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 ments and in sustained activation of p38 and JNK kinases.

7 2/3 and activation of the downstream IKK and JNK kinases.

8 olving the convergent action of two distinct JNK kinases.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

26 19 inhibits JNK kinase activity (IC(50) = 18 nM; K(i) = 1.5 nM) and

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

28 MKK4 ubiquitination required JNK kinase activity.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

59 1 (MEKK1) which activates the JNK activator, JNK kinase (JNKK), was similarly activated by antigen st

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

85 1-JNK/SAPK-c-Jun cascade (where JNKK/SEK1 is JNK kinase/SAPK kinase) was demonstrated by activation o

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

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

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

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

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

91 that additionally required serotonergic and Jnk kinase signaling pathways.

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

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

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

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