ライフサイエンスコーパス: c-Jun protein

1 myristate 13-acetate induction of endogenous c-Jun protein.

2 resulting in highly increased c-Jun mRNA and c-Jun protein.

3 , suggesting that LT promotes degradation of c-Jun protein.

4 ransactivation of AP-1 when coexpressed with c-Jun protein.

5 a critical role in regulating the amount of c-Jun protein.

6 s showed that MG132 prevented degradation of c-Jun protein.

7 ving NF-kappaB p50 dimers and excluding AP-1 c-jun protein.

8 at contains c-fos, c-jun, and phosphorylated c-jun protein.

9 hibited by expression of a dominant-negative c-Jun protein.

10 ylation of c-Jun, and subsequent increase in c-Jun protein.

11 nd DNA binding similarities to the mammalian c-Jun protein.

12 phorylation of MKK-4, phosphorylated-JNK and c-Jun proteins.

13 ese DNA-protein complexes and both c-Fos and c-Jun proteins.

14 ptotic effector protein and stabilization of c-jun protein, a potent pro-death effector in certain ce

15 Most importantly, the increase in c-Jun protein accumulation occurs with no corresponding

16 indicate substantially earlier increases in c-jun protein after nerve injury than previously reporte

17 ransected fibres, or by immunoreactivity for c-jun protein, an indicator of injury and regeneration,

18 cid also induced the expression of c-Fos and c-Jun protein and AP-1 activity.

19 The expression and phosphorylation of c-Jun protein and apoptosis in RGCs were examined after

20 ic acids induced the expression of c-Fos and c-Jun protein and increased activating protein 1 (AP-1)

21 n c-Jun, JunB, and c-Fos mRNA, as well as in c-Jun protein and its phosphorylated form.

22 Mutational analyses of the c-Jun protein and the AP-1 binding site in the promoter

23 uman skin with tRA inhibited UV induction of c-Jun protein and, consequently, AP-1.

24 The resulting functional activity of c-Jun proteins appears to be critical for cell prolifera

25 and involves both increases in the levels of c-Jun protein as well as phosphorylation of specific ser

26 evious studies have shown that expression of c-Jun protein, as well as the c-Jun amino-terminal kinas

27 Plk3 in HCE cells to directly phosphorylate c-Jun proteins at phosphorylation sites Ser-63 and Ser-7

28 crease in c-Jun mRNA or the half-life of the c-Jun protein but, rather, in the translatability of the

29 n N-terminal kinase (JNK) and phosphorylated c-Jun protein, but not total JNK protein, in livers of e

30 ss that involves phosphorylation of existing c-JUN protein by JNK and subsequent auto-activation of t

31 t homology with the SAPK binding site of the c-Jun protein, called the delta domain.

32 It also increased levels of c-Jun protein, causing its phosphorylation.

33 d inflammation by maintaining the balance of c-Jun protein consumed during infection.

34 cate that LT reduces c-Jun both by promoting c-Jun protein degradation via inactivation of MKK1/2-Erk

35 In contrast, expression of c-Jun protein does not appear to be a reliable indicator

36 de and arachidonic acid-stimulated c-Fos and c-Jun protein expression and AP-1 activity.

37 l lines examined causes a robust increase in c-Jun protein expression and phosphorylation and a corre

38 Inhibition of JNK activation or c-Jun protein expression significantly reduced 1, 25(OH)

39 diated knockdown of endogenous SRF, ELK1 and c-JUN protein expression significantly reduced TPA-stimu

40 Cytokine-induced c-Fos and phospho-c-Jun protein expression was inhibited by LXR ligands an

41 Moreover, c-Fos and phospho-c-Jun protein expression was inhibited by PPARalpha agon

42 inases ERK1 and ERK2, induction of c-fos and c-jun protein expression, and an increase in transcripti

43 uction of cJun-proximal TCR-RE complexes and c-Jun protein expression.

44 resulted in a rapid and robust induction of c-Jun protein expression.

