ライフサイエンスコーパス: c-fos gene

1 scription factor and increased expression of c-Fos gene.

2 cers underlies the broad inducibility of the c-fos gene.

3 is a repression of the ability to induce the c-fos gene.

4 s amphetamine-induced desensitization of the c-fos gene.

5 results in transcriptional activation of the c-fos gene.

6 cificity factor (CPSF73), was reduced at the c-FOS gene.

7 ired for Fyn activation and induction of the c-fos gene.

8 transcriptional activation of the endogenous c-fos gene.

9 activates the serum response element of the c-fos gene.

10 phosphoCREB-stimulated transcription of the c-fos gene.

11 transcriptional responses of the endogenous c-fos gene.

12 for STAT activation or for induction of the c-fos gene.

13 obes for a natural DNA sequence in the mouse c-fos gene.

14 the major CRE in the promoter region of the c-fos gene.

15 2+-induced transcription of prodynorphin and c-fos genes.

16 represses transcription of prodynorphin and c-fos genes.

17 response elements (DREs) in prodynorphin and c-fos genes.

18 NA response elements in the prodynorphin and c-fos genes.

19 element (DRE) of either the prodynorphin or c-fos genes.

20 um glucocorticoid kinase, inhibin alpha, and c-fos genes.

21 BMP2 inhibits PDGF-induced transcription of c-fos gene, a natural target of Elk-1 that normally form

22 s had no effect on AII-induced MAP kinase or c-fos gene activation.

23 The c-fos gene (also known as Fos) is induced by a broad ran

24 k factor 1 inhibits the transcription of the c-fos gene and antagonizes the activating effects of the

25 ells by functionally affecting expression of c-fos gene and AP-1 luciferase gene reporter activity.

26 hat PKC couples to the activation of the the c-fos gene and MAP kinases.

27 AII also activated the c-fos gene and mitogen-activated protein (MAP) kinases.

28 The activation of PKC, the c-fos gene, and MAP kinases was blocked by inhibition of

29 in the adenovirus 2 major late promoter, the c-fos gene, and the c-myc P1 and P2 promoters reveal var

30 rate that multiple enhancers surrounding the c-fos gene are crucial for ensuring robust c-fos respons

31 hermore, transcripts from the ARE-containing c-fos gene are selectively retained in the nucleus, whil

32 Using the c-fos gene as a candidate PRG, we addressed here how it

33 is required for regulated expression of the c-fos gene as well as other immediate-early genes and so

34 articipate in the process that represses the c-fos gene at the onset of cellular senescence.

35 induced c-fos expression, but also decreased c-fos gene basal expression.

36 null ES cells permitted transcription of the c-fos gene but was unable to rescue expression of myogen

37 ing to DNA response elements upstream of the c-fos gene (c-sis-inducible enhancer element; Stat 1 and

38 One CNS located in the first intron of the c-fos gene conferred regulation by cAMP-dependent protei

39 nsactivating a luciferase reporter driven by c-fos gene enhancer elements, suggesting that PRL allowe

40 tion of sialylated O-glycan and increases of c-fos gene expression and AP-1 activity, which are chara

41 a transcriptionally-mediated suppression of c-fos gene expression associated with the malignant tran

42 UVB significantly increased c-fos gene expression at both the transcriptional and pr

43 ctivation of MAP kinase and the induction of c-fos gene expression both correlated with STAT but not

44 nse factor (SRF), and Tax is known to induce c-fos gene expression by activating SRF-responsive trans

45 rdiac tissues and represses prodynorphin and c-fos gene expression by binding to DNA response element

46 This study investigated the pattern of c-fos gene expression corresponding with auditory adapta

47 gnaling components in mediating induction of c-fos gene expression downstream of epidermal growth fac

48 vlPOA) of rats was found to exhibit elevated c-fos gene expression during sleep, indicating that thes

49 he same area where neurons exhibit increased c-fos gene expression during sleep.

50 RelA contribute significantly to EGF-induced c-fos gene expression in a manner independent of the cla

51 ve of the present study was to determine how c-fos gene expression in brainstem structures after a br

52 nt with the hypothesis that the induction of c-fos gene expression in GnRH neurons leads to an increa

53 inistration of cholecystokinin (CCK) induced c-fos gene expression in NTS POMC-EGFP neurons, suggesti

54 Our results reveal that c-fos gene expression in the adult rat is attenuated in

55 with CRH there was a significant increase in c-fos gene expression in the CeA and in the hippocampal

56 dopamine-regulated CREB phosphorylation and c-fos gene expression in the striatum.

