydrogenase activity.
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
37                       Thus, multiple hits in NADH dehydrogenase and COX activity-impairing genes repr
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
41 strains expressed binary combinations of one NADH dehydrogenase and one quinol oxidase.
42                    The proton-pumping type-I NADH dehydrogenase and the aa3-type cytochrome c oxidase
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
49 of flavoenzymes, including xanthine oxidase, NADH dehydrogenase, and NADPH oxidase.
50 native oxidase activity and that alternative NADH dehydrogenases are also up-regulated in these plant
51 e or when devoid of quinones, implicating an NADH dehydrogenase as their source.
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
57 t represents a minor form of the respiratory NADH dehydrogenase complex (complex I).
58                               Defects of the NADH dehydrogenase complex are predominantly manifested
59  proteins and to a subunit of the eukaryotic NADH dehydrogenase complex I.
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
62 nd to those of the isolated P. denitrificans NADH-dehydrogenase complex.
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
66        Enzymologic analysis of mitochondrial NADH dehydrogenase (complex I) with submitochondrial par
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
74                                     However, NADH dehydrogenase-dependent respiration, as measured in
75  Saccharomyces cerevisiae is catalyzed by an NADH dehydrogenase designated Ndi1p.
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
78                                              NADH dehydrogenase gene mutations preferentially accumul
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.
82                       A rotenone-insensitive NADH dehydrogenase has been isolated from the mitochondr
83 tides (CsmR, CsmS, CsmT, CsmU, and a type II NADH dehydrogenase homolog).
84 lcarbodiimide, an inhibitor of mitochondrial NADH dehydrogenase I (also called complex I), inhibits t
85 ase A, and FNR) and membrane-bound proteins (NADH dehydrogenase I and succinate dehydrogenase).
86 nic message with the putative nuoF (encoding NADH dehydrogenase I chain F), secF (encoding protein ex
87 ansport chain, especially those encoding the NADH dehydrogenase I complex.
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
91        Aer-mediated responses were linked to NADH dehydrogenase I, although there was no absolute req
92 port chain, including cytochrome bo oxidase, NADH dehydrogenase I, NADH dehydrogenase II, and succina
93           Thus NADH dehydrogenase II but not NADH dehydrogenase I, respiratory quinones, or cytochrom
94  oxygen are associated with redox changes in NADH dehydrogenase I.
95 ssed the proton pumps cytochrome o (cyo) and NADH dehydrogenases I and II.
96                 However, mutants that lacked NADH dehydrogenase II and fumarate reductase, the most o
97          Null mutations in the gene encoding NADH dehydrogenase II averted autoxidation of vesicles,
98                                         Thus NADH dehydrogenase II but not NADH dehydrogenase I, resp
99                                              NADH dehydrogenase II did generate substantial H2O2 when
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
102                                              NADH dehydrogenase II that was purified from both wild-t
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.
106 on in the subunit for respiratory complex I, NADH dehydrogenase, in the ND6 gene.
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
109 ion to MPP(+) by a monoamine oxidase and (b) NADH dehydrogenase inhibition by MPP(+).
110 itochondrial ATP production, and rotenone, a NADH dehydrogenase inhibitor, were also tested.
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
113 spectively, by rotenone, which suggests that NADH dehydrogenase is present in these cells.
114 onella strain bearing mutations in complex I NADH dehydrogenases is refractory to the early NADPH oxi
115                     Mitochondrial complex I (NADH dehydrogenase) is a major contributor to neuronal e
116                                  Chloroplast NADH dehydrogenase-like (NDH) complex mediates cyclic el
117 y plays a role in the down-regulation of the NADH dehydrogenase-like complex-dependent plastoquinone
118 mplex (PGR) and one that is dependent of the NADH dehydrogenase-like complex.
119       ROS are produced from complex I by the NADH dehydrogenase located in the matrix side of the inn
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
123                     Here we describe a novel NADH dehydrogenase module of respiratory complex I that
124 n regulatory mtDNA elements, but only rarely NADH dehydrogenase mutations.
