ライフサイエンスコーパス: ATF1

1 ATF1 and CREB can be phosphorylated by Rsk2 which is a p

2 ATF1 can be phosphorylated by mitogen- and stress-activa

3 Activating transcription factor 1 (ATF1) and cAMP-responsive element (CRE)-binding protein

4 REB1) and activating transcription factor 1 (ATF1) are closely related members of the bZIP superfamil

5 horylates activating transcription factor 1 (ATF1) at serine 63 and enhances the transactivation and

6 REB), and activating transcription factor 1 (ATF1) pathway is involved in the mediation of the phenot

7 WSR1 with activating transcription factor 1 (ATF1) to give an oncogene EWSR1-ATF1.

8 phorylation of CREB, transcription factor 1 (ATF1), and ATF2, three transcription factors that bind t

9 CREB) and activating transcription factor 1 (ATF1), transcription factors that are downstream of p38

10 (EWS) and activating transcription factor 1 (ATF1).

11 bility of activating transcription factor-1 (ATF1) or the cAMP response element-binding protein (CREB

12 CREB) and activating transcription factor-1 (ATF1).

13 ediated repression of the ferritin H ARE; 2) ATF1 was sumoylated, but PIAS3, a SUMO E3 ligase, did no

14 S3 decreased ATF1 binding to the ARE; and 4) ATF1 knockdown with siRNA increased ferritin H expressio

15 gment the ability of Ca2+ influx to activate ATF1 or CREB consistent with a role for these kinases in

16 nt protein kinases (CaM kinases) to activate ATF1 or CREB.

17 (protein inhibitor of activated STAT3) as an ATF1-binding protein.

18 r, these data demonstrate that both AMPK and ATF1 are required for normal hematoma resolution.

19 We demonstrate that BRCA1 and ATF1 can physically associate in vitro, in yeast, and in

20 Consistent with the interaction of CREB and ATF1 at the TGA regulatory elements, expression of const

21 The results indicate that CREB and ATF1 play a central role in adipogenesis because express

22 nalyses with antibodies specific to CREB and ATF1 showed that these CREB family members associate wit

23 hosphorylated transcription factors CREB and ATF1 to the promoters of the genes encoding interleukin

24 ment-binding transcription factors, CREB and ATF1, also showed significant levels of interaction with

25 The LPS-stimulated activation of CREB and ATF1, the transcription of the cyclooxygenase-2 (COX-2)

26 MSK2 downstream targets, including CREB and ATF1.

27 -response element-binding protein (CREB) and ATF1 (activating transcription factor-1).

28 y blocked phosphorylation of Elk1, CREB, and ATF1, which constitutively bind to the FRA-1 promoter, b

29 antibody identified phosphorylated CREB1 and ATF1 and labeled the inner retina only in normal dogs.

30 Native CREB1 and ATF1 as well as phosphorylated CREB1/ATF1 was examined i

31 ing increased expression of native CREB1 and ATF1, as well as increased phosphorylation of these prot

32 the presence of EWSR1 fusions with CREB1 and ATF1, members of the CREB family of transcription factor

33 The expression levels of p-CREB1, CREB1, and ATF1 were examined by immunoblot and immunohistochemistr

34 led that other CREB family members, CREM and ATF1, are up-regulated and associate with the proximal C

35 cation, t(12;22)(q13;q12), involving EWS and ATF1 genes.

36 nteraction between the BRCA1 RING finger and ATF1, a member of the cAMP response element-binding prot

37 e sequence of FER-1 contains JunD, FosB, and ATF1.

38 ER stress induces CREB1 phosphorylation and ATF1/CREB1 binding to the Grp78 promoter.

39 tracellular expression of an inhibitory anti-ATF1 single chain antibody fragment (scFv4).

40 find that two sequence elements, which bind ATF1 and MEF2D transcription factors, are required in He

41 We further find that the FAP1 site binds ATF1 and CREB from HeLa nuclear extracts and that the ph

42 active CaM kinase I and IV can activate both ATF1 and CREB.

