ライフサイエンスコーパス: serum response element

1 ation of DNA synthesis and activation of the serum response element.

2 ssed the serum-induced activity of the c-fos serum response element.

3 h regulate c-fos gene expression through the serum response element.

4 butes to the transcriptional activation of a serum response element.

5 and transcriptional activation of the c-fos serum response element.

6 -1 receptor to the CArG element of the c-fos serum response element.

7 ement, an AP-1-like sequence adjacent to the serum response element.

8 hancer has a functional and highly conserved serum response element.

9 oter by CaMKII290 and Src required the c-fos serum response element.

10 atriuretic factor promoter that contains the serum response element.

11 /or factors that interact with TFII-I at the serum-response element.

12 he interferon beta enhancer, TATA boxes, and serum response elements.

13 tly reduced by specific mutations within the serum response element-1 domain of the egr-1 promoter.

14 and serum response factor proteins bound the serum response element-1 domain on the egr-1 promoter, a

15 t as a GAP for G12/13alpha, it impairs c-fos serum response element activation induced by either a co

16 at IFNalpha inhibits Erk phosphorylation and serum response element activation induced by expression

17 so indicated that Edg3 and Edg5 mediated the serum response element activation through transcriptiona

18 stress fiber formation, neurite retraction, serum response element activation, and increased DNA syn

19 y, Hsp90 is required for G alpha(12)-induced serum response element activation, cytoskeletal changes,

20 p90 and did not require functional Hsp90 for serum response element activation.

21 lock Gialpha-linked signaling, also inhibits serum response element activation.

22 Both TRIM28 and TRIM27 can regulate serum response element activity and were required for ma

23 , Leu and Met, to Ala impaired activity in a serum response element activity assay for both full-leng

24 ound to the rat insulin promoter II (RIP II) serum response element, an element conserved in both rat

25 onal level, Rgr enhances the activity of the serum response element and c-Jun.

26 gnificant decrease in the transactivation of serum response element and cAMP-response element.

27 volved in c-fos expression via regulation of serum response element and cAMP-response element.

28 f MAPKs leading to stimulation of both c-fos serum response element and E74-site-dependent transcript

29 ved when DNA-binding sites for both factors, serum response element and M-CAT respectively, were inta

30 hibitory effect on kisspeptin stimulation of serum response element and nuclear factor of activated T

31 regulate two transcription factor pathways, serum response element and nuclear factor of activated T

32 pha6beta4 induced transcription from the Fos serum response element and promoted cell cycle progressi

33 d the binding activity of SRF protein to the serum response element and reduced the capability of SRF

34 ired both the CArG DNA sequence of the c-fos serum response element and the Ca2+/cAMP response elemen

35 ion of c-fos transcription requires both the serum response element and the promoter proximal cyclic

36 perate to promote transcription from the Fos serum response element and transit through G1.

37 e BNP gene from the ANP gene, which utilizes serum response elements and an Sp1-like sequence.

38 tional level has been attributed to multiple serum response elements and their adjacent Ets motifs lo

39 isin induces activation of the intracellular serum-response element and NFkappaB signaling pathways a

40 lements [CRE], NF-kappaB binding sites [kB], serum response element, and ETS/ELK-1 binding site) and

41 f transcription using activating protein 1-, serum response element-, and cyclic AMP response element

42 rough multiple regulatory sites, including a serum response element, AP1, and TATA box.

43 runcation experiments suggested that several serum response elements are required for MAPK-mediated e

44 serum-induced transcriptional activation of serum response element as well as Ras-induced transcript

45 h as nuclear factor of activated T-cells and serum response element, as well as extracellular signal-

46 Serum response element binding protein (SRE BP) is a nov

47 eporter genes for the c-fos promoter and the serum response element by Edg3 and Edg5 transfected in J

48 Activation of the serum response element by v-Abl was inhibited by Rac N17

49 A serum-response element, comprised of the Ets and CArG mo

50 trongly enhanced TFII-I transactivation of a serum-response element-containing promoter in COS7 cells

51 In contrast, Pdcd4 did not inhibit serum response element-dependent transcription, indicati

52 Raf from activation of ERK1/2, induction of serum-response element-dependent gene expression, and in

53 region including EBS (ets binding site)-SRE (serum response element)-EBS and SRE-EBS-SRE sites.

54 in increased transcription of Egr-1 through serum response element/Ets motifs.

55 PRL-3 stimulated transcription driven by the serum response element in a Rho-dependent manner.

56 Ternary complex factors (TCFs) bind to the serum response element in the c-fos promoter and mediate

57 ctivate from the HTLV-1 21-bp repeats or the serum response element in the c-fos promoter.

58 moter fragment depended upon multiple intact serum response elements in combination with Sp1 sites fo

59 enhanced transcription of the Egr-1 gene via serum response elements in normal fibroblasts.

60 and partial agonist ligands require all six serum response elements in the Egr1 promoter to reach ma

61 blastic leukemia 1 (MKL1), which targets the serum response elements in the promoter of rat Slc1a2 ge

62 ne constructs demonstrated that the proximal serum response element is both necessary and sufficient

63 nced by activated RhoA, indicating that this serum response element is functional.

