ライフサイエンスコーパス: stress kinase

1 vity, but, instead, was dependent on the p38 stress kinase.

2 , which is not associated with activation of stress kinases.

3 tivation kinetics for the MAP3K MLK3 and JNK stress kinases.

4 ion of oxidative stress and its signaling to stress kinases.

5 3 kinase/Akt signaling and the activation of stress kinases.

6 e in hepatotoxicity, we examined the role of stress kinases.

7 activation of any of four diverse eIF2alpha stress kinases.

8 ein phosphatases in balancing the effects of stress kinases.

9 tested couple to activation of NFkappaB and stress kinases.

10 s provide new insight into the regulation of stress kinases.

11 portant for its stabilization in response to stress kinases activated following selective stress cond

12 dging fibrosis and associated with increased stress kinase activation and apoptosis.

13 kinase activation, supporting a link between stress kinase activation and apoptotic cell death in the

14 sensitize the cells to apoptosis induction, stress kinase activation and cell cycle arrest in respon

15 In addition, increased c-jun N-terminal stress kinase activation colocalized with aberrant tau i

16 viruses, we demonstrate a critical role for stress kinase activation in cell intrinsic and extrinsic

17 rst, markedly reduced CXCL1-induced NASH and stress kinase activation in HFD-fed mice.

18 Thus, early stress kinase activation initiated by TNF plays a key ro

19 astrocytes, including proteasome inhibition, stress kinase activation, mechanistic target of rapamyci

20 RAF promotes ERK activation, while RAF1 dims stress kinase activation.

21 CM-induced renal cell apoptosis by reducing stress kinases activation and (2) restored the survival

22 nd JNK, which indicated that the MHV-induced stress-kinase activation was not restricted to any parti

23 ve against oxidative damage and can decrease stress kinase activity, was decreased in the striatum of

24 to amplification in the activity of the p38 stress kinase and a diminution in the activity of the an

25 at-fed mice manifested striking induction of stress kinase and neural inflammasome activation at 3 mo

26 ed with palmitate (CM-P), phosphorylation of stress kinases and endoplasmic reticulum stress signalin

27 response, inasmuch as (i) the activation of stress kinases and gene expression in response to UV req

28 bypassed direct activation of the eIF2alpha stress kinases and instead relied on the inhibition of t

29 TNFalpha -induced apoptosis by inhibition of stress kinases and provide the first evidence that AKT i

30 g, generating more homogeneous activation of stress kinases and reducing apoptosis.

31 checkpoint is primarily mediated by the p38 stress kinases and requires the Chfr protein that is abs

32 actin stability is coordinately regulated by stress kinases and the ubiquitin-proteasomal network.

33 of receptor-associated kinase(s), NFkappaB, stress kinases, and transcription.

34 Stress kinases are well-described elements of the respon

35 al cellular RNA analyses have shown that the stress kinase ATM and the transcription factor p53 are i

36 , which could be attenuated by inhibitors of stress kinases but also by actinomycin D-inhibitor of tr

37 a suggest that the coordinated regulation of stress kinases by GSTp, as reflected by increased p38, E

38 In contrast, the activation of the stress kinases by hyperosmolarity, by the DNA-cross-link

39 The results also show that CDDO activates stress kinases by increasing levels of reactive oxygen s

40 both the cytotoxicity and the activation of stress kinases by palytoxin, we found that palytoxin is

41 ation of c-Jun NH(2)-terminal kinase and p38 stress kinases by PD169316 completely blocked all signs

42 nd Delta Hsp72EEVD blocked activation of the stress kinase c-jun N-terminal kinase (JNK) by TNF, and

43 Here, we demonstrate that the stress kinase c-Jun NH(2)-terminal kinase 1 (JNK1) is re

44 ion initiation factor 2alpha (eIF2alpha) and stress kinase c-Jun NH2-terminal kinase 1 (JNK1) (all P

45 ver, 3-AP and 3-AP-Me activated the cellular stress kinases c-Jun N-terminal kinase (JNK) and p38 mit

46 preceded by increased phosphorylation of the stress kinases c-Jun N-terminal kinase and p38, and of a

47 metal-inducible and stress-inducible genes, stress kinase cascades, and apoptosis.

48 eactivation events are dependent on cellular stress kinase DLK but independent of histone demethylase

49 a 2-fold increase in phosphorylation of the stress kinase ERK in control (but not Ames dwarf) mice a

50 ose inflammation via activation of JAK-STAT, stress kinases (ERK1/2, P38, JNK), and release of multip

51 ) and inhibitor of kappaB kinase (IKK-beta), stress kinases implicated in insulin resistance, and upr

52 The stimulation of stress kinases in arrestin double knockout cells could b

53 ant for the regulation of c-myc stability by stress kinases in response to selective stress condition

54 Furthermore, several major stress kinases involved in the development of Alzheimer'

55 phorylation of the key endoplasmic reticulum stress kinases IRE1alpha and PERK (PKR-like ER kinase) a

56 nt activation of Jun N-terminal kinase (JNK) stress kinase is a necessary step, licensing TBK1 phosph

57 randed RNA-activated protein kinase (PKR), a stress kinase, is involved in HIV/gp120-associated neuro

58 loss of plasma membrane integrity include a stress kinase JNK activated at early steps of recovery f

59 a significant increase in activation of the stress kinase JNK and production of the matrix metallopr

60 ROS and the stress kinase JNK mediate the accumulation of matrix met

61 In contrast, suppression of stress kinase JNK rendered cells thermoresistant.

62 provide the first evidence that AKT inhibits stress kinase JNK through activation of the NF kappa B p

63 ury is mediated in part by activation of the stress kinase JNK, but whether MIF modulates JNK in this

64 shock protein Hsp72 involves suppression of stress kinase JNK, we suggested that Hsp72-mediated JNK

65 lation of phosphorylated active forms of the stress kinase JNK.

