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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

50 tential molecular link between Nrf2 and CREB/ATF1.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

66 roprotective stimulus on activation of CREB1/ATF1.

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

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

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

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

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

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

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

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

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

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

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

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

79 2 phosphorylated ATF1 at Ser-63 and enhanced ATF1 transcriptional activity.

80 EWS-ATF1 activates the melanocyte transcription factor MITF,

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

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

83 eat a transforming pathway downstream of EWS-ATF1.

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

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

86 293T cells following introduction of an EWS/ATF1 expression vector.

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

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

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

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

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

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

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

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

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

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

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

98 .09, P = 7.4 x 10(-8)); rs1129406 (12q13) in ATF1 (OR = 1.11, P = 8.3 x 10(-9)), all reaching exome-w

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

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

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

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

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

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

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

106 activation and transcriptional activities of ATF1.

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

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

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

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

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

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

113 y acts through downstream phosphorylation of ATF1.

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

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

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

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

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

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

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

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

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

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

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

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

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

127 1 is a novel substrate of RSK2 and that RSK2-ATF1 signaling plays an important role in EGF-induced ne

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

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

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

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

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

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

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

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

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