64 In both HeLa TK- and NIH 3T3 cells the Serum Response Element is required for efficient UV-indu

65 Transcription from the serum response element, like activation of ERK1/2, is no

66 r required the presence of a CArG motif in a serum response element-like structure between -422 and -

67 a phenotypic high-throughput screen using a serum response element luciferase promoter, we identifie

68 ociation and Erk phosphorylation and elevate serum response element-luciferase (SRE-LUC) expression,

69 ls with insulin augmented the LPA-stimulated serum response element-luciferase activation to 12-fold,

70 well as inhibition of phospho-S6 protein and serum response element-luciferase activity.

71 effects of lysophosphatidic acid (LPA) on a serum response element-luciferase construct.

72 4)-AR subtype displayed a markedly increased serum response element-luciferase gene expression but no

73 a membrane (PM) and to activate Rho-mediated serum response element-luciferase gene transcription.

74 ion and negative regulation of Lck-dependent serum response element-luciferase reporter activity.

75 lated DNA synthesis, activated a transfected serum response element-luciferase reporter construct, an

76 addition, Syk-dependent transactivation of a serum response element-luciferase reporter in transfecte

77 LPA stimulated proliferation and signaled a serum response element-luciferase reporter of immediate-

78 nactive separately, evoked proliferative and serum response element-luciferase responses of OCCs but

79 lly required for coupling TCR stimulation to serum response element-mediated gene transcription.

80 STAT3 DNA binding and STAT3-mediated but not serum response element-mediated gene transcription.

81 on, demonstrating the Galpha13 dependence of serum response element-mediated transcription.

82 Elk-1 and cAMP response element-mediated and serum response element-mediated transcription.

83 or that binds to a CarG box motif within the serum response element of genes that are expressed in re

84 y forms a ternary complex that activates the serum response element of the c-fos gene.

85 ypotonic stress response element maps to the serum response element of the c-fos promoter.

86 nal mechanism, predominantly at the proximal serum response element of the c-fos promoter.

87 The factors binding to the serum response elements of the Egr1 promoter form a tern

88 ibition of transcriptional activation of the serum-response element of c-fos.

89 CArG* elements can be competed out by either serum response element or by an authentic CArG element f

90 controlled by the c-fos promoter, the c-fos serum response element or the transcription factors Elk-

91 d together with serum response factor to the serum response element present in the c-fos promoter and

92 cade or ternary complex formation at the fos serum response element promoter.

93 within the nucleus, correlated with enhanced serum-response element promoter activity.

94 tly increased basal activity of the CTGF and serum response element promoters, and enhanced induction

95 RIP2 activates AP-1 and serum response element regulated expression by inducing

96 stimulated ErbB4 activity as measured by the serum response element report assay and the BRCA1 mRNA e

97 nd LPC activate GPR4-dependent activation of serum response element reporter and receptor internaliza

98 astic increase in the ability to stimulate a serum response element reporter and the accumulation of

99 enuated D2 dopamine receptor agonist-induced serum response element reporter gene activity in Chinese

100 he catalytic activity of ECT2 as detected by serum response element reporter gene assays.

101 protein mediated LPA-induced activation of a serum response element reporter gene with LPA concentrat

102 duction is reproduced by a stably integrated serum response element reporter independently of mitogen

103 CC(A/T)(6)GG or serum response elements represent a common regulatory mo

104 nary complex factor pathway that targets the serum response element shows that extracellular ATP, via

105 e recognition elements of AP-1, AP-2, Msx-1, serum response elements, SP-1, and TCF-1.

106 MP response element (CRE) or mutation in the serum response element (SRE) and demonstrated that both

107 d and included a consensus octamer sequence, serum response element (SRE) and some short sequences wi

108 d resultant transcription by using the c-fos serum response element (SRE) as a target.

109 ion were assessed using the c-fos promoter's serum response element (SRE) as a target.

110 alysis of the c-fos promoter showed that the serum response element (SRE) at -325 to -296 was E2-resp

111 s of the human egr-1 promoter identified the serum response element (SRE) between nucleotides (nt) -4

112 phosphatidic acid (LPA) stimulates the c-Fos serum response element (SRE) by activating two distinct

113 onsive transcriptional activity to the c-fos serum response element (SRE) by interacting with serum r

114 also found to inhibit the activation of the serum response element (SRE) by preventing MAPK-mediated

115 3 reduced transcriptional activation via the serum response element (SRE) in response to anti-CD3 ant

116 The serum response element (SRE) in the c-fos promoter is ne

117 is a transcription factor which binds to the serum response element (SRE) in the c-fos promoter.