66 itive AMPK and activates the redox-sensitive stress kinase JNK.

67 cell death through a mechanism involving the stress kinase JNK.

68 e that anisomycin, a potent activator of the stress kinase JNK/SAPK, can induce Bcl2 phosphorylation

69 ng through p75NTR requires activation of the stress kinase, JNK.

70 e stimuli often correlates with induction of stress kinases, Jun-NH2 kinase (JNK).

71 ncurrent with drug-induced activation of the stress kinases, known to be linked with cell death pathw

72 phorylation and subsequent activation of p38 stress kinase, leading to Cdc25A degradation.

73 ng that the activation of the aforementioned stress kinases maintain breast acinar structures as part

74 ression in response to p38 but not the other stress kinase, N-terminal Jun kinase (JNK); p38-activati

75 results demonstrate that early activation of stress kinases or change of cellular redox states plays

76 s activation of multiple caspases and of the stress kinase p38 and c-Jun NH2-terminal kinase (JNK) wa

77 ies in Fancc(-/-) BM cells overactivates the stress kinase p38 and requires prolonged activation of t

78 m SB203580 and siRNA experiments suggest the stress kinase p38 is important for Ran gradient recovery

79 tion of Rho-associated kinase (ROCK) and the stress kinase p38, leads to further p53 elevation, causi

80 ve ERK activity as well as inhibition of the stress kinase p38.

81 of ERK1/2, as well as phosphorylation of the stress kinases p38 and c-Jun N-terminal protein kinase.

82 AKT/FOXO3 pathway by redox activation of the stress kinases p38 and JNK is instrumental in neuronal d

83 ependent induction of ASK1 and activation of stress kinases p38 and JNK.

84 r MP-induced p42/p44 MAPK, activation of the stress kinases p38 and JNK1 was PKC-independent.

85 (IKK)/nuclear factor kappaB (NF-kappaB) and stress kinase (p38 and c-Jun N-terminal kinase [JNK]) pa

86 L-3 from dependent lymphocytes activates the stress kinase, p38 MAPK, which phosphorylates Cdc25A, in

87 cells correlates with the activation of the stress kinases, p38 mitogen-activated protein (MAP) kina

88 Stress-induced activation of another stress-kinase, p38 (HOG1), is also blocked when the leve

89 Here we identify the stress kinase p38alpha as a nononcogenic signaling molec

90 ion and degradation of IkappaBalpha) and the stress kinase pathway (phosphorylation of ATF-2, p38, an

91 NF-kappaB and stress kinase pathway activation were determined by immu

92 evidence was found for activation of the JNK stress kinase pathway.

93 as a critical regulator of the NF-kappaB and stress kinase pathways and thus a key intermediary in ce

94 r SB203580 blocks OHT.ER-induced cell death, stress kinase pathways are likely involved.

95 hough TNF-alpha stimulates the NF-kappaB and stress kinase pathways in HSF, these effects of TNF-alph

96 h axonal transport is sufficient to activate stress kinase pathways initiating a biochemical cascade

97 cal changes that induce activation of axonal stress kinase pathways leading to abnormal tau hyperphos

98 Specifically, the stress kinase pathways p38 and JNK were modified in late

99 s as a scaffold to activate both the IKK and stress kinase pathways.

100 may mediate cross talk between the PI3K and stress kinase pathways.

101 include mitochondrial dysfunction, oxidative stress, kinase pathways, calcium dysregulation, inflamma

102 onse, specifically the endoplasmic reticulum stress kinase PERK.

103 The stress kinase PKR has been shown to phosphorylate B56alp

104 lly, inhibition of the endoplasmic reticulum stress kinase prior to TMAO treatment blocked all effect

105 uded activation of the endoplasmic reticulum stress kinase protein kinase R-like endoplasmic reticulu

106 molecular switch to initiate and amplify the stress kinase response in the TNF-alpha signaling pathwa

107 se embryonic fibroblasts deficient in the ER stress kinase RNA-activated protein kinase-like ER-resid

108 change in constitutively active Akt, or low-stress kinase signaling in ML-1 cells.

109 P and its processing by gamma-secretase, and stress kinase signaling pathways.

110 cysteine proteases also function to regulate stress kinase signalling cascades.

111 signalling pathways related to activation of stress kinases, similar to those observed in Alzheimer's

112 TLR4-dependent activation of the Ste20-type stress kinase SPAK, which binds, phosphorylates, and sti

113 In ischemic tissues, stress kinases such as c-Jun N-terminal kinases (JNKs),

114 utrophil infiltration, oxidative stress, and stress kinase (such as apoptosis signal-regulating kinas

115 hway leading to downstream signaling by this stress kinase to LKB1 and AMPK kinases, and activation o

116 Specific stress stimuli prompt dedicated stress kinases to phosphorylate eukaryotic initiation fa

117 eas retinoid agonists such as CD437 activate stress kinases via inhibition of the phosphatase MKP-1,

118 hepatic oxidative stress and its associated stress kinases via the induction of metallothionein, one

119 To map c-myc domains that are responsive to stress kinases, we monitored changes in the level of c-m

120 ed reactive oxygen species and activation of stress kinases, which can be reversed by IL-22 treatment

121 ole of ATF2 in this process, suggesting that stress kinases, which contribute to regulation of ATF2 s

122 ediated effects on the ribosome activate the stress kinases ZAKalpha and p38, which in turn drive an