ライフサイエンスコーパス: CREB

1 CREB activity (phosphorylated CREB) was also increased b

2 CREB family transcription factors are required for the e

3 CREB is a key transcription factor regulating circuit de

4 CREB is a transcription factor implicated in the pathoge

5 CREB is necessary for both Dc-ODP and Pc-ODP, whereas SR

6 CREB mediates effects of cyclic AMP on cellular gene exp

7 CREB overexpression in aged animals ameliorated the long

8 CREB-binding protein (CBP) and p300 are closely related

9 CREB-H, an ER-anchored transcription factor, plays a key

10 r cAMP-responsive element-binding protein 1 (CREB).

11 t and activity-induced expression of a CRH-1/CREB transcriptional target (gem-4 Copine), which parall

12 vement of macrophages in regulating an IL-10/CREB/WISP-1 signaling axis, with broad implications in l

13 cells in culture, implicates LINC00473 as a CREB effector.

14 lement-binding protein 3-like 1 (CREB3l1), a CREB/ATF family transcription factor, as a candidate pro

15 Deletion of a CREB-Neurod1-bound enhancer within the Lrrc10b-Syt7 supe

16 ssive transcription factor, which bound to a CREB site within the SIRT1 promoter and reduced SIRT1 le

17 Here we show that PAF increases Acetyl-CREB-binding protein (CBP/p300) histone acetyltransferas

18 tion domain of the histone acetyltransferase CREB-binding protein (CBP).

19 We also noted that the acetyltransferases CREB-binding protein and p300 both can acetylate ERK1/2.

20 However, both pathways activate CREB to induce IL-1Ra expression.

21 They also expressed high levels of activated CREB, a transcription factor implicated in generating al

22 a nuclear serine/threonine kinase, activates CREB through Ser271 phosphorylation; however, the regula

23 enhancer-linked transcriptional co-activator CREB-binding protein (CBP).

24 with antisense oligodeoxynucleotide against CREB reduced mechanical allodynia and lowered pC/EBPbeta

25 racellular signal-regulated kinase 1/2, AKT, CREB, and S6 by 1 or more of these GFs, and beta-catenin

26 smolytes promote mHtt aggregation, alleviate CREB dysfunction, and promote survival under stress to s

27 e in previous studies, aversive LTAM is also CREB dependent, and CREB activity is necessary immediate

28 rols metabolic reprograming through the AMPK/CREB/PGC-1alpha pathway in female mice.

29 on alpha(2)M*-GRP78 interaction, ERK1/2 and CREB phosphorylation, and unfolded protein response (UPR

30 -43 dysfunction inhibits CREB activation and CREB transcriptional output, and restoring CREB signalin

31 additional cell signaling pathways, AKT and CREB phosphorylation.

32 etween cells transfected with CREB alone and CREB plus HIPK2 over empty vector-transfected control di

33 onist, TRPC4 channel blocker, and CaMKII and CREB-binding protein/p300 inhibitors.

34 s, aversive LTAM is also CREB dependent, and CREB activity is necessary immediately after training.

35 l proteins (BDNF, Akt, mTOR, p70S6K, ERK and CREB) in the cerebral cortex and hippocampal formation t

36 ctors (TFs) glucocorticoid receptor (GR) and CREB within minutes and increases expression of TFs C/EB

37 er O-glycosylation plays a role in iron- and CREB-mediated regulation of leptin.

38 ownstream targets, such as ATF-2, c-Jun, and CREB (cAMP response element-binding protein), was disrup

39 the bone by inducing intracellular NFkB and CREB signalling in breast cancer cells, leading to autoc

40 kines and signaling pathways (i.e., NFkB and CREB) downstream of TLR4 compared to their GIV-depleted

41 g-term depression (required for Dc-ODP), and CREB in long-term potentiation (required for Pc-ODP).SIG

42 istone acetyltransferase paralogues p300 and CREB-binding protein (CBP) are key transcriptional co-ac

43 es revealed that activation of ERK, p38, and CREB is indispensable for the induction of IL-10 product

44 ylyl cyclase or PKA activity blocked p65 and CREB phosphorylation, CBP recruitment, and histone acety

45 led to increased phosphorylation of p65 and CREB.

