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1 ion channel, adenine nucleotide translocase, cyclophilin D).
2 KT binds to the mitochondrial matrix protein cyclophilin D.
3 e, whereas NIM811 blocks by interaction with cyclophilin D.
4 al upregulation of its activating component, cyclophilin D.
5 oes not provide the site of interaction with cyclophilin D.
6 n be inhibited by cyclosporin A mediated via cyclophilin D.
7 er may involve the peptidyl prolyl isomerase cyclophilin D.
8 ndrial permeability transition by binding to cyclophilin D.
9 t the protection was lost in neurons lacking cyclophilin D.
10 xygen species (ROS) and the participation of cyclophilin D, a component of the mitochondrial permeabi
11 m(s) by eliminating ubiquitous expression of cyclophilin D, a critical regulator of Ca(2+)-mediated o
12     Triple knockout mice lacking Bax/Bak and cyclophilin D, a key regulator of necrosis, fail to show
13                     Mechanistically, loss of cyclophilin D, a regulator of the mitochondrial permeabi
14 +) retention in brain mitochondria, and that cyclophilin D ablation abolished this effect.
15                                Surprisingly, cyclophilin D ablation completely abolished the phenotyp
16                As anticipated, we found that cyclophilin D ablation markedly increased Ca(2+) retenti
17 unique mechanism involving the regulation of cyclophilin D activity, a component of the mitochondrial
18                                            A cyclophilin-D affinity matrix was employed to isolate co
19 was bound to glutathione-agarose to form the cyclophilin-D affinity matrix.
20       Double-knockout mice lacking MCL-1 and cyclophilin D, an essential regulator of the mPTP, exhib
21               These chaperones interact with Cyclophilin D, an immunophilin that induces mitochondria
22                 Combined genetic blockade of cyclophilin D and acid sphingomyelinase renders the high
23               Both pathways were mediated by cyclophilin D and led to mitochondrial depolarization an
24 rial permeability transition pore (MPTP) via cyclophilin D and p53 as mechanisms of EPHOSS.
25 with the loss of interaction between ANT and cyclophilin D and the inability of ANT to adopt the cyto
26                                        Thus, cyclophilin D and the mitochondrial permeability transit
27                                        Thus, cyclophilin D and the mitochondrial permeability transit
28 pecific deficiency in central pathways of PA-cyclophilin D and transmembrane protein 16F-were more re
29                                 Accordingly, cyclophilin-D and mPTP were increased in heterozygous he
30  nuclear, p53, PEPCK1, superoxide dismutase, cyclophilin D, and Hsp10, and analyzed the deacetylation
31 member-induced cell death does not depend on cyclophilin D, and Ppif null fibroblasts are not protect
32 nthase complex promoted its interaction with cyclophilin D, and sensitized the opening of mitochondri
33  are formed via regulated necrosis involving cyclophilin D, and that they may be targeted independent
34  and anti-apoptotic BAX-BCL2 protein family, cyclophilin D, and the adenine nucleotide (ADP/ATP) tran
35 creased, whereas Hsp10, Hsp60, Hsp70, Hsp75, cyclophilin D, and voltage-dependent anion channel did n
36  nucleotide translocase (inner membrane) and cyclophilin-D, and forms at contact sites between the tw
37 the mitochondrial cis-trans prolyl isomerase cyclophilin D as in wild-type cells, indicating that cyc
38 ized that acetylation of mitochondrial CypD (cyclophilin D) at K166 contributes to endothelial dysfun
39                         It is concluded that cyclophilin D binding to the permeability transition por
40  HAX-1 were mediated through interference of cyclophilin-D binding to heat shock protein-90 (Hsp90) i
41 tical mitochondrial proteins mitofusin 2 and cyclophilin D, but not of transcription factor A of mito
42 nvestigated the submitochondrial location of cyclophilin D by following the fate of radiolabelled pro
43 PR formation is shear-dependent and requires cyclophilin D, calpain, and Rac1 activation.
44 lin D as in wild-type cells, indicating that cyclophilin D can modulate mPTP through substrates other
45 lar dystrophy, suggesting that inhibition of cyclophilin D could provide a new pharmacologic treatmen
46        However, this occurs independently of cyclophilin D (cyclosporine A insensitive) rather it is
47 arges the c-subunit ring and unhooks it from cyclophilin D/cyclosporine A binding sites in the ATP sy
48 he mitochondrial calcium uniporter (MCU) and cyclophilin D (CyD) are key players in induction of the
49  HFD-induced adipose tissue inflammation and cyclophilin D (CyP-D)-null mice that are protected again
50                                              Cyclophilin-D (Cyp-D) is a mitochondrial matrix peptidyl
51  the mitochondrial peptidyl prolyl isomerase cyclophilin-D (Cyp-D) reduces Vo(2).
