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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.
8 c, as compared with those with nondetectable cytochrome c (11% versus 1%; P<0.001).
9 l mortality than patients with nondetectable cytochrome c (6% versus 1%; P<0.001).
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
13           The resulting cleavage coverage of cytochrome c almost matched data provided by high-resolu
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
17  apoptosis, as evidenced by early release of cytochrome c and caspase 3/7 activation.
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
20                              Upon binding to cytochrome c and dATP, Apaf-1 oligomerizes into a heptam
21 turing activation of caspase 3/7, release of cytochrome c and loss of cell membrane integrity.
22                                              Cytochrome c and other apoptotic factors are released fr
23                                              Cytochrome c and p53-related apoptosis mechanisms were i
24 ures of the formation of the complex between cytochrome c and SET/TAF-Ibeta.
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
29 how a reduction of mitochondrial components, cytochrome c, and cytochrome b.
30 in blocking apoptosis by reduction of ferric cytochrome c, and gentle tuning of NO concentration in t
31                                      CRALBP, cytochrome C, and GNB3 showed that the RPE interdigitati
32 apped, translated into a solution containing cytochrome c, and monitored for 3-NBS leakage.
33 esults constitute the molecular mechanism of cytochrome c- and dATP-mediated activation of Apaf-1.
34 y electrons that would normally be passed to cytochrome c are donated directly to O2.
35 gment-elevation AMI patients with detectable cytochrome c, as compared with those with nondetectable
36      The resulting model gives insights into cytochrome c binding, nucleotide exchange and conformati
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
39  a novel and unexpected protein required for cytochrome c biogenesis in this pathogen.
40 1207 are involved in, but not essential for, cytochromes c biogenesis.
41 oss section (CCS), akin to that observed for cytochrome c but proceeding more smoothly.
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
44             Here we mimic phosphorylation of cytochrome c by replacing tyrosine 48 with p-carboxy-met
45                                              Cytochrome c can acquire peroxidase activity when it bin
46                   It was recently shown that cytochrome c can induce pore formation in cardiolipin-co
47 e for the extended lipid anchorage model for cytochrome c/cardiolipin binding.
48  (CcP)], suggesting both ascorbate (Asc) and cytochrome c (Cc) peroxidase activity.
49 ESI-QTOF-MS technique, formation of glycated cytochrome C containing up to 12 glucose moieties were o
50        In the oxidized state, this tetraheme cytochrome c contains three hemes with axial His/Met lig
51 ria differed primarily at a Raman biomarker, cytochrome c, corresponding to a bacteroid-specific term
52                                  Biomolecule cytochrome c (Cty c), a small molecule of a chain of ami
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
57                                   CRALBP and cytochrome C (Cyt C) immunolabeling revealed that hyperr
58 vine serum albumin (BSA), lysozyme (lyz) and cytochrome c (cyt c) in singular and competitive manner
59                        It is well known that cytochrome c (Cyt c) is a crucial death regulator that t
60                                              Cytochrome c (cyt c) is a small soluble heme protein cha
61                                              Cytochrome c (Cyt c) is an important biomarker in cell l
62                                              Cytochrome c (Cyt c) is commonly used as intrinsic bioma
63 cytochrome c synthase (HCCS) is required for cytochrome c (cyt c) maturation and therefore respiratio
64                  The multifunctional protein cytochrome c (cyt c) plays key roles in electron transpo
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
67                   Globular proteins, such as cytochrome c (cyt c), display an organized native confor
68                                              Cytochrome c (cyt c), required for electron transport in
69 hieved using redox cofactors namely oxidized cytochrome-c (Cyt-c) and Co-enzyme-Q (Co-Q) immobilized
70              The mesh is functionalized with cytochrome-c (cyt-c) and incorporated as a working elect
71 as an oligopeptide stopper, we have employed cytochrome C (CytC) as a protein stopper to produce the
72                          The combined use of cytochrome c (CYTc) loss-of-function mutants and respira
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
77 y 20-fold larger than the previously studied cytochrome c dimer.