118 The serum response element (SRE) is a promoter element essen

119 SRF binding activity as compared with c-fos serum response element (SRE) is important for conferring

120 of transcription factors associated with the serum response element (SRE) located upstream of c-fos w

121 The c-fos serum response element (SRE) mediates transcriptional ac

122 Luciferase constructs containing the serum response element (SRE) of growth-related gene prom

123 The serum response element (SRE) of the c-fos promoter is a

124 f nucleosomal histone H3 at both the ARE and serum response element (SRE) of the Egr-1 promoter, whic

125 d in transcriptional activation of the c-fos serum response element (SRE) promoter, whereas overexpre

126 ine nucleotide exchange factor (GEF)-induced serum response element (SRE) reporter activation in huma

127 ivate a truncated ANF promoter, containing a serum response element (SRE) required for phenylephrine-

128 The enhancer contains at its core the serum response element (SRE) that binds serum response f

129 The c-fos promoter contains a serum response element (SRE) that mediates ternary compl

130 utations at the sis inducible element (SIE), serum response element (SRE), c-fos AP-1 site (FAP1), or

131 One of the c-fos promoter elements, the serum response element (SRE), plays a central regulatory

132 cluding a cyclic AMP response element (CRE), serum response element (SRE), sis-inducible element (SIE

133 critical regulatory elements, including the serum response element (SRE), that mediate glutamate-ind

134 ted in activation of a transcription factor, serum response element (SRE), that was enhanced by p114R

135 several sequence elements, most notably the serum response element (SRE), the AP-1 binding site (FAP

136 These cis elements include a Serum Response Element (SRE), two Ets sites previously u

137 retic factor (ANF) gene, a promoter-proximal serum response element (SRE), which binds serum response

138 ular immediate early genes controlled by the serum response element (SRE), which contains both the se

139 The serum response element (SRE), which is pivotal for trans

140 n-mediated actin cytoskeleton remodeling and serum response element (SRE)-dependent gene transcriptio

141 l domain (amino acids 319-583) of radixin on serum response element (SRE)-dependent gene transcriptio

142 y activate numerous myogenic and nonmyogenic serum response element (SRE)-dependent promoters in CV1

143 tion factor that we found strongly activated serum response element (SRE)-dependent reporter genes th

144 f the Ras superfamily of proteins, activates serum response element (SRE)-dependent transcription thr

145 domains stimulated transcription of a c-fos serum response element (SRE)-driven reporter.

146 We found that two serum response element (SRE)-like DNA elements, one of w

147 other SSB proteins enhanced the HGF-induced serum response element (SRE)-luciferase activity.

148 teins to create aGPCR probes, we developed a serum response element (SRE)-luciferase-based screening

149 Because ERK1/2 and PI3K both stimulate serum response element (SRE)-mediated gene expression, a

150 evealed a subset necessary for activation of serum response element (SRE)-mediated transcription, a G

151 which form a ternary complex with the c- fos serum response element (SRE).

152 transcriptional control elements such as the serum response element (SRE).

153 urs primarily within the region containing a serum response element (SRE).

154 timulated transcription of c-fos through the Serum Response Element (SRE).

155 r-inducible factor binding element (SIE) and serum response element (SRE).

156 ho can activate transcription from the c-fos serum response element (SRE).

157 bility to stimulate transcription from c-fos serum response element (SRE).

158 ption of a reporter gene driven by the c-fos serum response element (SRE).

159 a 62 kDa ternary complex factor (TCF) and a serum response element (SRE).

160 f a reporter construct dependent only on the serum response element (SRE).

161 sus DNA sequence (CArG box) located within a serum response element (SRE).

162 fos promoter lies a key regulatory site, the serum response element (SRE).

163 addition to the SRF binding site (CArG box), serum response elements (SRE) also typically contain a b

164 athway, activating transcription through the serum-response element (SRE), is triggered by a rise in

165 site and the CArG box (collectively known as serum response element, SRE), and an ATF site, is also n

166 ytes with a reporter gene driven by a mutant serum response element, SRE.L, which responds to SRF act

167 sites, three of which exist as parts of two serum response elements (SREI and SREII).

168 ducibility, elimination of the five putative serum response elements (SREs) abolished the urea effect

169 the proximal -198 base pairs containing two serum response elements (SREs) and one cAMP-response ele

170 ts revealed that c-Abl utilizes three distal serum response elements (SREs) in the EGR1 promoter, whi

171 ection assays, deletion of the 3' cluster of serum response elements (SREs), but not the 5' cluster o

172 se the junB and c-fos promoters both contain serum response elements (SREs), the current studies test

173 alpha-actin promoter, depending upon intact serum response elements (SREs).

174 s of transcription factors that regulate the serum response element, suppression of death caspase act

175 ed with that of the classical c-Fos promoter serum response element, together with differences in the

176 nucleotide-independent fashion, Rho-induced serum response element transcriptional activity was not

177 The c-fos serum response element was necessary but not sufficient

178 A consensus serum response element was present within 100bp upstream

179 t analyses showed that the binding of SRF to serum response element was significantly increased by in

180 ression and ability to bind to the consensus serum response element, was altered long term in the pil

181 ved, but the CArG and CArG-like boxes of the serum response element were absent.

182 t on a reporter construct based on the c-fos serum response element, which is not dependent on Stat3

183 y troglitazone of the transactivation of the serum response element, which regulates c-fos expression

184 e atrial natriuretic factor gene through the serum response element, which was augmented by bone morp

185 ted transcriptional activation driven by the serum response element without altering the activation o