52 library of 256,000 drug-like macrocycles for cyclophilin D (CypD) affinity.
53  of diverse neuronal mitochondrial functions cyclophilin D (CYPD) and mitofusin-2 (MFN2), leucine zip
54 of these genetically verified regulators are cyclophilin D (CypD) and the adenine nucleotide transloc
55 rix may activate the mitochondrial chaperone cyclophilin D (CypD) and trigger permeability transition
56                                              Cyclophilin D (CypD) appears to be a critical component
57                ER-000444793 neither affected cyclophilin D (CypD) enzymatic activity, nor displaced o
58                                              Cyclophilin D (CypD) is a mitochondrial immunophilin and
59                                              Cyclophilin D (CypD) is a mitochondrial matrix peptidyl-
60                                              Cyclophilin D (CypD) is a mitochondrial protein that fac
61                                              Cyclophilin D (CypD) is a peptidyl-prolyl isomerase expr
62                                        While Cyclophilin D (CypD) is a well-characterized regulator o
63             The mitochondrial matrix protein cyclophilin D (CypD) is an essential component of the mi
64                                              Cyclophilin D (CyPD) is thought to sensitize opening of
65 Ppif-/-) of the mitochondrial matrix protein cyclophilin D (CypD) prevents perinatal KET-induced incr
66 drial permeability transition pore regulator cyclophilin D (CypD) promotes NGSIS, but not glucose-sti
67                                              Cyclophilin D (CypD) promotes opening of the mitochondri
68 production, while within ATP synthase is the cyclophilin D (CypD) regulated mitochondrial permeabilit
69 ficient for the mitochondrial matrix protein cyclophilin D (CypD) show robust protection from PVI dys
70 nknown component that requires the chaperone cyclophilin D (CypD) to activate.
71  protein 60 (Hsp60) directly associates with cyclophilin D (CypD), a component of the mitochondrial p
72                           Cells deficient in cyclophilin D (CypD), a component of the MPTP, are resis
73 ious studies have shown that cysteine 203 of cyclophilin D (CypD), a critical mPTP mediator, undergoe
74 oimmune encephalomyelitis (EAE) mice lacking cyclophilin D (CyPD), a key regulator of the mitochondri
75         We aimed at inhibiting mitochondrial cyclophilin D (CypD), a key regulator of the mPT, as a p
76 ng mice with a platelet-specific deletion of cyclophilin D (CypD), a mediator of necrosis, we found t
77 inhibition of the mitochondrial MAM protein, cyclophilin D (CypD), altered insulin signaling in mouse
78                            In the absence of cyclophilin D (CypD), an essential regulator of MPTP for
79  mitochondrial permeability transition pore, cyclophilin D (CypD), influenced endothelial metabolism
80 tween ANT3 and the peptidyl-prolyl isomerase cyclophilin D (CypD), mortalin decreased mitochondrial p
81 ion of adenine nucleotide translocase (ANT), cyclophilin D (CypD), or mitochondrial Ca(2+) uniporter
82                                              Cyclophilin D (CypD), the peptidylprolyl isomerase F (PP
83               The PTP is regulated by matrix cyclophilin D (CyPD), which also binds the lateral stalk
84 mitochondrial single-channel patch clamp and cyclophilin D (CypD)-deficient mice (Ppif (-/-)) with st
85        Here, we report an unexplored role of cyclophilin D (CypD)-dependent mitochondrial permeabilit
86 by which p53 activates the key mPT regulator cyclophilin D (CypD).
87 ochondria inner pore permeability regulator, Cyclophilin D (CypD).
88 ant platelets, is impaired in the absence of cyclophilin D (CypD).
89  physical interaction with the PTP regulator cyclophilin D (CypD).
90 , adenine nucleotide translocator (ANT), and cyclophilin D (CyPD).
