ライフサイエンスコーパス: fos gene

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

2 ranscriptional responses of the endogenous c-fos gene.

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

4 es for a natural DNA sequence in the mouse c-fos gene.

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

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

7 r cells was due to reduced expression of the FOS gene.

8 rs underlies the broad inducibility of the c-fos gene.

9 amphetamine-induced desensitization of the c-fos gene.

10 hibits the estrogen-driven activation of the FOS gene.

11 sults in transcriptional activation of the c-fos gene.

12 lator of PGE(2)-induced transcription of the fos gene.

13 ream transcript (FosDT) that is cogenic with Fos gene.

14 ficity factor (CPSF73), was reduced at the c-FOS gene.

15 ed for Fyn activation and induction of the c-fos gene.

16 anscriptional activation of the endogenous c-fos gene.

17 ctivates the serum response element of the c-fos gene.

18 hosphoCREB-stimulated transcription of the c-fos gene.

19 -induced transcription of prodynorphin and c-fos genes.

20 epresses transcription of prodynorphin and c-fos genes.

21 sponse elements (DREs) in prodynorphin and c-fos genes.

22 response elements in the prodynorphin and c-fos genes.

23 lement (DRE) of either the prodynorphin or c-fos genes.

24 glucocorticoid kinase, inhibin alpha, and c-fos genes.

25 MP2 inhibits PDGF-induced transcription of c-fos gene, a natural target of Elk-1 that normally forms

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

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

28 factor 1 inhibits the transcription of the c-fos gene and antagonizes the activating effects of the s

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

30 t PKC couples to the activation of the the c-fos gene and MAP kinases.

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

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

33 the adenovirus 2 major late promoter, the c-fos gene, and the c-myc P1 and P2 promoters reveal vario

34 te that multiple enhancers surrounding the c-fos gene are crucial for ensuring robust c-fos response

35 rmore, transcripts from the ARE-containing c-fos gene are selectively retained in the nucleus, while

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

37 s required for regulated expression of the c-fos gene as well as other immediate-early genes and some

38 ticipate in the process that represses the c-fos gene at the onset of cellular senescence.

39 duced c-fos expression, but also decreased c-fos gene basal expression.

40 ll ES cells permitted transcription of the c-fos gene but was unable to rescue expression of myogenic

41 Induction of the cellular fos gene (c-fos) is one of the earliest transcriptional

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

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

44 nt and activity of p300/CBP molecules at the Fos gene correlated with higher histone H4 acetylation a

45 activating a luciferase reporter driven by c-fos gene enhancer elements, suggesting that PRL allowed

46 on of sialylated O-glycan and increases of c-fos gene expression and AP-1 activity, which are charact

47 imulated SRE- and AP1-binding activities and fos gene expression and its translocation in a MAP kinas

48 transcriptionally-mediated suppression of c-fos gene expression associated with the malignant transf

49 UVB significantly increased c-fos gene expression at both the transcriptional and prot

50 ivation of MAP kinase and the induction of c-fos gene expression both correlated with STAT but not Sr

51 e factor (SRF), and Tax is known to induce c-fos gene expression by activating SRF-responsive transcr

52 iac tissues and represses prodynorphin and c-fos gene expression by binding to DNA response elements

53 This study investigated the pattern of c-fos gene expression corresponding with auditory adaptati

54 aling components in mediating induction of c-fos gene expression downstream of epidermal growth facto

55 POA) of rats was found to exhibit elevated c-fos gene expression during sleep, indicating that these

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

57 lA contribute significantly to EGF-induced c-fos gene expression in a manner independent of the class

58 of the present study was to determine how c-fos gene expression in brainstem structures after a brie

59 with the hypothesis that the induction of c-fos gene expression in GnRH neurons leads to an increase

60 ted that PRIP also directly up-regulated the FOS gene expression in human breast cancer cells.

61 ults in robust (5- to 10-fold) activation of Fos gene expression in many brain regions that are inner

62 istration of cholecystokinin (CCK) induced c-fos gene expression in NTS POMC-EGFP neurons, suggesting

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

64 th CRH there was a significant increase in c-fos gene expression in the CeA and in the hippocampal su

65 opamine-regulated CREB phosphorylation and c-fos gene expression in the striatum.

