ライフサイエンスコーパス: cyclophilin D

1 ion channel, adenine nucleotide translocase, cyclophilin D).

2 e, whereas NIM811 blocks by interaction with cyclophilin D.

3 oes not provide the site of interaction with cyclophilin D.

4 er may involve the peptidyl prolyl isomerase cyclophilin D.

5 ndrial permeability transition by binding to cyclophilin D.

6 t the protection was lost in neurons lacking cyclophilin D.

7 n be inhibited by cyclosporin A mediated via cyclophilin D.

8 KT binds to the mitochondrial matrix protein cyclophilin D.

9 m(s) by eliminating ubiquitous expression of cyclophilin D, a critical regulator of Ca(2+)-mediated o

10 Triple knockout mice lacking Bax/Bak and cyclophilin D, a key regulator of necrosis, fail to show

11 Mechanistically, loss of cyclophilin D, a regulator of the mitochondrial permeabi

12 +) retention in brain mitochondria, and that cyclophilin D ablation abolished this effect.

13 Surprisingly, cyclophilin D ablation completely abolished the phenotyp

14 As anticipated, we found that cyclophilin D ablation markedly increased Ca(2+) retenti

15 unique mechanism involving the regulation of cyclophilin D activity, a component of the mitochondrial

16 A cyclophilin-D affinity matrix was employed to isolate co

17 was bound to glutathione-agarose to form the cyclophilin-D affinity matrix.

18 Double-knockout mice lacking MCL-1 and cyclophilin D, an essential regulator of the mPTP, exhib

19 These chaperones interact with Cyclophilin D, an immunophilin that induces mitochondria

20 Combined genetic blockade of cyclophilin D and acid sphingomyelinase renders the high

21 Both pathways were mediated by cyclophilin D and led to mitochondrial depolarization an

22 rial permeability transition pore (MPTP) via cyclophilin D and p53 as mechanisms of EPHOSS.

23 with the loss of interaction between ANT and cyclophilin D and the inability of ANT to adopt the cyto

24 Thus, cyclophilin D and the mitochondrial permeability transit

25 Thus, cyclophilin D and the mitochondrial permeability transit

26 Accordingly, cyclophilin-D and mPTP were increased in heterozygous he

27 nuclear, p53, PEPCK1, superoxide dismutase, cyclophilin D, and Hsp10, and analyzed the deacetylation

28 member-induced cell death does not depend on cyclophilin D, and Ppif null fibroblasts are not protect

29 nthase complex promoted its interaction with cyclophilin D, and sensitized the opening of mitochondri

30 are formed via regulated necrosis involving cyclophilin D, and that they may be targeted independent

31 and anti-apoptotic BAX-BCL2 protein family, cyclophilin D, and the adenine nucleotide (ADP/ATP) tran

32 creased, whereas Hsp10, Hsp60, Hsp70, Hsp75, cyclophilin D, and voltage-dependent anion channel did n

33 nucleotide translocase (inner membrane) and cyclophilin-D, and forms at contact sites between the tw

34 It is concluded that cyclophilin D binding to the permeability transition por

35 HAX-1 were mediated through interference of cyclophilin-D binding to heat shock protein-90 (Hsp90) i

36 nvestigated the submitochondrial location of cyclophilin D by following the fate of radiolabelled pro

37 PR formation is shear-dependent and requires cyclophilin D, calpain, and Rac1 activation.

38 lar dystrophy, suggesting that inhibition of cyclophilin D could provide a new pharmacologic treatmen

39 arges the c-subunit ring and unhooks it from cyclophilin D/cyclosporine A binding sites in the ATP sy

40 HFD-induced adipose tissue inflammation and cyclophilin D (CyP-D)-null mice that are protected again

41 Cyclophilin-D (Cyp-D) is a mitochondrial matrix peptidyl

42 rix may activate the mitochondrial chaperone cyclophilin D (CypD) and trigger permeability transition

43 Cyclophilin D (CypD) appears to be a critical component

44 ER-000444793 neither affected cyclophilin D (CypD) enzymatic activity, nor displaced o

45 Cyclophilin D (CypD) is a mitochondrial immunophilin and

46 Cyclophilin D (CypD) is a mitochondrial matrix peptidyl-

47 The mitochondrial matrix protein cyclophilin D (CypD) is an essential component of the mi

48 Cyclophilin D (CyPD) is thought to sensitize opening of

49 production, while within ATP synthase is the cyclophilin D (CypD) regulated mitochondrial permeabilit