125                         The sodium-dependent NADH dehydrogenase (Na(+)-NQR) is a key component of the
126                         The sodium-dependent NADH dehydrogenase (Na(+)-NQR) is the main ion transport
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
131              We determined the activities of NADH dehydrogenase (ND), succinate dehydrogenase, and cy
132  gene for subunit 1 of the respiratory chain NADH dehydrogenase (ND1), complete genes for cytochrome
133        In contrast, deletion of the external NADH dehydrogenases NDE1 and NDE2, which feed electrons
134  both major clades of Erodium contain intact NADH dehydrogenase (ndh) genes, but the 11 ndh genes are
135                                        While NADH dehydrogenase (NDH) is a critical site of this O(2)
136                                  Exposure of NADH dehydrogenase (NDH), the flavin subcomplex of compl
137  type 2 NADH:quinone oxidoreductase complex (NADH dehydrogenase [NDH]) from M. capsulatus Bath, along
138 metformin-resistant Saccharomyces cerevisiae NADH dehydrogenase NDI1 was overexpressed.
139 s rescued by bypassing complex I using yeast NADH dehydrogenase Ndi1.
140  restored by ectopic expression of the yeast NADH dehydrogenase Ndi1.
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
143 s, which encode the major, energy-generating NADH dehydrogenase of the cell.
144                                              NADH dehydrogenase or complex I (CI) is affected in most
145                     Mutations of respiratory NADH dehydrogenases prevent nitrotyrosine formation and
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
148                     Mutants that lacked both NADH dehydrogenases respired very slowly, as expected; h
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
152                Here, we demonstrate that the NADH dehydrogenase subunit 1 self-peptide is seen by mat
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
155 n unusual ATC (non-AUG) codon initiating the NADH dehydrogenase subunit 2 (ND2) gene.
156 l function of the mtDNA mutations, we cloned NADH dehydrogenase subunit 2 (ND2) mutants based on prim
157                       By using mitochondrial NADH dehydrogenase subunit 2 (ND2) sequences and 467 amp
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.
160                                              NADH dehydrogenase subunit 2, encoded by the mtDNA, has
161 s (cardiac alpha-actin, cyclin G1, stathmin, NADH dehydrogenase subunit 2, titin and prostatic bindin
162 3'-terminal sequence of mitochondria-encoded NADH dehydrogenase subunit 3 (ND-3).
163                             We sequenced the NADH dehydrogenase subunit 3 (ND3) gene from a sample of
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
169  acids in cytochrome c oxidase subunit 1 and NADH dehydrogenase subunit 5.
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
175 rring peptide derived from the mitochondrial NADH-dehydrogenase subunit 1 gene (9-mer peptide).
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
178 the slo3 mutant was defective in splicing of NADH dehydrogenase subunit7 (nad7) intron 2.
179 ial for the translation of the mitochondrial NADH dehydrogenase subunit7 (nad7) mRNA.
180 3.8-kb mtDNA deletion in the region encoding NADH dehydrogenase subunits 1 and 2 and cytochrome c oxi
181         We observed that transcripts of most NADH dehydrogenase subunits are edited inefficiently in
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
184                              A new family of NADH dehydrogenases, the flavin oxidoreductase (FlxABCD,
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
187                                     Multiple NADH dehydrogenases, transcription factors of unknown fu
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
195         Loss of murine Ndufs4, which encodes NADH dehydrogenase (ubiquinone) iron-sulfur protein 4, r
196              Furthermore, we also identified NADH dehydrogenase [ubiquinone] 1 alpha subcomplex subun
197 he unexpected loss of respiratory complex I (NADH dehydrogenase), universally present in all 300+ oth
198                     As anticipated, however, NADH dehydrogenase was inhibited by these rotenoids.
199            The presence of three subunits of NADH dehydrogenase was observed in immunoblots of mitoch
200 ochondrial proteins, including aconitase and NADH dehydrogenases, were oxidized and their activities

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