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1 16S rDNA, 28S rDNA, Cytochrome oxidase I and Cytochrome b).
2 Atovaquone targets parasite cytochrome b.
3 nits and the mitochondrially encoded subunit cytochrome b.
4 eveals the presence of the Y268S mutation in cytochrome b.
5 eakened interaction between this subunit and cytochrome b.
6 ansfer to the Rieske iron-sulfur protein and cytochrome b.
7 ion, which eliminates the proton acceptor in cytochrome b.
8 mitochondrial components, cytochrome c, and cytochrome b.
9 cripts for cytochrome oxidase II (COXII) and cytochrome b.
10 These cysts highly express cytochrome b.
11 lasmic mutation in a subunit of complex III, cytochrome b.
12 llowed by sequencing of a 201-bp fragment of cytochrome b.
13 ochondrial disease-related mutation in human cytochrome b.
14 ia a feedback loop that senses hemylation of cytochrome b.
15 nsformation of heme ligand sets reported for cytochrome bd.
16 herichia coli cells harbouring CpcA-labelled cytochrome bd 1 ubiquinol oxidase in the cytoplasmic mem
17 b light chain and encodes p22(phox) protein; cytochrome b-245 or NADPH oxidase 2, and encodes Nox2 or
18 dismutase, and NADPH oxidase-complex adaptor cytochrome b-245, alpha-polypeptide (p22phox) proteins,
19 ecies (ROS) because selective Cybb (encoding cytochrome b-245, beta polypeptide, also known as NOX2)
22 cytochrome P450 reductase (CPR) and Mn(III) cytochrome b 5 (Mn cyt b 5); the manganese derivative of
23 ological partner proteins myoglobin (Mb) and cytochrome b(5) (b(5)) reveal interprotein ET rates comp
24 ently link cytochrome P450 2E1 (CYP2E1) with cytochrome b(5) (b(5)) through the formation of specific
26 nimals and contains three domains similar to cytochrome b(5) (b(5)), CHORD-SGT1 (CS), and cytochrome
29 pation of cytochrome b(5) reductase (CYB5R), cytochrome b(5) (CYB5), and molybdenum cofactor sulfuras
30 me P450 2B4 were compared in the presence of cytochrome b(5) (cyt b(5)) and NADPH-cyt P450 reductase
31 tuted with Zn-deuteroporphyrin and monitored cytochrome b(5) (cyt b(5)) binding and electron transfer
33 [POR; HRN (hepatic reductase null) line] or cytochrome b(5) [HBN (hepatic cytochrome b(5) null) line
35 ome b(5) oxidoreductase (Ncb5or), comprising cytochrome b(5) and cytochrome b(5) reductase domains, i
37 bicelles containing uniformly (15)N-labeled cytochrome b(5) are presented and theoretical analyses o
39 chrome b(5) has been deleted in all tissues [cytochrome b(5) complete null (BCN)], which surprisingly
40 ctivities were also significantly reduced by cytochrome b(5) deletion, leading to significantly lower
41 o the previous finding in the liver-specific cytochrome b(5) deletion, suggesting that extrahepatic c
42 However, neither AL10 nor AL21 contain the cytochrome b(5) domain normally present in this class of
46 iver-specific deletion, complete deletion of cytochrome b(5) leads to a neonatal increase in the expr
47 ructure analysis reveals similarities to the cytochrome b(5) motif, neither of the two axial histidin
50 The endoplasmic reticulum-associated NADH cytochrome b(5) oxidoreductase (Ncb5or) is widely distri
52 n Leishmania, we attempted to create NAD(P)H cytochrome b(5) oxidoreductase from L. major (LmNcb5or)
53 b(5) deletion, suggesting that extrahepatic cytochrome b(5) plays a significant role in its disposit
57 igate whether other reducing enzymes such as cytochrome b(5) reductase (b5R), cytochrome P450 reducta
58 ified enzymes suggested the participation of cytochrome b(5) reductase (CYB5R), cytochrome b(5) (CYB5
59 provide strong evidence that cytochrome b(5)/cytochrome b(5) reductase can act as a sole electron don
60 whether this is because cytochrome b(5) and cytochrome b(5) reductase can act as the sole electron d
61 ase (Ncb5or), comprising cytochrome b(5) and cytochrome b(5) reductase domains, is widely distributed
62 PH concentrations below the apparent K(m) of cytochrome b(5) reductase, but well above that for POR,
63 Several lines of evidence indicate that the cytochrome b(5) reductase-like protein controls the oxid
64 he growth defect caused by overexpression of cytochrome b(5) reductase-like protein could be partiall
67 dipocytes, whereas down-regulation of MOSC1, cytochrome b(5) type A (CYB5A), CYB5R1, CYB5R2, or CYB5R
68 ation of MOSC2 and the mitochondrial form of cytochrome b(5) type B (CYB5B) significantly inhibited t
71 elate the nonfunctional property of a mutant cytochrome b(5) with its inability to insert into the li
74 y charge-clustered mutants of rat microsomal cytochrome b(5), E11Q and E44Q, with the same total char
75 shows respective K(m) values for ascorbate, cytochrome b(5), NO, and O(2) of 0.25 mm, 0.3 microm, 40
76 hich to further investigate the functions of cytochrome b(5), particularly in extrahepatic tissues.
