ライフサイエンスコーパス: JNK kinase

1 We show that JNKK2 is a highly specific JNK kinase.

2 ctivated protein kinases, including ERK1 and JNK kinase.

3 osphorylation of the upstream JNK activator, JNK kinase.

4 horylated the MAP kinase kinases, MEK 1, and JNK kinase.

5 the combined action of JAK, SRC, c-ABL, and JNK kinases.

6 pathophysiologic arm is mediated by p38 and Jnk kinases.

7 ments and in sustained activation of p38 and JNK kinases.

8 2/3 and activation of the downstream IKK and JNK kinases.

9 olving the convergent action of two distinct JNK kinases.

10 P3, UNC-16 physically interacts with JNK and JNK kinases.

11 (ERK1) and ERK2, p38, and c-Jun N-terminal (JNK) kinases.

12 iously identified c-Jun NH2-terminal kinase (JNK) kinase 1/mitogen-activated protein kinase (MAPK) ki

13 pression of catalytically inactive mutant of JNK kinase 2 (JNKK2(AA)).

14 ctivation by MEKK2 was mediated by the MAPKK JNK kinase 2 (JNKK2) rather than by JNKK1 through format

15 ession of a catalytically inactive mutant of JNK kinase 2 and RNA interference of stress-activated pr

16 results demonstrate that cisplatin activates JNK kinase 3.8 +/- 0.2-fold more efficiently in DNA mism

17 Inhibitors of ERK1/2 and JNK kinases abolished and significantly decreased H. pyl

18 ila IkappaB kinase-activating kinase and the JNK kinase-activating kinase.

19 n contrast, OPGL enhanced both NF-kappaB and JNK kinase activation and increased the expression of c-

20 g RNA knockdown established that the p38 and JNK kinase activation following DeltaE3L infection was d

21 ion, and attenuated v-Src-stimulated ERK and JNK kinase activation.

22 CDC42HsN17 prevented S. typhimurium-induced JNK kinase activation.

23 tor activation in neurons, including PKC and JNK kinases activation, elevation of somatic and dendrit

24 se 2 (ERK2) and c-Jun NH(2)-terminal kinase (JNK) kinase activation.

25 Rac1 blockade inhibits p38/JNK kinase activities and the spontaneous anoikis of D4-

26 ine revealed that active Rac3 drives Pak and JNK kinase activities by two separate pathways.

27 or LY294002 decreased cell survival, Akt and JNK kinase activities, ets-2 phosphorylation, and Bcl-x

28 19 inhibits JNK kinase activity (IC(50) = 18 nM; K(i) = 1.5 nM) and

29 Inhibition of JNK kinase activity using dominant-negative constructs r

30 The PPP-CNP activated MLK3, its downstream JNK kinase activity, and down-regulated AKT pathway sign

31 MKK4 ubiquitination required JNK kinase activity.

32 ption factors responding to stress-activated JNK kinases and also for the Cdt1 licensing factor that

33 ally expressed, CIKS stimulates IKK and SAPK/JNK kinases and it transactivates an NF-kappaB-dependent

34 lular regulated (ERK), and c-jun N-terminal (JNK) kinases and induced AP-1 activation.

35 he Ras/mitogen-activated protein kinase, Rac/JNK kinase, and phosphatidylinositol 3-kinase (PI-3 kina

36 Rgr induces phosphorylation of ERKs, p38 and JNK kinases, and increases the levels of the GTP-bound f

37 urthermore, the activation of the ERK1/2 and JNK kinases, as well as the transcription factor NF-kapp

38 s activation of FGF receptors and of ERK and JNK kinases, because it can be blocked by inhibitors of

39 ciating c-Src tyrosine kinase and downstream JNK kinase by pharmacological and molecular means suppre

40 Dominant-negative versions of JNK kinase, c-Jun, and IKK beta interfered In CD3- plus

41 lator in the HPK1 --> TAK1 --> MKK4/SEK1 --> JNK kinase cascade and indicate the involvement of JNK i

42 nd that MLK3 mediates activation of MEKK-SEK-JNK kinase cascade by Rac1 and Cdc42.

43 ) family, suggesting that stimulation of the JNK kinase cascade can lead to caspase activation.

44 and that the HGK --> TAK1 --> MKK4, MKK7 --> JNK kinase cascade may mediate the TNF-alpha signaling p

45 PB induction, nor is activation of the SAPK/JNK kinase cascade responsible for down-regulating PB re

46 xpression led to the suppression of the MKK4/JNK kinase cascade.

47 nduce activation of c-Jun N-terminal kinase (JNK) kinase cascades, it is not known whether they utili

48 Expression of dominant negative JNK kinases decreased cPLA(2) promoter activity in NSCLC

49 Mechanistically, the JNK kinases directly bind to and phosphorylate PIN1 at S

50 ed expression of MKP5, a JNK phosphatase, in JNK kinase-expressing cells decreased T81 phosphorylatio

51 tion of JNK1 and JNK2 genes or inhibition of JNK kinase function rendered Delta24RGD-treated cells re

52 nM), excellent selectivity against ROCK and JNK kinases (>400-fold), potent inhibition of cofilin ph

53 Although the activation of JNK kinase has been implicated in BRCA1-induced apoptosi

54 Also, we found that loss of ben, but not the JNK kinase hemipterous, resulted in an upregulation of h

55 odule, as it is blocked by null mutations in JNK kinase [hemipterous (hep)] and JNK [basket (bsk)].