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
84 , which serves as the axial heme ligand when cytochrome c functions as an electron carrier.
85 and release of apoptosis-inducing factor and cytochrome c Furthermore, this protection was mediated b
86                                              Cytochrome C had multiple charges in non-glycated state,
87                                        Serum cytochrome c had no diagnostic utility for AMI (area und
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
91              Encapsulation of oxidized horse cytochrome c in 1-decanoyl-rac-glycerol/lauryldimethylam
92 ax pore facilitates future study of releases cytochrome C in atomic detail.
93 e of the cell covered biosensor by releasing Cytochrome C in cytoplasm.
94                  The distribution pattern of cytochrome c in individual cells was used as a measure o
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
98  models of the OMM, is investigated to probe cytochrome c-induced permeability.
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
101                                          How cytochrome C is released from the mitochondria to the cy
102                                Specifically, cytochrome c is shown to be translocated into cell nucle
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,
105                      The glycated species of cytochrome C, lysozyme, and beta-casein formed during gl
106                                              Cytochrome c [M + 5H](5+) ions present in one conformer
107  (NANOG, MYOD), antibodies, native proteins (cytochrome C), magnetic nanoparticles (MNPs), and nuclei
108 ologous, nucleus-, and mitochondrion-encoded cytochrome c maturase systems.
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
111  suggesting loss of the entire mitochondrial cytochrome c maturation pathway from Ophioglossum.
112 e, with a low energy barrier, the release of cytochrome C may be readily achieved through energy fluc
113         The Collision Cross Section (CCS) of cytochrome c measured with the TMIMS is in agreement wit
114 ork for understanding the molecular basis of cytochrome c-mediated blocking of SET/TAF-Ibeta, which s
115                      Mitochondrial biogenic (cytochrome c, mitochondrial transcription factor A), mor
116               The more extended [M + 7H](7+) cytochrome c monomer presents as two conformers undergoi
117                                              Cytochrome c nitrite reductases perform a key step in th
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
120                                              Cytochrome c oxidase (CcO) catalyzes the reduction of ox
121 on of the electron transport chain component cytochrome c oxidase (CcO) in cancer progression.
122                                              Cytochrome c oxidase (CcO) is a transmembrane protein th
123                                              Cytochrome c oxidase (CcO) is the last electron acceptor
124                                   The enzyme cytochrome c oxidase (CcO) or complex IV (EC 1.9.3.1) is
125                                              Cytochrome c oxidase (CcO) reduces oxygen to water and u
126                        Proton pumping A-type cytochrome c oxidase (CcO) terminates the respiratory ch
127                                              Cytochrome c oxidase (CcO), the terminal enzyme in the e
128 T is assumed to rely on photon absorption by cytochrome c oxidase (CCO), the terminal enzyme in the m
129                                Biogenesis of cytochrome c oxidase (CcO), the terminal enzyme of the m
130 ctor of the mitochondrial respiratory enzyme cytochrome c oxidase (CcO).
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
136                                              Cytochrome c oxidase (COX) was initially purified more t
137       Copper is required for the activity of cytochrome c oxidase (COX), the terminal electron-accept
138                                              Cytochrome c oxidase (COX), the terminal enzyme of the m
139 sed mitochondrial iron loading and levels of cytochrome c oxidase (COX), which led to mitochondrial d
140 tes to fail in the assembly of mitochondrial cytochrome c oxidase (COX).
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
144                                              Cytochrome c oxidase activity was significantly reduced
145 lls, for example, mitochondrial respiration, cytochrome c oxidase activity, and ATP production.
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
148                                              Cytochrome c oxidase activity, uncoupling protein 1 expr
149 itochondrial respiratory chain complex IV or cytochrome c oxidase activity.
150 he respiratory chain by up-regulation of the cytochrome c oxidase activity.
151 tected the activity of mitochondrial enzymes cytochrome c oxidase and aconitase in differentiating NS
152 tected the activity of mitochondrial enzymes cytochrome c oxidase and aconitase.
