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   1 lations of the half reaction of reduction of cytochrome c.                                           
     2  tRNA but is regulated by the redox state of cytochrome c.                                           
     3 es decorated on multiwalled carbon nanotubes/cytochrome c.                                           
     4 tide exchange on Apaf-1 following binding of cytochrome c.                                           
     5 a: hydrogen peroxide, mitochondrial DNA, and cytochrome c.                                           
     6  induce cell death through direct release of cytochrome c.                                           
     7 an enhanced ability to transfer electrons to cytochrome c.                                           
  
  
    10  isotopes at the fundamental distribution of cytochrome c(+8) (m/z approximately 1549) were nearly ba
    11 by DESI-MS, were 100% for melittin, 100% for cytochrome c, 90% for myoglobin, and 65% for bovine seru
    12 gly, D62-DPPC acyl chains were unaffected by cytochrome c accumulation, while cardiolipin showed majo
  
    14 mbrane potential loss, increase of cytosolic cytochrome c and Bax levels, decrease of Bcl-2 levels an
    15 er resolution images of individual proteins (cytochrome C and BSA) as well as of protein complexes (h
    16 e used as a biosensor for directly detecting cytochrome c and carbohydrate antigen 199 in air after t
  
    18 ated Bid at Asp-52 increasing the release of cytochrome c and caspase-3 activation, and thus creating
    19 ly activated Bax and increased activities of cytochrome c and caspase-9 and -3 that, in turn, led to 
  
  
  
  
  
    25 accepts electrons with similar efficiency to cytochrome c and that the cell has strategies to coordin
    26  of mitochondrial activity by phosphorylated cytochrome c and to develop novel therapeutic approaches
    27  (flavoprotein, succinate dehydrogenase, and cytochrome c) and the synthesis and activity of key deni
    28  Bax expression, a disturbed distribution of cytochrome c, and cleaved caspase-3 positive staining in
  
    30 in blocking apoptosis by reduction of ferric cytochrome c, and gentle tuning of NO concentration in t
  
  
    33 esults constitute the molecular mechanism of cytochrome c- and dATP-mediated activation of Apaf-1.   
  
    35 gment-elevation AMI patients with detectable cytochrome c, as compared with those with nondetectable 
  
    37 Compared with reduced cytochrome c, oxidized cytochrome c binds to tRNA with a weaker affinity, which
    38  novel fluorescence assay, we show here that cytochrome c binds to tRNA with an affinity comparable w
  
  
  
    42 erobic electron acceptors include oxygen and cytochrome c, but an acceptor that can function under an
    43  electrons coming from NADH and ubiquinol to cytochrome c, but it is also capable of producing signif
  
  
  
  
  
    49 ESI-QTOF-MS technique, formation of glycated cytochrome C containing up to 12 glucose moieties were o
  
    51 ria differed primarily at a Raman biomarker, cytochrome c, corresponding to a bacteroid-specific term
  
    53 rving as respiratory electron shuttle, ferri-cytochrome c (cyt c) acts as a peroxidase; i.e., it cata
    54 ns and ER stress as shown by increased HSP60/Cytochrome C (Cyt C) and CHOP-ATF3 levels respectively. 
    55 d, catalytic circuit based on photosystem I, cytochrome c (cyt c) and human sulfite oxidase (hSOX).  
    56 cribe advancements in sensing technology for cytochrome c (cyt c) detection, at point-of-care (POC) a
  
    58 vine serum albumin (BSA), lysozyme (lyz) and cytochrome c (cyt c) in singular and competitive manner 
  
  
  
  
    63 cytochrome c synthase (HCCS) is required for cytochrome c (cyt c) maturation and therefore respiratio
  
    65 has been suggested that the alkaline form of cytochrome c (cyt c) regulates function of this protein 
    66 s of the spontaneous reversible unfolding of Cytochrome c (Cyt c) under native conditions have led to
  
  
    69 hieved using redox cofactors namely oxidized cytochrome-c (Cyt-c) and Co-enzyme-Q (Co-Q) immobilized 
  
    71 as an oligopeptide stopper, we have employed cytochrome C (CytC) as a protein stopper to produce the 
  