50 protein 60 (Hsp60) directly associates with cyclophilin D (CypD), a component of the mitochondrial p

51 Cells deficient in cyclophilin D (CypD), a component of the MPTP, are resis

52 ious studies have shown that cysteine 203 of cyclophilin D (CypD), a critical mPTP mediator, undergoe

53 oimmune encephalomyelitis (EAE) mice lacking cyclophilin D (CyPD), a key regulator of the mitochondri

54 We aimed at inhibiting mitochondrial cyclophilin D (CypD), a key regulator of the mPT, as a p

55 inhibition of the mitochondrial MAM protein, cyclophilin D (CypD), altered insulin signaling in mouse

56 In the absence of cyclophilin D (CypD), an essential regulator of MPTP for

57 mitochondrial permeability transition pore, cyclophilin D (CypD), influenced endothelial metabolism

58 The PTP is regulated by matrix cyclophilin D (CyPD), which also binds the lateral stalk

59 mitochondrial single-channel patch clamp and cyclophilin D (CypD)-deficient mice (Ppif (-/-)) with st

60 Here, we report an unexplored role of cyclophilin D (CypD)-dependent mitochondrial permeabilit

61 by which p53 activates the key mPT regulator cyclophilin D (CypD).

62 ochondria inner pore permeability regulator, Cyclophilin D (CypD).

63 ant platelets, is impaired in the absence of cyclophilin D (CypD).

64 physical interaction with the PTP regulator cyclophilin D (CypD).

65 , adenine nucleotide translocator (ANT), and cyclophilin D (CyPD).

66 that deletion or reduction in the levels of cyclophilin D (CypD, also called Ppif), a mitochondrial

67 Cyclophilin D (CypD, encoded by Ppif) is an integral par

68 r mitochondrial Ca(2+) retention, similar to cyclophilin D (CypD, PPIF) knockdown with sustained Delt

69 The peptidylprolyl isomerase, cyclophilin D (CypD, PPIF), is a positive regulator of t

70 utcome of this approach was the finding that cyclophilin D deletion enhanced the R6/2 brain mitochond

71 Mouse models lacking cyclophilin D demonstrate convincingly that cyclophilin

72 and mitochondrial damage are prevented in a cyclophilin D-dependent manner.

73 mediating mitochondrial depolarization in a cyclophilin D-dependent manner.

74 ice deficient in peptidylprolyl isomerase D (cyclophilin D, encoded by Ppid) by administration of L-a

75 ted R6/2 mice with normal, reduced or absent cyclophilin D expression and examined the effect of incr

76 Suppression of cyclophilin-D expression or enforced detachment of hexok

77 ow expression of a glutathione S-transferase/cyclophilin-D fusion protein in Escherichia coli XL1 cel

78 with megakaryocyte-directed deletion of the cyclophilin D gene.

79 In the adult rat brain, cyclophilin D immunoreactivity was abundant in neurons b

80 gh two pathways: modulation of mitochondrial cyclophilin D, implicated in mitochondrial permeability

81 by Mg(2+)/ADP; (ii) that expression of human cyclophilin D in mitochondria of Drosophila S2R(+) cells

82 The high levels of cyclophilin D in neuronal mitochondria result in their g

83 rdiomyocyte-specific transgene expression of cyclophilin D in Ppif(-/-) mice rescued the enhanced hyp

84 e primarily the result of the high levels of cyclophilin D in synaptic mitochondria, reflecting the g

85 ed mice lacking Ppif and mice overexpressing cyclophilin D in the heart.

86 The cyclophilin-D in the fusion was functionally normal as j

87 heterozygous hearts, but genetic ablation of cyclophilin-D in these hearts significantly alleviated t

88 (translocase of outermembrane 40) and CypD (cyclophilin D) in grade III and grade IV HD patients and

89 KT-mediated cell death involve dynamin-2 and cyclophilin D, in a process that can be prevented by the

90 Similarly, the cyclophilin D-inhibiting drug alisporivir and the acid s

91 ermeability transition pore opening with the cyclophilin D inhibitor cyclosporin A restored Deltapsi(

92 A cyclophilin D inhibitor, cyclosporine A, disrupts the Cy

93 peripheral stalk, provides the site at which cyclophilin D interacts.