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
157                            The mitochondrial cytochrome c oxidase assembles in the inner membrane fro
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
161                            Here we isolate a cytochrome c oxidase assembly intermediate in preparator
162                                              Cytochrome c oxidase assembly requires the synthesis of
163  the COX1 mRNA is coupled to the assembly of cytochrome c oxidase by a mechanism that involves Mss51.
164 phism fingerprinting of the protein-encoding cytochrome c oxidase ccoN gene.
165 otein synthesis but rather have a problem in cytochrome c oxidase complex (COX) assembly.
166                              Deficiencies of cytochrome c oxidase complex IV, which reduces O2 in mit
167 x1, Cox2, and Cox3, comprise the core of the cytochrome c oxidase complex.
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
170 ble reduction of oxygen to bound peroxide at cytochrome c oxidase determining the net flux.
171                          Fluorophore-labeled cytochrome c oxidase displayed a similar increase when r
172                           Proton transfer in cytochrome c oxidase from the cellular inside to the bin
173                           Proton transfer in cytochrome c oxidase from the cellular inside to the bin
174                                 The ba3-type cytochrome c oxidase from Thermus thermophilus is a memb
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
178                       Here, metabarcoding of cytochrome c oxidase I (COI) region of mitochondrial DNA
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
181 nd decreased levels of mitochondrial complex cytochrome c oxidase I/IV and lower ATP levels.
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
187                    The O-->E intermediate of cytochrome c oxidase is the first redox state in its cat
188 ong with a correlation between the number of cytochrome c oxidase operons and heterotrophic or diazot
189                     Defects in mitochondrial cytochrome c oxidase or respiratory chain complex IV (CI
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
193  voltage-dependent anion channel (VDAC), and cytochrome c oxidase subunit 4 (COX IV).
194              Two DNA barcode regions, namely cytochrome c oxidase subunit I (COI) and cytochrome b (c
195 sed on a single mitochondrial locus, such as cytochrome c oxidase subunit I (COI).
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
199       Pyrosequencing of genetic marker, COI (cytochrome c oxidase subunit I) and subsequent sequence
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
203                      Conditional deletion of cytochrome c oxidase, the terminal enzyme in the respira
204 , whereas mice deficient in the synthesis of cytochrome c oxidase, which have reduced COX, were prote
205 d inhibition are significantly attenuated in cytochrome c oxidase-deficient mice.
206 ions in individual muscle fibres with 20% of cytochrome c oxidase-deficient myofibres accumulating tw
207 (2+) centres of soluble guanylate cyclase or cytochrome c oxidase.
208 m by association of the bc1 complex with the cytochrome c oxidase.
209 e a biosynthesis and/or transfer to maturing cytochrome c oxidase.
210 ation by potently inhibiting the heme-copper cytochrome c oxidase.
211 tner of Cox17 in transferring copper ions to cytochrome c oxidase.
212 ated MT-CO2, the mtDNA-encoded subunit II of cytochrome c oxidase; and (3) reduced spare respiratory
213 ol-cytochrome c reductase; cyt. bc1) and IV (cytochrome c oxidase; CytcO).
214                 Muscle studies showed global cytochrome-c oxidase deficiency in all patients tested a
215  the oxidation state of mitochondrial enzyme cytochrome-c-oxidase (oxCCO) have the potential to yield
216                                              Cytochrome c oxidases of facultative members of the comm
217                                    cbb3-type cytochrome c oxidases, which catalyze the terminal step
218                        Compared with reduced cytochrome c, oxidized cytochrome c binds to tRNA with a
219                                    Ubiquinol cytochrome c oxidoreductase (bc1 complex) serves as an i
220 es the Rieske iron-sulfur protein subunit of cytochrome c oxidoreductase (complex III of the electron
221 e, the flexible pore may selectively aid the cytochrome C passage.
