ライフサイエンスコーパス: jun gene

1 th factor (EGF) induction of a transfected c-jun gene.

2 tivation is increased transcription of the c-jun gene.

3 n cells that harbor a null mutation in the c-jun gene.

4 wn-regulation, respectively, of the GR and c-jun genes.

5 Weight loss reduced expression of FOS and JUN genes and down-regulated oxidative stress pathways a

6 If the products of the c-fos and/or c-jun genes are essential components in the cascade of eve

7 JNK and subsequent auto-activation of the c-JUN gene by recruitment of c-JUN and ATF2 to two AP-1 si

8 observation that AP-1 sequences within the c-JUN gene can function as transcriptional amino acid-resp

9 The junD gene contains no introns and generates a single mRN

10 c-jun gene deletion reduced c-Src expression, hyperactivat

11 la homolog of the mammalian proto-oncogene c-Jun gene (Djun).

12 s indicate that heat shock activates c-Fos/c-Jun gene expression and AP-1 DNA binding and suggests th

13 on is followed by an increase in c-fos and c-jun gene expression and enhanced activating protein 1 (A

14 The induction of c-fos and c-jun gene expression by bFGF or by PMA was blocked by the

15 n has been linked to prolonged activation of jun gene expression by the cytokine.

16 A dose-dependent upregulation of c-fos and c-jun gene expression by the PKC activator PMA was also ob

17 suggested that up-regulation of c-fos and c-jun gene expression does not directly contribute to the

18 cate that exogenous bFGF induces c-fos and c-jun gene expression in cultured rat Muller cells through

19 creases in c-fos in the mNTS and cRVLM and c-jun gene expression in the mNTS and rRVLM caused by NP-e

20 e that the coordinate regulation of GR and c-jun gene expression is dose-dependent and cell type-spec

21 Induction of c-fos and c-jun gene expression started at a bFGF concentration of 0

22 The temporal pattern of c-jun gene expression was similar to that of c-fos, wherea

23 DAC inhibitors suppressed the induction of c-jun gene expression, resulting in reduced COX-2 transcri

24 or, did not inhibit bFGF-induced c-fos and c-jun gene expression, whereas forskolin (5 microM), an ad

25 PMA transiently increases egr-1 and c-jun gene expression.

26 ound to the c-Jun promoter and upregulated c-Jun gene expression.

27 vity and an efficient inducer of c-fos and c-jun gene expression.

28 es multiple layers of control that safeguard junD gene expression and functional activity.

29 P-1) activity results from the activation of junD gene expression and plays a critical role in regula

30 Polyamines negatively regulate junD gene expression posttranscriptionally, and increase

31 hal; therefore, transgenic mice encoding a c-Jun gene flanked by LoxP sites (c-jun(f/f)) were used.

32 These findings indicate that the c-jun gene has a biphasic response to hypoxia consisting o

33 To determine the role of the endogenous c-jun gene in apoptosis, we performed mammary epithelial c

34 uates the expression of the closely linked c-jun gene in neurons implicated in centrally mediated hyp

35 ers at nucleotide resolution along the human JUN gene in normal fibroblasts and found very efficient

36 moter and transcribed sequences of the human JUN gene in UV-irradiated diploid fibroblasts.

37 is needed for the expression of the GR and c-jun genes in F9 cells.

38 al kinase/stress-activated protein kinase, c-jun gene induction, activation of caspase-3/CPP32-like p

39 JunD levels by ectopic overexpression of the junD gene or by depleting cellular polyamines repressed

40 acetylase 1 (HDAC1) and recruits it to the c-Jun gene promoter, resulting in an inhibition of histone

41 l level by its direct association with the c-jun gene promoter.

42 The expression of the endogenous c-jun gene, regulated through a promoter-proximal AP-1-bin

43 The c-jun gene regulates cellular proliferation and apoptosis

44 mmunodeficiency virus (HIV), and the human c-Jun gene's enhancer (CJE), an element newly identified h

45 nts blocked EGF induction of a transfected c-jun gene suggesting that MSK1 or a similar family member

46 pathetic neurons of mice carrying a mutant c-Jun gene that lacks Ser63/Ser73 phosphorylation sites (j

47 ade use of null mutations in the c-fos and c-jun genes that were produced by gene targeting to invest

48 f histone H3 associated with the c-fos and c-jun genes through an ERK-dependent pathway.

49 utostimulate the expression of the c-Jun and JunD genes, thus leading to lower production of c-Jun an

50 of MKK1/2-Erk1/2 signaling and by blocking c-Jun gene transcription via inactivation of MKK4-JNK1/2 s

51 a and the endoplasmic reticulum as well as c-jun gene transcription.

52 nsequence of MEF2C activation is increased c-jun gene transcription.

53 amine depletion did not increase the rate of junD gene transcription but significantly increased the

54 The junD gene transcription was examined by nuclear run-on a

55 bryonic lethality, somatic deletion of the c-jun gene was conducted using floxed c-jun (c-jun(f/f)) c

56 Since transcription of the JUN gene was UV-induced in all fibroblast strains, inclu

57 y targeting the excision of the endogenous c-jun gene within the mouse mammary epithelium, we have id