ライフサイエンスコーパス: c-Jun N-terminal kinase 1

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1 al-regulated protein kinase 2 (ERK2) but not c-Jun N-terminal kinase 1.

2 ism dependent on the selective activation of c-Jun N-terminal kinase 1.

3 Activation of c-Jun N-terminal kinase 1/2 (JNK) can delay oxidant-indu

4 We also found that silencing c-Jun N-terminal kinase 1/2 (JNK1/2) decreased PARP-1 ub

5 38, while no discernible increase in phospho-c-Jun N-terminal kinase 1/2 (JNK1/2) levels was observed

6 orylation, whereas the activation of p38 and c-Jun N-terminal kinase 1/2 kinases were unaffected.

7 10 delta(D910A/D910A) NK cells had a reduced c-Jun N-terminal kinase 1/2 phosphorylation in response

8 and STAT5 were unaffected, but activation of c-Jun N-terminal kinase 1/2 was delayed.

9 ch depends on the phosphorylation of p38 and c-Jun N-terminal kinase 1/2.

10 c-Jun-N-terminal kinase 1/2 (JNK1/2) activation is a cau

11 ticulum (ER) stress induction and subsequent c-jun-N-terminal kinase 1/2 (JNK1/2) activation.

12 Additionally, IkappaB kinase beta and c-Jun N-terminal kinase 1 activation in THP-1 cells indu

13 sequentially by discoidin domain receptor 1, c-Jun N-terminal kinase 1, and phosphorylated JunB, whic

14 the extracellular regulated kinase (ERK) 2, c-Jun N-terminal kinase 1 (JNK), and p38 kinase.

15 iNOS induction were paralleled by increased c-Jun N-terminal kinase 1 (JNK-1) phosphorylation.

16 c-Jun N-terminal kinase-1 (JNK-1) is a stress-regulated

17 ng extracellular regulated kinase-2 (Erk-2), c-Jun N-terminal kinases-1 (JNK-1), and p38.

18 acellular signal-regulated kinase 1 [ERK-1], c-Jun N-terminal kinase 1 [JNK-1], and p38 MAPK) from ei

19 Furthermore, inhibition or deletion of c-jun N-terminal kinase 1 (JNK1) abrogated PUMA inductio

20 ion of Mn-superoxide dismutase and XIAP, and c-Jun N-terminal kinase 1 (JNK1) activation.

21 itively identified yet, we have examined the c-Jun N-terminal kinase 1 (JNK1) activity on p53 by expr

22 nses mediated by TLR1/2 heterodimers through c-Jun N-terminal kinase 1 (JNK1) activity.

23 nals via protein : protein interactions with c-Jun N-terminal kinase 1 (JNK1) and ASK1 (apoptosis sig

24 ibitory effect on autophagy via reduction of c-Jun N-terminal kinase 1 (JNK1) and B-cell lymphoma 2 (

25 t MAP kinase activity but can stimulate both c-Jun N-terminal kinase 1 (JNK1) and ERK6/p38 gamma.

26 lar-signal regulated kinase 1/2 (ERK1/2) and c-jun N-terminal kinase 1 (JNK1) and/or JNK2, but not p3

27 Here, we show that mice lacking c-Jun N-terminal kinase 1 (JNK1) exhibit reduced patholo

28 oxin, nocodazole) stimulated the activity of c-jun N-terminal kinase 1 (JNK1) in MCF-7 cells.

29 The increased superoxide content induces c-Jun N-terminal kinase 1 (JNK1) kinase activity, which

30 ellular signal-regulated kinase 2 (ERK2) and c-Jun N-terminal kinase 1 (JNK1) MAPK in EGF-stimulated

31 lvement of mitogen-activated protein kinase, c-Jun N-terminal kinase 1 (JNK1), and extracellular sign

32 ignal-regulated protein kinases (ERK1/2) and c-Jun N-terminal kinase 1 (JNK1), and have shown that ov

33 ar signal-regulated protein kinase 2 (ERK2), c-jun N-terminal kinase 1 (JNK1), and p38.

34 utant of Erk2 or p38 kinase, but not that of c-Jun N-terminal kinase 1 (JNK1), blocked UVB-induced Ak

35 we found that the genetic loss of the MAPK, c-Jun N-terminal kinase 1 (JNK1), enhances IL-10 product

36 imer formation, which in turn blocked JNKK2, c-Jun N-terminal kinase 1 (JNK1), extracellular signal-r

37 n, hypoglycemic treatment strongly activated c-Jun N-terminal kinase 1 (JNK1), leading to the phospho

38 ented by a dominant negative mutant of ERK2, c-Jun N-terminal kinase 1 (JNK1), or p38 kinase and in k

39 kinase (SEK), which regulate the activity of c-Jun N-terminal kinase 1 (JNK1).

40 ignal-regulated protein kinase 2 (ERK2), and c-Jun N-terminal kinase 1 (JNK1).

41 or dominant negative forms of Vav, Rac1, and c-Jun N-terminal kinase-1 (JNK1).

42 signal-regulated kinase 1/2 (ERK1/2) but not c-Jun N-terminal kinase-1 or p38 MAP kinase was observed

43 gulated kinase 1/2 (phospho-ERK) and phospho-c-Jun N-terminal kinase 1 (phospho-JNK) in the striatum

44 NTT4/Rxt1), enzymes (aryl sulfotransferase, c-jun N-terminal kinase 1, serum/glucocorticoid-induced

45 n increased phosphorylation of Akt, p38, and c-Jun N-terminal kinase 1 that was also beta2-integrin d

46 mitogen-activated protein kinase gamma, and c-Jun N-terminal kinase 1), which in turn might be due t

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