43 scFv4 disrupted the binding of both ATF1 and CREB in electrophoretic mobility shift assays a

44 These results clearly showed that the cdk3-ATF1 signaling axis is critical for cell proliferation a

45 cells and si-cdk3 suppresses Ras(G12V)/cdk3/ATF1-induced foci formation in NIH3T3 cells.

46 oxes 2 and 5, NF-Y to CCAAT boxes, and CREB, ATF1, and CREM to CRE.

47 phosphorylation of ERK1/2, p38, MSK1, CREB, ATF1, AKT and STAT6.

48 recognition motifs which interact with CREB, ATF1, and ATF2 but not with ATF4/CREB2.

49 tein-activation transcription factor-1 (CREB-ATF1) proteins that bind these promoter elements from th

50 r Th (eTh) cells have reduced levels of CREB-ATF1 proteins, their nuclear extracts exhibit reduced CR

51 their nuclear extracts exhibit reduced CREB-ATF1 binding and greater Jun and Jun-ATF2 binding to dis

52 CREB/ATF1 depletion did not attenuate lipid accumulation in c

53 including the RFX factor components and CREB/ATF1 family transcription factors, to promote MHC class

54 tential molecular link between Nrf2 and CREB/ATF1.

55 ccharide-induced activation of p38 MAPK-CREB/ATF1 pathway and DC maturation.

56 indicate that dysregulation of p38 MAPK-CREB/ATF1 signaling axis underlies the altered function and p

57 and function by modulating the p38 MAPK-CREB/ATF1 signaling axis.

58 iting for the LPS-induced activation of CREB/ATF1 and the transcription of the COX-2 and IL-1 beta ge

59 Loss of CREB/ATF1 blocked adipogenic conversion of 3T3-L1 cells in cu

60 Depletion of CREB/ATF1 did not suppress the expression of C/EBP beta as we

61 shows an increase in phosphorylation of CREB/ATF1 in HIB-1B cells after norepinephrine treatment.

62 The increased phosphorylation of CREB/ATF1 in Nrf2(-/-) iDCs was sensitive to p38 MAPK inhibit

63 Loss of CREB/ATF1 inhibited adipogenic conversion even in cells ectop

64 Loss of CREB/ATF1 prevented the expression of PPARgamma, C/EBP alpha,

65 ally, Western blot analysis for phospho-CREB/ATF1 shows an increase in phosphorylation of CREB/ATF1 i

66 AMP-responsive element binding protein CREB/ATF1 transcription factors and using the electrophoretic

67 APK2 phosphorylates its nuclear targets CREB/ATF1, serum response factor, and E2A protein E47 and its

68 ed by specific combinations of c-Jun, CREB1, ATF1, and ATF2 dimers.

69 We show that expression of EWSR1-CREB1/ATF1 fusion in hES cells recapitulates the core gene sig

70 Positive association of CREB1/ATF1 phosphorylation with photoreceptor protection sugge

71 roprotective stimulus on activation of CREB1/ATF1.

72 p-CREB1/ATF1 immunolabeling was assessed in normal and rcd1 dogs

73 ignificant increase in the number of p-CREB1/ATF1-labeled photoreceptor nuclei.

74 EB1 and ATF1 as well as phosphorylated CREB1/ATF1 was examined in normal canine retina by immunoblot.

75 the CIITA enhanceosome including RFX, CREB1/ATF1 and NFY.

76 This study was conducted to assess the CREB1/ATF1 pathway in photoreceptor disease and protection.

77 ross-reacted with antibodies for CREB, CREM, ATF1, ATF2, and c-Jun, while proteins binding the varian

78 did not alter the expression of CREB, CREM, ATF1, ATF2, or ATF4 proteins.

79 tion activating function; 3) PIAS3 decreased ATF1 binding to the ARE; and 4) ATF1 knockdown with siRN

80 EWSR1-ATF1 is constitutively active to drive ATF1-dependent gene transcription to cause tumorigenesis

81 n of other CREB protein family members, i.e. ATF1 and CREM.

82 CaM kinase II was unable to activate either ATF1 or CREB.

83 Cotransfection of either ATF1 or CREB in the presence of scFv restored basal leve

84 show that, in contrast to c-Jun, SRF, Elk1, ATF1 and CREB proteins bind to SRE and ATF sites of the

85 2 phosphorylated ATF1 at Ser-63 and enhanced ATF1 transcriptional activity.