91  that deletion or reduction in the levels of cyclophilin D (CypD, also called Ppif), a mitochondrial
92                                              Cyclophilin D (CypD, encoded by Ppif) is an integral par
93 r mitochondrial Ca(2+) retention, similar to cyclophilin D (CypD, PPIF) knockdown with sustained Delt
94                The peptidylprolyl isomerase, cyclophilin D (CypD, PPIF), is a positive regulator of t
95 utcome of this approach was the finding that cyclophilin D deletion enhanced the R6/2 brain mitochond
96                         Mouse models lacking cyclophilin D demonstrate convincingly that cyclophilin
97  and mitochondrial damage are prevented in a cyclophilin D-dependent manner.
98  mediating mitochondrial depolarization in a cyclophilin D-dependent manner.
99                     Our study identified the cyclophilin D-dependent mitochondrial proton leak and un
100 l intermittent hypoxic (IH) stress activated cyclophilin D-dependent mitochondrial proton leak and un
101 ice deficient in peptidylprolyl isomerase D (cyclophilin D, encoded by Ppid) by administration of L-a
102 ted R6/2 mice with normal, reduced or absent cyclophilin D expression and examined the effect of incr
103                               Suppression of cyclophilin-D expression or enforced detachment of hexok
104 ow expression of a glutathione S-transferase/cyclophilin-D fusion protein in Escherichia coli XL1 cel
105  with megakaryocyte-directed deletion of the cyclophilin D gene.
106                      In the adult rat brain, cyclophilin D immunoreactivity was abundant in neurons b
107 gh two pathways: modulation of mitochondrial cyclophilin D, implicated in mitochondrial permeability
108 by Mg(2+)/ADP; (ii) that expression of human cyclophilin D in mitochondria of Drosophila S2R(+) cells
109                           The high levels of cyclophilin D in neuronal mitochondria result in their g
110 rdiomyocyte-specific transgene expression of cyclophilin D in Ppif(-/-) mice rescued the enhanced hyp
111 e primarily the result of the high levels of cyclophilin D in synaptic mitochondria, reflecting the g
112 ed mice lacking Ppif and mice overexpressing cyclophilin D in the heart.
113                                          The cyclophilin-D in the fusion was functionally normal as j
114 heterozygous hearts, but genetic ablation of cyclophilin-D in these hearts significantly alleviated t
115  (translocase of outermembrane 40) and CypD (cyclophilin D) in grade III and grade IV HD patients and
116 KT-mediated cell death involve dynamin-2 and cyclophilin D, in a process that can be prevented by the
117                               Similarly, the cyclophilin D-inhibiting drug alisporivir and the acid s
118 -induced mPTP opening and desensitization by cyclophilin D inhibition.
119 ochondrial ATP synthase but still blocked by cyclophilin D inhibition.
120 ermeability transition pore opening with the cyclophilin D inhibitor cyclosporin A restored Deltapsi(
121                                            A cyclophilin D inhibitor, cyclosporine A, disrupts the Cy
122  in the pyrrolidine headgroup of a series of cyclophilin D inhibitors gives a dramatic enhancement in
123                                              Cyclophilin D inhibitors that prevent opening of the mit
124 peripheral stalk, provides the site at which cyclophilin D interacts.
125                                              Cyclophilin D is a mitochondrial protein that promotes m
126  cyclophilin D demonstrate convincingly that cyclophilin D is an essential component and a key regula
127                                Inhibition of cyclophilin D is protective against glucocorticoid-induc
128        An X-ray structure of 33 bound to rat cyclophilin D is reported.
129                                     To date, cyclophilin D is the only confirmed component of mPTP.
130  A mitochondrial isoform in mammalian cells, cyclophilin D, is a component of the permeability transi
131                              Mitochondria of cyclophilin D knockout mice are particularly resistant t
132  The transients were absent in cultures from cyclophilin D knockout mice, leaving the slow depolariza
133 hibitor cyclosporine A, sanglifehrin, and in cyclophilin D knockout mice.