77 tive SERR enhancement of the anionic protein cytochrome b(5), whereas functionalization with SiO(2) a
78 esterone receptor membrane component 1) is a cytochrome b(5)-related drug-binding orphan receptor ess
79 esterone receptor membrane component 1) is a cytochrome b(5)-related protein that is up-regulated in
84 adicals per PS II, and the yield of oxidized cytochrome b 559 by optical difference spectroscopy is 0
85 w that human erythrocyte membranes contain a cytochrome b(561) (Cyt b(561)) and hypothesize that it m
88 tion (CHGB, exon 4, Glu348Glu; P=0.002), and cytochrome b-561 (CYB561, intron 1, C719G; P<0.001), an
90 omplication, we have engineered a variant of cytochrome b(562) (cyt c-b(562)) featuring a c-type link
91 eins, namely, the heme binding capability of cytochrome b(562) and the antibiotic degrading beta-lact
93 was then replaced by a DNA cassette encoding cytochrome b(562) with differing linking sequences at ea
96 haped relationship to the reduction state of cytochrome b(566), suggesting that superoxide production
97 s not required for catalytic turnover of the cytochrome b 6 f complex, the role of the single chlorop
100 encoding the cytochrome b(6) subunit of the cytochrome b(6) f complex, was selected to expand our un
101 hown in single flash turnover experiments of cytochrome b(6) reduction and oxidation, the R214H mutat
102 single core genome locus, petB, encoding the cytochrome b(6) subunit of the cytochrome b(6) f complex
105 compared the lipid binding properties of the cytochrome b(6)f and bc(1) complexes that function in ph
106 also reported that the Chl a molecule in the cytochrome b(6)f complex does not change orientation in
107 The crystal structure of the cyanobacterial cytochrome b(6)f complex has previously been solved to 3
112 ells accumulate 14 to 20% less photosystems, cytochrome b(6)f complex, and ATP synthase but 30% more
113 However, the residual fraction of assembled cytochrome b(6)f complexes exhibits single-turnover elec
114 the presence of two distinguishable pools of cytochrome b(6)f complexes with different functions that
115 ential component of the cytochrome bc(1) and cytochrome b(6)f complexes, and it is exported across th
116 rising multiple subunits and many cofactors, cytochrome b(6)f from the chloroplast of the green alga
118 Accordingly, measurements of flash-induced cytochrome b(6)f turnover and respiration pointed to a r
120 pressure selects parasites with mutations in cytochrome b, a respiratory protein with low but essenti
122 e p22 phagocytic oxidase subunit (p22(phox)) cytochrome b alpha gene (CYBA) C242T, crystallizable gam
124 n 300 samples were collected and analyzed at cytochrome b and 11 microsatellites loci for investigati
125 eractions between the Rieske protein and the cytochrome b and c sites and provide part of the driving
127 omplex formation depended on the presence of cytochrome b and Cox3, supporting the idea that supercom
128 refore, TtRp likely translocates between the cytochrome b and cytochrome c sites by passive diffusion
129 lity of the Fe/S protein to move between the cytochrome b and cytochrome c(1) subunits of the enzyme.