86 EWS-ATF1 activates the melanocyte transcription factor MITF,

87 EWS-ATF1, the fusion product of a balanced chromosomal trans

88 tion of a chimeric transcription factor, EWS-ATF1, which is formed as the result of a disease-specifi

89 eat a transforming pathway downstream of EWS-ATF1.

90 otential is driven by a chimeric protein EWS-ATF1 (Ewing's sarcoma protein-activating transcription f

91 Conditional expression of the EWS-ATF1 human cDNA in the mouse generates CCS-like tumors w

92 293T cells following introduction of an EWS/ATF1 expression vector.

93 Contribution of the chimeric EWS/ATF1 protein to maintenance of the tumor phenotype was i

94 he transcriptional activity of exogenous EWS/ATF1 and EWS/FLI1 and suggests that post-translational m

95 The level of EWS/ATF1 expression was found to be significantly higher in

96 The EWS/ATF1 and EWS/FLI1 fusion proteins associated with Clear

97 tudies demonstrate a direct role for the EWS/ATF1 fusion protein in maintaining tumor cell viability

98 usions, in particular, EWSR1-CREB1 and EWSR1-ATF1, in human embryonic stem (hES) cells, which are cap

99 verely impaired cell proliferation and EWSR1-ATF1-driven transcription.

100 the epigenetic mechanisms utilized by EWSR1-ATF1 to establish regulatory networks in CCS, and points

101 esulting in expression of the chimeric EWSR1-ATF1 or EWSR1-CREB1 fusion proteins, driving sarcomagene

102 Conversely, EWSR1-ATF1 depletion results in a marked reconfiguration of 3D

103 We found that PRMT5 enhances EWSR1-ATF1-mediated gene transcription to sustain CCSST cell p

104 No EWSR1-ATF1-targeted therapies have been identified due to the

105 ouse tumors generated by expression of EWSR1-ATF1 from the Rosa26 locus demonstrated no other repeate

106 on factor 1 (ATF1) to give an oncogene EWSR1-ATF1.

107 ivity is dependent on phosphorylation, EWSR1-ATF1 is constitutively active to drive ATF1-dependent ge

108 We find that EWSR1-ATF1 displays a distinct DNA binding pattern that requir

109 ma, an aggressive cancer driven by the EWSR1-ATF1 fusion gene.

110 5) as a novel protein to interact with EWSR1-ATF1.

111 deplete CREB and the closely related factor ATF1 to explore the ability of the master adipogenic reg

112 igate the roles of the transcription factors ATF1 and CREB.

113 Deletion of all three transcription factors (ATF1, CREB1, and CREM) together led to a significant red

114 the three CREB-family transcription factors (ATF1, CREB1, or CREM).

115 CREB-family transcription factors (ATF1, cyclic AMP-responsive element-binding protein 1, a

116 ubgroup: VL kappa-III, VH miscellaneous) for ATF1 was similar to that of the parental mAb and the Fab

117 In contrast, little induction is seen for ATF1 or CREM.

118 This site is related to but distinct from ATF1/CREB binding sites.

119 ther LORE-dependent, hypoxia-inducible gene, ATF1, was similarly affected in the Deltamga2 strain.

120 .09, P = 7.4 x 10(-8)); rs1129406 (12q13) in ATF1 (OR = 1.11, P = 8.3 x 10(-9)), all reaching exome-w

121 r CREB-like transcription factors, including ATF1 and cAMP-responsive element modulator (CREM), may p

122 with these results, overexpression of c-Jun, ATF1, ATF2, or CREB1 in transiently transfected osteobla

123 vates an AMPK (AMP-activated protein kinase)/ATF1 (activating transcription factor-1) pathway that di

124 hermore, eriodictyol inhibited RSK2-mediated ATF1 transactivation and tumor promoter-induced transfor

125 ppear to play a major role in SUMO1-mediated ATF1 sumoylation or ATF1 transcription activating functi

126 L1, THAP1-USF1-BRCA2, ZNF263-USF1-UBA52, MYC-ATF1-UBA52, ELK1-EGR1-CCT4, and YY1-EGR1-INO80C) could a

127 Unlike normal ATF1, whose transcription activity is dependent on phosp

128 ed EGF induction of c-jun expression but not ATF1 phosphorylation.