56 s of Basket (Bsk), or of one of the upstream JNK kinases, Hemipterous or Mkk4, these axons overextend

57 In contrast, wild-type MEKK1 or JNK kinase induced NF-kappaB activation alone or in comb

58 sitol 3 kinase inhibitor Wortmannin, and the JNK kinase inhibitor SP600125.

59 protein kinase kinase inhibitors), SP600125 (JNK kinase inhibitor), and wortmannin (phosphatidylinosi

60 phosphorylated, was inhibited by SP600125, a JNK kinase inhibitor.

61 lls requires activation of a Ras/Rac1/MEKK-1/JNK kinase/JNK signal transduction leading to phosphoryl

62 However, inhibition of JNK kinase (JNKK) in ras-transformed cells with normally

63 K kinase 1 (MEKK1) activity, which activates JNK kinase (JNKK), the kinase that phosphorylates and ac

64 1 (MEKK1) which activates the JNK activator, JNK kinase (JNKK), was similarly activated by antigen st

65 ared by hep mutant animals, deficient in the JNK kinase (JNKK/MKK7) substrate for SLPR, suggesting th

66 However, coexpression of JNK kinase kinase (MEKK) effectively increased JNK activ

67 SEK)-1 and suppressed by a dominant negative JNK kinase kinase (MEKK)-1.

68 Using inducible dominant-active (DA) JNK kinase kinase (MEKK1) expression in Jurkat cells, we

69 Daxx was found to activate the JNK kinase kinase ASK1, and overexpression of a kinase-d

70 ch can be reversed by over-expression of the JNK kinase kinase Wnd.

71 In contrast, the dominant-active JNK kinase kinase, MEKK1, induced CD28RE/AP-1 luciferase

72 mal JNK-scaffold POSH (Plenty-of-SH3s) and a JNK kinase kinase, TAK1, in regulating growth activation

73 es (MLKs) function as Jun-N-terminal kinase (JNK) kinase kinases to transduce extracellular signals d

74 In this study we show that a JNK kinase known as the stress-activated protein kinase/

75 he downstream phosphorylated Chk1, Chk2, and JNKs, kinases known to inactivate cdc25C.

76 sponse to T-cell activation, the Jun kinase (JNK) kinase MAP kinase kinase 7 (MKK7) is alternatively

77 KC, MLCK, cyclin G-associated kinase, EphA1, JNK kinase, MAP kinase 1), phosphatases (meprin, PTPK, p

78 s suggest that ligand-directed activation of JNK kinases may generally provides an alternate mode of

79 e male and the induction of apoptosis by the JNK kinase, MEKK1.

80 idence suggests two c-Jun N-terminal kinase (JNK) kinases, MKK4 and MKK7, transactivate JNK, in vivo

81 ated antiapoptotic factor GADD45beta and the JNK kinase MKK7 as a therapeutic target in MM.

82 add45beta depends on direct targeting of the JNK kinase, MKK7/JNKK2.

83 ated protein kinase kinase kinase 1 (MEKK1), JNK kinase, or JNK inhibits NF-kappaB activation by thio

84 as dominant-negative mutants of MAPK kinase, JNK kinase, or Ras completely blocked strain-dependent r

85 Transient expression of a kinase inactive JNK kinase partially inhibited induction of SM-alpha-act

86 assembly by promoting dissociation, while a JNK kinase pathway and AZ assembly proteins inhibit diss

87 Interestingly, our analysis reveals that the JNK kinase pathway plays a crucial role in the tyrosine

88 MEKK1, an upstream activator of the ERK and JNK kinase pathway, but not induced following p53 expres

89 e kinase known to activate the ERK, p38, and JNK kinase pathways.

90 hibitors to assess whether c-Jun N-terminal (JNK) kinases regulate hepatitis C virus (HCV) replicatio

91 mutations in Caenorhabditis elegans JNK and JNK kinases result in similar mislocalization of synapti

92 1-JNK/SAPK-c-Jun cascade (where JNKK/SEK1 is JNK kinase/SAPK kinase) was demonstrated by activation o

93 directly phosphorylating and activating the JNK kinase SEK-1 (MKK4 and -7).

94 co-transfection with a constitutively active JNK kinase (SEK)-1 and suppressed by a dominant negative

95 H 3T3 cells when a dominant-negative form of JNK kinase, Sek1/MKK4 is expressed in these cells.

96 for Rac1 in activation of the prodeath MLK3-JNK kinase signaling pathway and delayed neuronal cell d

97 Activation of NFkappaB, Erk, and JNK kinase signaling pathways were inhibited in a VopS-d

98 that additionally required serotonergic and Jnk kinase signaling pathways.

99 egulated kinase and c-Jun N-terminal kinase (JNK) kinase stimulation by TNFalpha.

100 s is regulated by Mg(2+), PI(3,5)P2, and P38/JNK kinases, thus paralleling regulation of TPC2 current

101 n component of AP-1; whilst agonists of SAPK/JNK kinases trigger transient N-terminal phosphorylation

102 NKG2D-induced activation of JNK kinase was also blocked by inhibitors of Src protein