ライフサイエンスコーパス: mitochondrial membrane depolarization

1 e induced by PA-LTx was followed by a strong mitochondrial membrane depolarization.

2 of Bak activation, cytochrome c release, and mitochondrial membrane depolarization.

3 ong, and Bcl-x(L) that were accompanied with mitochondrial membrane depolarization.

4 levels of the death receptor DR5 and caused mitochondrial membrane depolarization.

5 MAPK), and caspase-3 and was associated with mitochondrial membrane depolarization.

6 lease H(2)O(2), which can cause apoptosis by mitochondrial membrane depolarization.

7 disrupted plasma and acrosome membranes, and mitochondrial membrane depolarization.

8 sol is not a consequence of events requiring mitochondrial membrane depolarization.

9 spholipid asymmetry, caspase activation, and mitochondrial membrane depolarization.

10 to the cytosol followed by subsequent inner mitochondrial membrane depolarization.

11 DB treatment of HCC827 cells leads to mitochondrial membrane depolarization.

12 species generation, lipid peroxidation, and mitochondrial membrane depolarization.

13 RNA expression, and evoke cell death through mitochondrial membrane depolarization.

14 ficient Drosophila Schneider cells exhibited mitochondrial membrane depolarization, a 60% decrease in

15 cytochrome c and apoptosis-inducing factor, mitochondrial membrane depolarization, activation of a s

16 terized by concentration- and time-dependent mitochondrial membrane depolarization, activation of cas

17 Simvastatin attenuates mitochondrial membrane depolarization after exposure to

18 o safeguard mechanisms, induced by transient mitochondrial membrane depolarization and activation of

19 ibited mitochondrial respiration and induced mitochondrial membrane depolarization and apoptosis in a

20 elect lymphoma cell lines and induced potent mitochondrial membrane depolarization and apoptosis when

21 n treatment of cells led to a tumor-specific mitochondrial membrane depolarization and ATP depletion

22 both APT-1 and APT-1-TPP rescue DOX-induced mitochondrial membrane depolarization and ATP depletion

23 Because mitochondrial membrane depolarization and calcium are kn

24 posure to K5 ultimately led to apoptosis via mitochondrial membrane depolarization and caspase activa

25 l by these enzymes ultimately contributed to mitochondrial membrane depolarization and cell death.

26 th was caspase-dependent and associated with mitochondrial membrane depolarization and cytochrome c r

27 to proceed via a classical pathway involving mitochondrial membrane depolarization and cytochrome c r

28 Mitochondrial membrane depolarization and cytochrome c r

29 A interference, or genetic deletion prevents mitochondrial membrane depolarization and cytotoxicity i

30 -rosamine and Indo-1 revealed FimH-dependent mitochondrial membrane depolarization and elevated [Ca(2

31 DA receptor activation, leading to increased mitochondrial membrane depolarization and excitotoxic ce

32 ibition or gene silencing of TXN resulted in mitochondrial membrane depolarization and increased ROS

33 The mechanism involved mitochondrial membrane depolarization and inhibition of

34 membrane depolarization in synaptosomes, and mitochondrial membrane depolarization and nuclear apopto

35 nosine triphosphate (ATP) levels, leading to mitochondrial membrane depolarization and reduced mitoch

36 Other factors that regulated the mitochondrial membrane depolarization and subsequent los

37 HSC death conferred by NO occurred through mitochondrial membrane depolarization and through a casp

38 ecreased AKT phosphorylation at Ser-473, (2) mitochondrial membrane depolarization, and (3) activated

39 optotic events such as cytochrome c release, mitochondrial membrane depolarization, and activation of

40 cells showed extensive cytochrome c release, mitochondrial membrane depolarization, and caspase activ

41 affected mitochondrial respiration, elicited mitochondrial membrane depolarization, and disrupted mit

42 cell death was preceded by NAD(+) depletion, mitochondrial membrane depolarization, and MPT.

43 ic NMDA exposure triggers AIF translocation, mitochondrial membrane depolarization, and phosphatidyl

44 ase in the level of reactive oxygen species, mitochondrial membrane depolarization, and premature sen

45 phosphorylation of RyR2, SR Ca(2+) leak and mitochondrial membrane depolarization are critically inv

46 Ca(2+) overload, as a consequence of partial mitochondrial membrane depolarization by mitoK(ATP) chan

47 Low MOI reduced mitochondrial membrane depolarization, caspase-3 and cas

48 species (ROS) at the cellular level, causing mitochondrial membrane depolarization, cleavage of DNA,

49 the intracellular level of ROS and prevented mitochondrial membrane depolarization, correlating with

50 o significantly reduced H(2)O(2) generation, mitochondrial membrane depolarization, cytochrome c rele

51 following staurosporine treatment results in mitochondrial-membrane depolarization, cytochrome c rele

52 AT-101 also induced potent mitochondrial membrane depolarization (Delta Psi m) and

53 (reg) cell deficiencies, present with B cell mitochondrial membrane depolarization, elevated ROS and

54 cytes, HBx activation of NF-kappaB prevented mitochondrial membrane depolarization; however, when NF-

55 to Abeta resulted in caspase activation and mitochondrial membrane depolarization in dendrites and c

56 itochondrial respiratory chain and prevented mitochondrial membrane depolarization in response to a p

57 ndent neurotrophic support may contribute to mitochondrial membrane depolarization in sensory neurons

58 A caspase inhibitor prevented Abeta-induced mitochondrial membrane depolarization in synaptosomes, a

59 FRD produced mitochondrial membrane depolarization in WT mice but not

60 sis (defined by annexin V staining) prior to mitochondrial membrane depolarization, in contrast to cy

61 a(2+) levels and inhibited beta-Lap-mediated mitochondrial membrane depolarization, intracellular ATP

62 he mitochondrial response to stress, such as mitochondrial membrane depolarization, is increased in t

63 n of MATalpha1 K48 prevented ethanol-induced mitochondrial membrane depolarization, MATalpha1 depleti

64 LL-rearranged leukemia cells did not undergo mitochondrial membrane depolarization or apoptosis despi

65 occurrence of shared early events, including mitochondrial membrane depolarization, permeability tran

66 s, including phosphatidylserine exposure and mitochondrial membrane depolarization, PMN-SA had sustai

67 apoptosis to a non-apoptotic form, caused by mitochondrial membrane depolarization, probably initiate

68 with activation of c-Jun-N-terminal kinase, mitochondrial membrane depolarization, release of cytoch

69 All antineoplastic agents tested caused mitochondrial membrane depolarization that was inhibited

70 The mitochondrial membrane depolarization triggered proteoly

71 Mitochondrial membrane depolarization was detected in fl

72 However, mitochondrial membrane depolarization was not detected i

73 conditions of inflammatory stress and led to mitochondrial membrane depolarization, whereas inhibitio

74 nitiation of protein kinase C signaling, and mitochondrial membrane depolarization with resultant apo