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

67 ay that activates CREB phosphorylation and c-fos gene expression is likely activated by Ca(2+) entry

68 We conclude that c-fos gene expression occurs transiently in granule cells

69 ary complex factors (TCFs), which regulate c-fos gene expression through the serum response element.

70 ticity, and (3) stress are proposed to use c-fos gene expression to signal molecular changes in neuro

71 ave shown that nitric oxide (NO) regulates c-fos gene expression via cGMP-dependent protein kinase (G

72 Specifically, activation of c-fos gene expression was found to occur exclusively throu

73 c-fos gene expression was increased by PMA but not involve

74 3-kinase signaling pathway in UVB-induced c-fos gene expression was investigated in a human keratino

75 Patterns of c-fos gene expression were compared between Saffan-anesthe

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

77 s of p38 MAP kinase and ERK on UVB induced c-fos gene expression were studied in a human keratinocyte

78 ess generates only a small contribution to c-fos gene expression while novel stimuli are potent signa

79 loproteinase-13 (MMP-13), c-jun, junB, and c-fos gene expression, binding of activator protein 1 (AP1

80 iated by the induction of c-jun, junB, and c-fos gene expression, by the binding of AP1 to DNA, by in

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

82 ile not inhibiting smooth muscle-unrelated c-fos gene expression, suggesting that RGC-32 is an import

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

84 luc) was generated to continuously monitor c-fos gene expression.

85 through serum-responsive factor to regulate FOS gene expression.

86 d that PRIP deficiency substantially reduced FOS gene expression.

87 transcription factor significantly reduces c-fos gene expression.

88 nd respond to leptin with a stimulation of c-fos gene expression.

89 athway that led to CREB phosphorylation or c-fos gene expression.

90 icate that novelty of sound stimuli induce c-fos gene expression.

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

92 Multiple members of the jun and fos gene families were frequently expressed at the mRNA

93 ntained specific members of both the jun and fos gene families.

94 s, Fos-like antigen 1 (FOSL1) is a member of Fos gene family and is a known proto-oncogene.

95 y, meq is perhaps the only member of the jun-fos gene family completely viral in origin.

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

97 ation of an active promoter complex at the c-fos gene, including the linkage of specific signal respo

98 We evaluated patterns of c-fos gene induction as a monitor of spinal neurons respon

99 racellular signal-related kinase (ERK) and c-fos gene induction.

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

101 ere processed immunocytochemically for the c-fos gene product, Fos and related antigens.

102 tive Src (SrcK-) blocked activation of the c-fos gene promoter by CaMK II 290, a constitutively activ

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

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

105 iting histone deacetylase 1 (HDAC1) to the c-fos gene promoter, which, in turn, deacetylates surround

106 ining the TATA elements from the hsp70 and c-fos gene promoters but failed to significantly activate

107 he role of MAP kinases in retinoid-induced c-fos gene regulation.

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

109 Whereas Egr1 and Fos genes responded only to variations in average GnRH c

110 ltering the chromosomal environment of the c-fos gene, thereby rendering it more accessible to the si

111 JNK regulates Elk-1 transactivation at the c-fos gene to promote the formation of AP-1 complexes impo

112 38 almost completely abrogated UVB induced c-fos gene transcription and c-Fos protein synthesis.

113 c-Fos gene transcription was lower in tumorigenic HBE cell

114 xpression, (2) Ras-dependent activation of c-fos gene transcription, inferred from the induction of a

115 bition of Akt also attenuated PDGF-induced c-fos gene transcription, with concomitant inhibition of E

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

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

118 Activation of the c-fos gene was blocked by coexpression with a Raf-C4 catal

119 The c-fos gene was one of the earliest vertebrate genes shown

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

121 The Finkel-Biskis-Jinkins osteosarcoma (FOS) gene was significantly increased in patients, and t

122 Finally, by re-expressing the FOS gene, we confirmed that the inhibited tumor formatio

123 of housekeeping genes, but not of p21 and c-fos genes, which are involved in the DNA damage response