    73 tion (MOMP) via BAK and BAX oligomerization, cytochrome c (cytc) release, and caspase activation are 
    74 polarization of mitochondria, and release of cytochrome c, demonstrating its important role as an ant
    75 onality: The phosphomimetic mutation impairs cytochrome c diffusion between respiratory complexes, en
    76 after three initial reports of NECD from the cytochrome c dimer complex, no further evidence of the e
  
    78 hrome c indicate that formation of mammalian cytochrome c dimers in vivo would require catalysis.    
    79 e cofactors (hemes b and copper for CcoN and cytochromes c for CcoO and CcoP) were present within the
    80 e detection of apoptosis based on release of cytochrome c from mitochondria in lysates human embryoni
    81  Escherichia coli cells harbouring wild-type cytochrome c from Rhodothermus marinus (Rma cyt c) were 
    82 ution, we enhanced the catalytic function of cytochrome c from Rhodothermus marinus to achieve more t
    83 ases are often activated upon the release of cytochrome c from the mitochondria, which is promoted by
  
    85 and release of apoptosis-inducing factor and cytochrome c Furthermore, this protection was mediated b
  
  
    88 ect electrochemistry and electrocatalysis of cytochrome c immobilized on the MWCNTs-TiN composite mod
    89 e basal portion of the RPE, as identified by cytochrome C immunoreactivity, and that the hyporeflecti
    90  Mitochondria were preserved as indicated by Cytochrome c immunostaining in the spinal cord, which ma
  
  
  
  
    95 cytochrome P450 but fully active in reducing cytochrome c In the DeltaGly-141 mutants, the backbone a
    96 d had greater amounts of cytosolic mtDNA and cytochrome c, increased apoptosis, and more IL-1beta sec
    97 association kinetics for yeast versus equine cytochrome c indicate that formation of mammalian cytoch
  
    99  depicts a low barrier for the permeation of cytochrome C into the Bax C-terminal mouth, with the pat
   100  collision cross sections of native-like, 7+ cytochrome c ions increase monotonically from 15.1 to 17
  
  
   103  decreased activity with cytochrome P450 and cytochrome c It formed a flexible loop, which transientl
   104 hanges in mitrochondrial membrane potential, cytochrome c leakage, activation of family of caspases, 
  
  
   107  (NANOG, MYOD), antibodies, native proteins (cytochrome C), magnetic nanoparticles (MNPs), and nuclei
  
   109  bacteria, including Rhodobacter capsulatus, cytochrome c maturation (Ccm) is carried out by a membra
   110  in these PPR proteins resulted in defective cytochrome c maturation and activation of mitochondrial 
  
   112 e, with a low energy barrier, the release of cytochrome C may be readily achieved through energy fluc
  
   114 ork for understanding the molecular basis of cytochrome c-mediated blocking of SET/TAF-Ibeta, which s
  
  
  
   118 owed that the information on the chromophore cytochrome c obtained by resonance SIRM at 532 nm excita
   119 y, we analyzed Cu delivery to the cbb3 -type cytochrome c oxidase (cbb3 -Cox) of Rhodobacter capsulat
  
  
  
  
  
  
  
  
   128 T is assumed to rely on photon absorption by cytochrome c oxidase (CCO), the terminal enzyme in the m
  
  
   131  particular the cytochrome bc1 (complex III)-cytochrome c oxidase (complex IV) supercomplex (termed I
   132 present study, we found that the decrease in cytochrome c oxidase (COX) activity was ascribable to a 
   133 alized respiratory terminal oxidases (RTOs), cytochrome c oxidase (Cox) and cytochrome bd quinol oxid
   134 itochondrial protein with essential roles in cytochrome c oxidase (COX) assembly and the regulation o
   135 frequently associated with cardiomyopathy is cytochrome c oxidase (COX) deficiency caused by mutation
  
  
  
   139 sed mitochondrial iron loading and levels of cytochrome c oxidase (COX), which led to mitochondrial d
  
   141 ction by measuring H2O2, lipid peroxidation, cytochrome c oxidase activity and mitochondrial ATP.    
   142 s occur in mild hypoxia, where mitochondrial cytochrome c oxidase activity is unimpaired, suggesting 
   143 synthase activity was lower (P < 0.0001) and cytochrome c oxidase activity per Mt unit was higher (P 
  
  
   146 l density, mDNA/nDNA ratio), and functional (cytochrome c oxidase activity, ATP synthesis rate) marke
   147 ned AMP-dependent kinase activation improved cytochrome c oxidase activity, rescued the motor phenoty
  