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
226                                    Microbial cytochrome c peroxidases (Ccp) have been studied for 75
227                                     Although cytochrome c phosphorylation-in particular, at tyrosine
228  The resulting oxygenation of cardiolipin by cytochrome c provides an early signal for the onset of a
229                  When the vesicle-associated cytochrome c Raman spectrum is compared with a spectrum
230                                              Cytochrome c recognizes the tertiary structural features
231 ytochrome bc1 :aa3 consists of a menaquinone:cytochrome c reductase (bc1 ) and a cytochrome aa3 -type
232                                In this work, cytochrome c reductase (CcR) biofunctionalized self asse
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
236 function of the subunit b of the menaquinone:cytochrome c reductase.
237 tween mitochondrial complexes III (ubiquinol-cytochrome c reductase; cyt. bc1) and IV (cytochrome c o
238                tRNA binding both facilitates cytochrome c reduction and inhibits the peroxidase activ
239        Superoxide generation was measured by cytochrome C reduction in the presence and absence of N-
240 ene (SCO2), which is critical for preventing cytochrome c release and activation of the intrinsic apo
241 Bid interaction at mitochondria, suppressing cytochrome c release and apoptosis.
242 chondrial outer membrane (MOM), which causes cytochrome c release and apoptosis.
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
246 trinsic apoptosis inducer, c-FLIP suppressed cytochrome c release from mitochondria.
247                    Rifampicin also inhibited cytochrome c release from the mitochondria and caspase 3
248 ther confirmed by mitochondrial swelling and cytochrome c release induced by Ca(2+) overload.
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
251 e oxygen species generation, Bax activation, cytochrome C release, and apoptosis.
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.
257 ndrial translocation of BAX and BAX-mediated cytochrome c release.
258 ic interference with cristae remodelling and cytochrome c release.
259  XIAP occurs independently of Drp1-regulated cytochrome c release.
260 spases activation, Bcl-xL sequestration, and cytochrome c release.
261  both Drp1 binding to Mff and stress-induced cytochrome c release.
262 not lead to cerebral caspase-3 activation or cytochrome-c release.
263  biochemical characterization, uncovered how cytochrome c releases the autoinhibition of Apaf-1 throu
264                   At multivariable analysis, cytochrome c remained a significant independent predicto
265 ns of the inner mitochondrial membrane where cytochrome c resides.
266           The observation that tRNA binds to cytochrome c revealed a previously unexpected mode of ap
267                                              Cytochrome c serum concentrations do not have diagnostic
268                    We prospectively assessed cytochrome c serum levels at hospital presentation in 2
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
272 nted, display remodelled cristae and release cytochrome c, thereby driving apoptosis.
273 imilar to the previously reported results on cytochrome c, these fragment ions form near residues kno
274             Rather than inert passing of the cytochrome C through a rigid pore, the flexible pore may
275 insight in atomic detail into the release of cytochrome C through Bax oligomeric pores.
276 r binding affinity of rebaudioside A towards cytochrome c, thus supporting their host-guest relations
277 on distance of 11 nm, and delivering reduced cytochrome c to complex IV.
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.
281  have been studied only for the formation of cytochrome c-type hemoproteins.
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
284                  Direct electron transfer of cytochrome c was achieved on the CNT film electrode.
285          A muFFE separation of myoglobin and cytochrome c was also demonstrated on a 3D-printed devic
286 g 753 AMI patients in the prognostic cohort, cytochrome c was detectable in 280 (37%) patients.
287              The direct electron transfer by cytochrome c was further supported by HOMO-LUMO calculat
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
293          To verify selective interactions of cytochrome c with cardiolipin, these experiments were re
294             In this work, the interaction of cytochrome c with cardiolipin-containing phospholipid ve
295 effects of confinement on the interaction of cytochrome c with cardiolipin.
296 ion of a domain-swapped dimer of yeast iso-1-cytochrome c with the detergents, CYMAL-5, CYMAL-6, and
297 nerated by enzymatic digestion of the equine cytochrome c with trypsin.
298 different proteins (Trp-cage, myoglobin, and cytochrome c) with folding time constants that differ by
299                                 Reduction of cytochrome C would change the ionic state of the cells m
300  that only a modest deformation of monomeric cytochrome c would suffice to form the hydrocarbon bindi

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