94 Cyclophilin D is a mitochondrial protein that promotes m

95 cyclophilin D demonstrate convincingly that cyclophilin D is an essential component and a key regula

96 An X-ray structure of 33 bound to rat cyclophilin D is reported.

97 A mitochondrial isoform in mammalian cells, cyclophilin D, is a component of the permeability transi

98 Mitochondria of cyclophilin D knockout mice are particularly resistant t

99 The transients were absent in cultures from cyclophilin D knockout mice, leaving the slow depolariza

100 hibitor cyclosporine A, sanglifehrin, and in cyclophilin D knockout mice.

101 These pathologic responses were abrogated in cyclophilin D-knockout mice.

102 the two mitochondrial fractions, we compared cyclophilin D levels in primary cortical neurons and ast

103 Primary rat cortical neurons possess higher cyclophilin D levels than do primary astrocytes.

104 Mechanistically, alterations in cyclophilin-D levels by HAX-1 were contributed by the ub

105 re attributed to specific down-regulation of cyclophilin-D levels leading to reduction in mPTP activa

106 dings reveal the role of HAX-1 in regulating cyclophilin-D levels via an Hsp90-dependent mechanism, r

107 AX-1 overexpressing cardiomyocytes increased cyclophilin-D levels, as well as mPTP activation upon ox

108 ion, whereas proteosomal inhibition restored cyclophilin-D levels.

109 tochondria following import established that cyclophilin D locates only to the matrix.

110 nucleotide translocase (inner membrane) and cyclophilin-D (matrix) assembles at contact sites betwee

111 ase functionality, but it was independent of cyclophilin-D-mediated mitochondrial permeability transi

112 defined by the requirement for mitochondrial cyclophilin D nor to autophagy as defined by the require

113 ynaptic mitochondria were greatly reduced in cyclophilin D null [Ppif-/- (peptidylprolyl isomerase F)

114 examined the effects of genetic ablation of cyclophilin D on gender differences in mice expressing G

115 erfusion-induced cell death in vivo, whereas cyclophilin D-overexpressing mice show mitochondrial swe

116 rs including reactive oxygen species, matrix cyclophilin D, Pi (inorganic phosphate), and matrix pH.

117 such as adenine nucleotide translocator and cyclophilin D (possibly voltage-dependent anion channel)

118 e we show that deletion of the gene encoding cyclophilin D (Ppif) rendered mitochondria largely insen

119 revents ROS-elicited necrosis by suppressing cyclophilin D (PPIF), a regulator of ROS escape from mit

120 o an in vitro expressed mature protein and a cyclophilin D purified from rat heart mitochondria.

121 Genetic ablation of the Ppif gene, encoding cyclophilin D, restored beta-cell mass and decreased TUN

122 Targeted deletion of the cyclophilin D subunit of the mPT complex abrogated the e

123 reported sirtuin substrate proteins such as cyclophilin D, superoxide dismutase, and PEPCK1 were not

124 ed that striatal mitochondria contained more cyclophilin D than cortical mitochondria.

125 ator, a voltage-dependent anion channel, and cyclophilin D (the Ppif gene product), a prolyl isomeras

126 avage of integrin-associated proteins and by cyclophilin D/TMEM16F-dependent phospholipid scrambling.

127 ions of cyclosporine A, which interacts with cyclophilin D to delay mPTP opening, were necessary to i

128 HAX-1 overexpression enhanced cyclophilin-D ubiquitination, whereas proteosomal inhibi

129 mponents that modulate PTP activity, such as cyclophilin D, voltage-dependent anion channel, adenine

130 n contrast, the ectopic expression of ANT or cyclophilin D was effective at preventing cell death.

131 Precursor [(35)S]cyclophilin D was expressed in vitro from a PCR-generate

132 ndrial buffering of Ca(2+) in the absence of cyclophilin D was maintained throughout disease course a

133 A cDNA encoding cyclophilin-D was cloned from a rat liver library and li

134 Synaptic mitochondria had higher levels of cyclophilin D when compared with nonsynaptic mitochondri

135 Cyclophilin D (which is encoded by the Ppif gene) is a m

136 d uncoupling was not affected by deletion of cyclophilin D, which is a component of the permeability

137 sirtuin-3 activity led to the activation of cyclophilin-D, which mediated an increased binding of he

138 he pathway involving enhanced interaction of cyclophilin D with ATP synthase mediates L-arginine-indu