  
  
   151 tected the activity of mitochondrial enzymes cytochrome c oxidase and aconitase in differentiating NS
  
   153 e bc1 complex in the absence of a functional cytochrome c oxidase and identify a supercomplex indepen
   154 pression of ATP synthase's catalytic domain, cytochrome c oxidase and its tyrosine phosphorylation, m
   155 al fragment of Rcf2 associate with monomeric cytochrome c oxidase and respiratory chain supercomplexe
   156  biochemical deconvolution cascade suggested cytochrome c oxidase as the potential target of IPE clas
  
   158  Our analyses show that Oms1 participates in cytochrome c oxidase assembly by stabilizing newly synth
   159 present in the promoter of the mitochondrial cytochrome c oxidase assembly gene (SCO2), which is crit
   160 dicate that KLF6-dependent regulation of the cytochrome c oxidase assembly gene is critical for maint
  
  
   163  the COX1 mRNA is coupled to the assembly of cytochrome c oxidase by a mechanism that involves Mss51.
  
  
  
  
   168 ociated with electron and proton transfer in cytochrome c oxidase could, in principle, be used to dis
   169 th MICOS disassembly, abnormal cristae, mild cytochrome c oxidase defect, and sensitivity to glucose 
  
  
  
  
  
   175 an 844 base pair region of the mitochondrial Cytochrome c oxidase gene, present at approximately 1 pp
   176 elevated expression of several mitochondrial cytochrome C oxidase genes, suggesting increased aerobic
   177 argeting short (127-314 bp) fragments of the cytochrome c oxidase I (CO1) DNA barcode region were dev
  
   179 in expression of the mitochondrially encoded cytochrome C oxidase I (MTCO1), complex I activity, and 
   180 techniques based on two mitochondrial genes (cytochrome c oxidase I and 16S rRNA) we prove the existe
  
   182  atomistic molecular dynamics simulations of cytochrome c oxidase in an explicit membrane-solvent env
   183 e a is an essential cofactor for function of cytochrome c oxidase in the mitochondrial electron trans
   184 on function (Q) of the redox center CuA from cytochrome c oxidase is attained by tuning the accessibi
   185 on of the protonation rate at the surface of cytochrome c oxidase is found when the lipid area surrou
   186 rmore, a reaction step that in the wild-type cytochrome c oxidase is linked to simultaneous proton up
  
   188 ong with a correlation between the number of cytochrome c oxidase operons and heterotrophic or diazot
  
   190  unravel the use of the mitochondrial marker cytochrome c oxidase subunit 1 (coxI) as barcode for Lon
   191  in a stretch of 22 identical amino acids in cytochrome c oxidase subunit 1 and NADH dehydrogenase su
   192 e KRIPP1 knockdown, A/U-tailed mRNA encoding cytochrome c oxidase subunit 1 declined concomitantly wi
  
  
  
   196 in the mtDNA [NADH dehydrogenase 6 (ND6) and cytochrome c oxidase subunit I (COI)] or nuclear DNA [ad
   197 tures) over a 6-mo period were identified by cytochrome c oxidase subunit I barcoding (>2-mm mobile o
   198      For the second objective, mitochondrial cytochrome c oxidase subunit I sequences of 16 individua
  
   200 ichiometric imbalance between mitochondrial (cytochrome c oxidase subunits 1 and 2) and nuclear (succ
   201 t the unusual sensitivity of skeletal muscle cytochrome c oxidase to sulfide poisoning in ethylmaloni
   202 pressions of mediators of energy metabolism (cytochrome c oxidase) and mediators of neuronal activity
  
   204 , whereas mice deficient in the synthesis of cytochrome c oxidase, which have reduced COX, were prote
  
   206 ions in individual muscle fibres with 20% of cytochrome c oxidase-deficient myofibres accumulating tw
  
  
  
  
  
   212 ated MT-CO2, the mtDNA-encoded subunit II of cytochrome c oxidase; and (3) reduced spare respiratory 
  
  
   215  the oxidation state of mitochondrial enzyme cytochrome-c-oxidase (oxCCO) have the potential to yield
  
  
  
  
   220 es the Rieske iron-sulfur protein subunit of cytochrome c oxidoreductase (complex III of the electron
  