130 Rieske protein is mobile, moving between the cytochrome b and cytochrome c1 components during turnove
132 is both required for efficient synthesis of cytochrome b and for protection of the newly synthesized
133 Tyr to Cys mutation cross-links together the cytochrome b and iron-sulfur subunits and renders the ba
134 e Q(o) site by weakening the binding between cytochrome b and ISP through hydrogen bonding provided b
135 when the iron-sulfur cluster is proximal to cytochrome b and minimizing binding of the product, redu
136 results suggest that functional variation in cytochrome b and NADH dehydrogenase could mechanisticall
137 ommunication between the two active sites of cytochrome b and open new possibilities for the utilizat
138 systems whereas two negative control genes (cytochrome b and peptidase inhibitor 3) show no signific
140 the downregulation of the redox activity of cytochromes b and c in freezing yeast cells in a contact
141 lled protein structures of the mtDNA marker (cytochrome b) and estimated the environmental envelopes
142 mino N form H-bonds with conserved Asp228 of cytochrome b, and the formylamino O H-bonds via a water
143 inct step preceding transfer of electrons to cytochrome b, and with conformational gating models that
147 ssed mitochondrial precursor transcript (ND5-cytochrome b) but had no effect on steady-state levels o
149 he idea that alanine substitution at S322 of cytochrome b causes conformational changes at the Q(o) s
150 which we sequenced two mitochondrial genes, cytochrome b (cob) and cytochrome oxidase (cox1), for mu
151 is, we generated a data set of mitochondrial cytochrome b (cob) and mitochondrial cytochrome c oxidas
152 mitochondrial NADH dehydrogenase5 (nad5) and cytochrome b (cob) transcripts at the nad5-1550 and cob-
153 resulted in sequestration of Cbp3-Cbp6 in a cytochrome b-containing complex, thereby making Cbp3-Cbp
156 evolves about 60% as rapidly as that of host cytochrome b, corresponding to approximately 1.2% sequen
157 This was thought to be mediated by duodenal cytochrome b (Cybrd1), a ferric reductase enzyme residen
159 ypeptide derived from the C-terminal half of cytochrome b (Cyt b) encoded by the mitochondrial genome
160 atin-induced apoptosis due to an increase of cytochrome b (Cyt b) expression and its release from mit
161 tive open reading frame of the mitochondrial cytochrome b (cyt b) gene in melanoma cells established
162 l DNA (mtDNA) cytochrome oxidase I (COI) and cytochrome b (Cyt b) gene markers, we inferred the origi
163 ts and newly designed from the mitochondrial cytochrome b (cyt b), cytochrome oxidase I (COI), and 12
164 ur DNA sequences were analysed-mitochondrial cytochrome b (cyt b), nuclear elongation factor-1alpha (
165 tutions in the atovaquone-binding regions of cytochrome b (cytb) and the azithromycin-binding region
167 one, a ubiquinone analogue, targets C. felis cytochrome b (cytb), of which 30 unique genotypes have b
168 skippers based on three mitochondrial genes (cytochrome b (Cytb), the NADH dehydrogenase subunit 1 (N
169 ely cytochrome c oxidase subunit I (COI) and cytochrome b (cytb), were analysed in silico to identify
171 Species-specific primers were designed from cytochrome b, cytochrome oxidase I, and 16S rRNA genes t
172 etal transporter 1 (DMT1) 3.2-fold, duodenal cytochrome b (Dcytb) 1.8-fold, and transferrin receptor
173 ensitive than with a mitochondrial probe for cytochrome b despite higher copy numbers of mitochondria
176 Respiratory chain complex III and possibly cytochrome b function are essential for this increase.
177 ected to an NGS approach targeting two short cytochrome b gene (cytb) fragments on the Illumina MiSeq
179 Our research revealed that a mutation in the cytochrome b gene (G126S) in 35% tested T. urticae popul
181 y applying a previously established parasite cytochrome b gene mutation rate (0.012 mutations per sit
182 A sequences of portions of the mitochondrial cytochrome b gene obtained from gorilla parasites closel
184 ain reaction (PCR) (nested PCR targeting the cytochrome b gene) and quantitative PCR as reference sta
185 sing conserved regions of mitochondrial DNA (cytochrome b gene) was performed to evaluate the halal a
187 e diversity in New World Myotis by analyzing cytochrome-b gene variation from an expansive sample ran
188 d targeting mitochondrial ND5, ATPase 6, and cytochrome b genes to amplify 172, 163, 141, 129 and 108
191 y using stopped flow, the reduction rates of cytochromes b(H) and c(1) were 403 s(-1) (t(1/2) 1.7 ms)
192 rane potential, and redox states of NADH and cytochromes b(H), b(L), c(1), c, and a,a(3)] were compar
194 g two one-electron carriers, a low potential cytochrome b heme and the "Rieske" iron-sulfur cluster.