129 CRE complex contains CREB and ATF2, but not ATF1.

130 that may permit variation in the ability of ATF1 and CREB to respond to changes in intracellular Ca2

131 icate BRCA1 in transcriptional activation of ATF1 target genes, some of which are involved in the tra

132 activation and transcriptional activities of ATF1.

133 human HSF1, interfering with the assembly of ATF1-containing transcription complexes.

134 1), which contains the DNA binding domain of ATF1, a B-ZIP protein.

135 PIAS3 antagonizes the repressor function of ATF1, at least in part by blocking its DNA binding, and

136 A serine 63 to alanine mutation of ATF1 acts to block epidermal growth factor (EGF) inducti

137 gh the ATF1 site requires phosphorylation of ATF1 at serine 63.

138 ls, eriodictyol inhibited phosphorylation of ATF1 but had no effect on the phosphorylation of RSK, ME

139 y acts through downstream phosphorylation of ATF1.

140 lts suggest that PIAS3 is a new regulator of ATF1 that regulates the ARE-mediated transcription of th

141 Indeed, knockdown of Akt, CREB, or ATF1 in t-Darpp-expressing cells reduced Bcl2 protein le

142 nown which of the isoforms of CREB, CREM, or ATF1 are expressed in the neurons that undergo long-term

143 om mice deficient in AMPK (Prkab1(-/)(-)) or ATF1 (Atf1(-/-)).

144 ce deficient in either AMPK (Prkab1(-/-)) or ATF1 (Atf1(-/-); n=6 each).

145 Eriodictyol or knockdown of RSK2 or ATF1 also suppressed Ras-mediated focus formation.

146 r role in SUMO1-mediated ATF1 sumoylation or ATF1 transcription activating function; 3) PIAS3 decreas

147 on of Rsk related kinases that phosphorylate ATF1 and CREB.

148 RSK2 phosphorylated ATF1 at Ser-63 and enhanced ATF1 transcriptional activit

149 proteins bind to the 3' enhancer (PU.1, PIP, ATF1, CREM, c-Fos, c-Jun, and E2A), but the mechanism of

150 monoclonal antibody (mAb41.4) that prevents ATF1 binding to DNA and reduces CRE-driven promoter acti

151 that requires the EWSR1 domain and promotes ATF1 retargeting to new distal sites, leading to chromat

152 ectors cAMP-response element-binding protein/ATF1 as mediators of UV-induced p38alpha-dependent DUSP1

153 Here we have identified the closely related ATF1 and CREB1 as nuclear co-factors that form in vivo c

154 actor induction of c-jun expression requires ATF1 and MEF2 sites in the c-jun promoter.

155 ARE regulation showed that 1) PIAS3 reversed ATF1-mediated repression of the ferritin H ARE; 2) ATF1

156 1 is a novel substrate of RSK2 and that RSK2-ATF1 signaling plays an important role in EGF-induced ne

157 Overall, these results indicate that RSK2-ATF1 signaling plays an important role in neoplastic cel

158 ate that Site I and Site IV together support ATF1- and CREB-induced trans-activation of the H4 promot

159 A directed against cdk3 (si-cdk3) suppresses ATF1 activity, resulting in inhibition of proliferation

160 Here we found that ATF1 (activating transcription factor 1) is a transcript

161 Here, we report that ATF1 is a novel substrate of RSK2 and that RSK2-ATF1 sig

162 ptional activation through c-Jun but not the ATF1, ATF2, or CREB transcription factor.

163 activation of the c-jun promoter through the ATF1 site requires phosphorylation of ATF1 at serine 63.

164 ear fractionation reveals that there are two ATF1 isoforms which appear to differ with respect to DNA

165 ition, we show that NLRC5 can cooperate with ATF1 and the transcriptional coactivators CBP/p300 and g

166 ar transcriptomic changes when rescuing with ATF1, CREB1, or CREM.