57 a Rho kinase and myocardin and also regulate c-fos gene expression independently via CaMK.

58 hway that activates CREB phosphorylation and c-fos gene expression is likely activated by Ca(2+) entr

59 We conclude that c-fos gene expression occurs transiently in granule cell

60 rnary complex factors (TCFs), which regulate c-fos gene expression through the serum response element

61 asticity, and (3) stress are proposed to use c-fos gene expression to signal molecular changes in neu

62 have shown that nitric oxide (NO) regulates c-fos gene expression via cGMP-dependent protein kinase

63 Specifically, activation of c-fos gene expression was found to occur exclusively thr

64 c-fos gene expression was increased by PMA but not invol

65 PI 3-kinase signaling pathway in UVB-induced c-fos gene expression was investigated in a human kerati

66 Patterns of c-fos gene expression were compared between Saffan-anest

67 Patterns of c-fos gene expression were site-specific and correlated

68 cts of p38 MAP kinase and ERK on UVB induced c-fos gene expression were studied in a human keratinocy

69 tress generates only a small contribution to c-fos gene expression while novel stimuli are potent sig

70 alloproteinase-13 (MMP-13), c-jun, junB, and c-fos gene expression, binding of activator protein 1 (A

71 ediated by the induction of c-jun, junB, and c-fos gene expression, by the binding of AP1 to DNA, by

72 n had no effect on AP-1 activation, c-jun or c-fos gene expression, or CREB phosphorylation.

73 while not inhibiting smooth muscle-unrelated c-fos gene expression, suggesting that RGC-32 is an impo

74 While Epo is known to activate c-fos gene expression, the mechanism of AP-1 activation

75 s transcription factor significantly reduces c-fos gene expression.

76 and respond to leptin with a stimulation of c-fos gene expression.

77 pathway that led to CREB phosphorylation or c-fos gene expression.

78 ndicate that novelty of sound stimuli induce c-fos gene expression.

79 s/luc) was generated to continuously monitor c-fos gene expression.

80 ic acid receptors (RARs) and AP-1 (c-Jun and c-Fos) gene expression, chronic ethanol (36% of total ca

81 y to inhibit endogenous transcription of the c-fos gene in NIH3T3 cells at micromolar concentrations.

82 rmation of an active promoter complex at the c-fos gene, including the linkage of specific signal res

83 We evaluated patterns of c-fos gene induction as a monitor of spinal neurons resp

84 xtracellular signal-related kinase (ERK) and c-fos gene induction.

85 ays is also required for the response of the c-fos gene itself to UV stimulation.

86 were processed immunocytochemically for the c-fos gene product, Fos and related antigens.

87 gative Src (SrcK-) blocked activation of the c-fos gene promoter by CaMK II 290, a constitutively act

88 and the reduction in transcription involved c-fos gene promoter elements from -327 to +40.

89 uced methylation at CpG dinucleotides in the c-Fos gene promoter, effects reversed by MET treatment.

90 ruiting histone deacetylase 1 (HDAC1) to the c-fos gene promoter, which, in turn, deacetylates surrou

91 taining the TATA elements from the hsp70 and c-fos gene promoters but failed to significantly activat

92 the role of MAP kinases in retinoid-induced c-fos gene regulation.

93 The induction of transactivation by the c-fos gene regulator Elk-1 mirrored this requirement for

94 altering the chromosomal environment of the c-fos gene, thereby rendering it more accessible to the

95 t JNK regulates Elk-1 transactivation at the c-fos gene to promote the formation of AP-1 complexes im

96 p38 almost completely abrogated UVB induced c-fos gene transcription and c-Fos protein synthesis.

97 c-Fos gene transcription was lower in tumorigenic HBE ce

98 expression, (2) Ras-dependent activation of c-fos gene transcription, inferred from the induction of

99 hibition of Akt also attenuated PDGF-induced c-fos gene transcription, with concomitant inhibition of

100 c-fos mRNA and protein levels by decreasing c-fos gene transcription.

101 Previous studies have reported that the c-fos gene via formation of activator protein-1 (AP-1) t

102 Activation of the c-fos gene was blocked by coexpression with a Raf-C4 cat

103 The c-fos gene was one of the earliest vertebrate genes show

104 taining for the protein product (Fos) of the c-fos gene was used as an index of neuronal activation.

105 ls of housekeeping genes, but not of p21 and c-fos genes, which are involved in the DNA damage respon