197 a mean of approximately 76, indicating that cytochrome bd-I is concentrated in mobile patches in the
198 uent catalytic steps of the Escherichia coli cytochrome bd-I oxidase were investigated by means of ul
200 echanisms to evade nitrosative stresses, the cytochrome bd-I respiratory oxidase is the main contribu
202 (YTL01) that expresses functional GFP-tagged cytochrome bd-I terminal oxidase complexes under wild-ty
205 s of our tests suggest that the evolution of cytochrome b in Peromyscus is chiefly governed by purify
213 f quinol with oxygen that are observed after cytochrome b is reduced were unaffected by the E272Q sub
216 omplex has a dual function for biogenesis of cytochrome b: it is both required for efficient synthesi
218 otential inhibits electron transfer from the cytochrome b(L) to b(H) hemes, thereby promoting the for
219 milar reduction kinetic is also observed for cytochrome b(L), indicating a simultaneous reduction of
221 es that encode components of NADPH oxidases (cytochrome b light chain and encodes p22(phox) protein;
223 eals an operon (cydAB) apparently encoding a cytochrome bd-like oxidase homologous to oxidases in Esc
224 eric [NiFe]-hydrogenase that lacks a typical cytochrome b membrane anchor subunit, which transfers el
225 d with point mutations in the Q(o) pocket of cytochrome b, most notably near the conserved Pro(260)-G
226 dox potential of the FeS cluster, or a E272Q cytochrome b mutation, which eliminates the proton accep
227 II subunit Rieske iron sulfur protein in the cytochrome b-null cells and treatment of wild-type cells
230 gene markers, Cytochrome Oxidase I (COI) and Cytochrome b oxidase (COB), have been used to assess DNA
231 with data showing that CydX is required for cytochrome bd oxidase activity, copurification experimen
232 the naphthoquinones, which pass electrons to cytochrome bd oxidase and the anaerobic terminal reducta
233 around E. coli that identified high-affinity cytochrome bd oxidase as an essential bacterial gene pro
234 pothesis that CydX is a subunit of the CydAB cytochrome bd oxidase complex that is required for compl
240 e propose that the sulfide resistance of the cytochrome bd oxidase is a key trait that permits respir
242 , we show that the electron flow through the cytochrome bd oxidase is sufficient to maintain respirat
244 production of reactive oxygen species by the cytochrome bd oxidase was below the detection level of 1
245 that the alternate terminal bd-type oxidase (cytochrome bd oxidase) is capable of maintaining a membr
256 n for 12s rRNA) in: third codon positions of cytochrome B, probably because, unlike rRNAs, specific m
258 dases (RTOs), cytochrome c oxidase (Cox) and cytochrome bd quinol oxidase (Cyd), are present in the p
261 in a non-linear inhibition of the extent of cytochrome b reduction by quinol together with a shift o
264 different single amino acid substitutions in cytochrome b rendering the yeast resistant to the inhibi
268 ern South China Seas using the mitochondrial cytochrome b sequences and Bayesian Skyline Plot analyse
274 erial system, we show that mutation G167P in cytochrome b shifts the equilibrium distribution of ISP-
276 he quinone when the Rieske protein is in the cytochrome b site, as the residue experiencing the remar
278 we show that a conserved Tyr residue of the cytochrome b subunit of cytochrome bc(1) is critical for
279 ia eutropha, including the membrane-integral cytochrome b subunit, was investigated electrochemically
282 ex, thereby making Cbp3-Cbp6 unavailable for cytochrome b synthesis and thus reducing overall cytochr
283 ntermediates, thereby causing a reduction in cytochrome b synthesis via a feedback loop that senses h
284 e, we report that Cbp3-Cbp6 also coordinates cytochrome b synthesis with bc(1) complex assembly.
285 acquisition that triggers the progression of cytochrome b through successive assembly intermediates.
287 ochrome b were observed in 2 cases (ratio of cytochrome b to ND1: 0.80 [95% CI, 0.68-0.92] vs 0.99 [9
288 . monocytogenes has two terminal oxidases, a cytochrome bd-type (CydAB) and a cytochrome aa 3-type me
290 In Escherichia coli, the biogenesis of both cytochrome bd-type quinol oxidases and periplasmic cytoc
291 e test for evidence of positive selection on cytochrome b variation within and among species of the e
293 extraction of DNA, followed by nested PCR of cytochrome b, was the optimal strategy, allowing reliabl
294 munoreactivities of cytochrome oxidase 1 and cytochrome b were found in HD patients relative to contr
296 t cells deficient in the complex III subunit cytochrome b, which are respiratory incompetent, increas
298 volves interactions of the newly synthesized cytochrome b with assembly factors and structural comple
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