   222 ndrial respiration via the energy-conserving cytochrome c pathway in both strains, the mutant was una
   223 idopsis (especially after restriction of the cytochrome c pathway) but cannot compensate for the lack
   224 re, we report the 1.5-A crystal structure of cytochrome c peroxidase (CCP) compound I (CmpI) using da
   225  A member of class I heme peroxidases [TcAPx-cytochrome c peroxidase (CcP)], suggesting both ascorbat
  
  
   228  The resulting oxygenation of cardiolipin by cytochrome c provides an early signal for the onset of a
  
  
   231 ytochrome bc1 :aa3 consists of a menaquinone:cytochrome c reductase (bc1 ) and a cytochrome aa3 -type
  
   233 c stimuli and increases the NO synthesis and cytochrome c reductase activities of eNOS, thereby enhan
   234 fide bond cross-link caused a >/=95% loss of cytochrome c reductase activity that was reversible with
   235 cient to explain the stimulation of both the cytochrome c reductase and NO synthase activities of eNO
  
   237 tween mitochondrial complexes III (ubiquinol-cytochrome c reductase; cyt. bc1) and IV (cytochrome c o
  
  
   240 ene (SCO2), which is critical for preventing cytochrome c release and activation of the intrinsic apo
  
  
   243 7 and mitochondrial translocation of Bax and cytochrome c release but not c-Jun N-terminal kinase act
   244 lium to ketamine resulted in apoptosis, with cytochrome c release from mitochondria and significant s
   245  against the accumulation and toxicity (i.e. cytochrome c release from mitochondria) of intracellular
  
  
  
   249 process that correlates with LFG blockage of cytochrome c release to the cytosol and caspase activati
   250  respiration, and ATP production and induced cytochrome c release, although the lack or inactivation 
  
   252 o the MOM bypasses the need for Mff to evoke cytochrome c release, and occludes the effect of SENP3 o
   253 tage-thresholds of mPT opening inferred from cytochrome c release, but intact cells showed no differe
   254 reactive oxygen species (ROS) production and cytochrome c release, indicating that lumican-induced di
   255 fragmentation, mitochondrial depolarization, cytochrome c release, reactive oxygen species generation
   256 K homo-oligomer formation thereby preventing cytochrome c release-mediated mitochondrial dysfunction.
  
  
  
  
  
  
   263  biochemical characterization, uncovered how cytochrome c releases the autoinhibition of Apaf-1 throu
  
  
  
  
  
   269 pathological changes and increased levels of cytochrome c, Smac/DIABLO and AIF in the cytosol while t
   270 ubunits: the catalytic CcoN subunit, the two cytochrome c subunits (CcoO and CcoP) involved in electr
   271 ccurs due to mutations in the human gene for cytochrome c that results in enhanced mitochondrial apop
  
   273 imilar to the previously reported results on cytochrome c, these fragment ions form near residues kno
  
  
   276 r binding affinity of rebaudioside A towards cytochrome c, thus supporting their host-guest relations
  
   278  occurs through the release of mitochondrial cytochrome c to the cytosol, where it promotes activatio
   279 ranslocates to the mitochondria and oxidizes cytochrome c to yield H2O2, which in turn initiates cell
   280 these findings provide new insights into the cytochrome c-tRNA interaction and apoptotic regulation. 
  
   282 obilities of single multiply charged ions of cytochrome c, ubiquitin, myoglobin, and bovine serum alb
   283  reactivity of the reduced FMN domain toward cytochrome c; (v) response to calmodulin binding; and (v
  
  
  
  
   288 s compound is a non-competitive inhibitor of cytochrome c When tested in cellular assays, ADDA 5 dose
   289 the SH3 domain, dihydrofolate reductase, and cytochrome c, where the transparent window vibrational p
   290 tion and inhibits the peroxidase activity of cytochrome c, which is involved in its release from mito
   291 ICR MS are explored with a tryptic digest of cytochrome c with both ECD and IRMPD as fragmentation mo
   292 on proceeds through selective interaction of cytochrome c with cardiolipin, resulting in protein unfo
  
  
  
   296 ion of a domain-swapped dimer of yeast iso-1-cytochrome c with the detergents, CYMAL-5, CYMAL-6, and 
  
   298 different proteins (Trp-cage, myoglobin, and cytochrome c) with folding time constants that differ by
  
   300  that only a modest deformation of monomeric cytochrome c would suffice to form the hydrocarbon bindi
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