134                Improved exercise capacity in cyclophilin-D knockout mice associated with enhanced oxy
135                       Compared with WT mice, cyclophilin D-knockout littermates did not develop bioen
136 These pathologic responses were abrogated in cyclophilin D-knockout mice.
137 the two mitochondrial fractions, we compared cyclophilin D levels in primary cortical neurons and ast
138  Primary rat cortical neurons possess higher cyclophilin D levels than do primary astrocytes.
139              Mechanistically, alterations in cyclophilin-D levels by HAX-1 were contributed by the ub
140 re attributed to specific down-regulation of cyclophilin-D levels leading to reduction in mPTP activa
141 dings reveal the role of HAX-1 in regulating cyclophilin-D levels via an Hsp90-dependent mechanism, r
142 AX-1 overexpressing cardiomyocytes increased cyclophilin-D levels, as well as mPTP activation upon ox
143 ion, whereas proteosomal inhibition restored cyclophilin-D levels.
144 tochondria following import established that cyclophilin D locates only to the matrix.
145  nucleotide translocase (inner membrane) and cyclophilin-D (matrix) assembles at contact sites betwee
146 ase functionality, but it was independent of cyclophilin-D-mediated mitochondrial permeability transi
147 tant mitochondrial calcium overload triggers cyclophilin-D-mediated necrosis.
148 nificant reduction in fibrin accumulation in cyclophilin D-/-mice.
149 defined by the requirement for mitochondrial cyclophilin D nor to autophagy as defined by the require
150 ynaptic mitochondria were greatly reduced in cyclophilin D null [Ppif-/- (peptidylprolyl isomerase F)
151  examined the effects of genetic ablation of cyclophilin D on gender differences in mice expressing G
152 erfusion-induced cell death in vivo, whereas cyclophilin D-overexpressing mice show mitochondrial swe
153 rs including reactive oxygen species, matrix cyclophilin D, Pi (inorganic phosphate), and matrix pH.
154  such as adenine nucleotide translocator and cyclophilin D (possibly voltage-dependent anion channel)
155                                              Cyclophilin D (PPIF or CypD) is a peptidyl-prolyl cis-tr
156 e we show that deletion of the gene encoding cyclophilin D (Ppif) rendered mitochondria largely insen
157 revents ROS-elicited necrosis by suppressing cyclophilin D (PPIF), a regulator of ROS escape from mit
158 ne derivatives targeted to the mitochondrial cyclophilin D protein.
159 o an in vitro expressed mature protein and a cyclophilin D purified from rat heart mitochondria.
160  Genetic ablation of the Ppif gene, encoding cyclophilin D, restored beta-cell mass and decreased TUN
161                     Targeted deletion of the cyclophilin D subunit of the mPT complex abrogated the e
162 PTP opening persists in the absence of CypD (cyclophilin D), suggesting the existence of a CypD-indep
163  reported sirtuin substrate proteins such as cyclophilin D, superoxide dismutase, and PEPCK1 were not
164 ed that striatal mitochondria contained more cyclophilin D than cortical mitochondria.
165 ator, a voltage-dependent anion channel, and cyclophilin D (the Ppif gene product), a prolyl isomeras
166 avage of integrin-associated proteins and by cyclophilin D/TMEM16F-dependent phospholipid scrambling.
167 ions of cyclosporine A, which interacts with cyclophilin D to delay mPTP opening, were necessary to i
168                HAX-1 overexpression enhanced cyclophilin-D ubiquitination, whereas proteosomal inhibi
169 mponents that modulate PTP activity, such as cyclophilin D, voltage-dependent anion channel, adenine
170 n contrast, the ectopic expression of ANT or cyclophilin D was effective at preventing cell death.
171                             Precursor [(35)S]cyclophilin D was expressed in vitro from a PCR-generate
172 ndrial buffering of Ca(2+) in the absence of cyclophilin D was maintained throughout disease course a
173                              A cDNA encoding cyclophilin-D was cloned from a rat liver library and li
174   Synaptic mitochondria had higher levels of cyclophilin D when compared with nonsynaptic mitochondri
175                                              Cyclophilin D (which is encoded by the Ppif gene) is a m
176 sporin A inhibits pore opening by binding to cyclophilin D, which interacts with the pore.
177 d uncoupling was not affected by deletion of cyclophilin D, which is a component of the permeability
178  sirtuin-3 activity led to the activation of cyclophilin-D, which mediated an increased binding of he
179 he pathway involving enhanced interaction of cyclophilin D with ATP synthase mediates L-arginine-indu

 
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