45 In this study, we show that c-Jun protein in fibroblasts regulates production and pa

46 utant were consistent with a higher level of c-Jun protein in MEKK1(-/-) cells than in corresponding

47 In addition, UVB induced both c-Fos and c-Jun proteins in B82K+ cells, whereas neither were indu

48 y and increased expression of c-jun mRNA and c-Jun protein; in contrast, sphingosine moderately stimu

49 ative way of measuring the time of course of c-jun protein induction following sciatic nerve transect

50 agonizes UV activation of AP-1 by inhibiting c-Jun protein induction.

51 c-Jun protein inhibition occurred via a posttranscriptio

52 Transcriptional activation of the c-Jun protein is dependent on its phosphorylation at Ser

53 However, neither the mechanism through which c-Jun protein is increased nor the level of its post-inj

54 gnal-regulated protein kinase (ERK), and the c-JUN protein kinase (JNK) in this phosphorylation event

55 apoptosis requires activation of N-terminal c-Jun protein kinase (JNK) that phosphorylates and inact

56 ignaling pathway that activates the SEK1/JNK/c-Jun protein kinase cascade.

57 ion of activated protein-1, stress-activated c-Jun protein kinase, and mitogen-activated protein kina

58 vation of PU.1 by Ras is blocked by a mutant c-Jun protein lacking the basic domain.

59 The reduced c-Jun protein level resulting from exogenous expression

60 ling the cells to maintain relatively normal c-Jun protein levels and cell proliferation.

61 her, these findings indicate that LT reduces c-Jun protein levels via two distinct mechanisms, thereb

62 ITPR2 and c-Jun protein levels were evaluated in Huh7 cells, in li

63 rbol ester, transient increases in c-Fos and c-Jun protein levels were observed at 2-4 h, followed by

64 ession of Mayven resulted in an induction of c-Jun protein levels, as well as increased AP-1 (activat

65 proteasome inhibitor MG132 largely restored c-Jun protein levels, suggesting that LT promotes degrad

66 ), p44/p42-MAPK/ERK1/2 (Thr-202/Tyr-204), or c-Jun protein levels.

67 prostate cancer, up-regulation of c-Fos and c-Jun proteins occurs in advanced disease and is correla

68 SAPK/JNK) pathway showed that phosphorylated c-Jun proteins, phosphorylated JNK proteins, and JNK act

69 ns of c-fos and c-jun, a 14-fold increase in c-Jun protein phosphorylation, and an increase in in vit

70 Interestingly, c-Jun protein rebounded to normal levels 4 h following U

71 AP-1 binding and c-Jun protein returned to basal levels in DRGs as periph

72 nificant increases in the phosphorylation of c-Jun protein (ser63).

73 change in the phosphorylation pattern of the c-jun protein, shifting that pattern from a Ser63/73 dom

74 footprinting analysis with purified Sp1 and c-jun proteins showed that Sp1 binding could facilitate

75 on contains an AP-1 site that binds JunB and c-Jun proteins specifically in Th2 cells and not in Th1

76 ificant increase in c-Jun mRNA abundance and c-Jun protein synthesis.

77 ATF-1; (iii) PGN induced phosphorylation of c-Jun, protein synthesis of JunB and c-Fos, and transcri

78 The c-Jun proteins that are early transcription factor molec

79 lcium contain Fra-1, Fra-2, Jun B, Jun D and c-Jun proteins that bind to the AP-1 DNA binding sequenc

80 ll death, while increased phosphorylation of c-Jun protein was associated with resistance to cell dea

81 c-Jun protein was first detected within 3 h of proximal

82 In the crypt, c-Jun protein was highly expressed in progenitor cells a

83 Increased amounts of phosphorylated c-Jun protein were also found with wtVT1 and anisomycin.

84 response element binding protein (CREB) and c-Jun proteins were included in the CRE binding complex.

85 Expression of Ha-Ras led to induction of c-Jun protein, which showed functional cooperation with

86 rk1/2 pathway inactivation similarly reduces c-Jun protein, which was also restored by MG132 pre-expo