46 2 led to sequential activation of p90RSK and CREB, which consequently bound to IL10 promoter and init

47 in Het mice, whereas the levels of PDE4B and CREB were not altered.

48 ion, with subsequent NF-kappaB signaling and CREB phosphorylation.

49 We show that NMDAR signaling and CREB-mediated transcription maintain nascent corticospin

50 recovery after surgery, including STAT3 and CREB phosphorylation, are not affected by MP.

51 ant increase of phosphorylated Synapsin1 and CREB, which affect synaptic vesicle mobilization and gen

52 ng Ribosome Affinity Purification (TRAP) and CREB-target gene repositories.

53 significantly reduced SOCE-induced VASP and CREB phosphorylation.

54 dilator-stimulated phosphoprotein (VASP) and CREB.

55 ings reveal an essential role for Zfp189 and CREB-Zfp189 interactions in mediating a central transcri

56 vel role for the CLOCK protein to antagonize CREB-mediated transcriptional activity at the tyrosine h

57 This receptor-dependent effect, as well as CREB phosphorylation, was blocked by a construct derived

58 unknown despite the fact that the astrocytic CREB is also activity-driven and neuroprotective.

59 This TGF-beta-CREB-Hedgehog signaling axis allows a key metabolic tiss

60 how experience shapes the interplay between CREB and neuronal activity in the neocortex of awake mic

61 We found minimal overlap between CREB signatures in astrocytes and neurons.

62 ellular regulators and roles of CRTCs beyond CREB.

63 requires the cAMP-response element binding (CREB) interaction domain of the histone acetyltransferas

64 nophosphate (cAMP) response element binding (CREB)/CREB binding protein-mediated expression of the pu

65 P), and cyclic AMP-response element-binding (CREB) protein (CBP).

66 horylation of cAMP response element-binding (CREB) protein on the IL-10 promoter.

67 ucts indicate that the regulation of BDNF by CREB family after BDNF-TrkB signaling is generally conse

68 y contrast, the gene networks coordinated by CREB in astrocytes are unknown despite the fact that the

69 ed by TK and PI-3K pathways and modulated by CREB, HSF-4a, HDACs, and modified histones.

70 tes, the top triad of functions regulated by CREB consists of 'Gene expression', 'Mitochondria', and

71 ed the transcriptional programs regulated by CREB in astrocytes as compared to neurons using, as stud

72 ed SOCE via TRPC4 channels stimulates CaMKII/CREB-dependent GMC proliferation and ECM protein product

73 ting SD-mediated effects on hippocampal cAMP-CREB-BDNF, cAMP-PKA-LIMK1-cofilin, and RhoA-ROCK2 pathwa

74 otein kinase A (PKA) is a well-characterized CREB activation mechanism.

75 egulated by MDV U(S)3 and identified chicken CREB (chCREB) as a substrate of MDV U(S)3.

76 The transcriptional coactivartor CREB-regulated transcription coactivator-1 (CRTC1) is re

77 ocks the interaction between the coactivator CREB-binding protein (CBP) and beta-catenin, resulting i

78 ors depleted the transcriptional coactivator CREB-binding protein from the NF-kappaB complex in the n

79 prevents its interaction with a coactivator, CREB-binding protein, and subsequently reduces the BDNF

80 cription factor complex and its coactivators CREB-binding protein (CBP)/p300 and mixed-lineage leukem

81 ide 3-kinase (PI3K) pathway, with consequent CREB-dependent transcription of antiinflammatory genes,

82 The key mechanism controlling CREB-H activity involves its ER retention and forward tr

83 phate (cAMP) response element binding (CREB)/CREB binding protein-mediated expression of the purinerg

84 ion of RIbeta, but not of RIIbeta, decreased CREB phosphorylation.

85 hat iron down-regulates leptin by decreasing CREB glycosylation, resulting in increased CREB phosphor

86 Ca(2+)-dependent CREB/c-fos activation via Ca(2+)-calmodulin kinase IV (C

87 via mechanisms involving cAMP/PKA-dependent CREB activation.

88 ific transcriptional reprogramming to direct CREB or G9a (a repressive histone methyltransferase) to

89 r133 but not Ser271, suggesting two distinct CREB regulatory mechanisms by HIPK2 and PKA.

90 7ac at the promoter, recruits the C/EBPbeta (CREB-binding protein) and CBP transcription factors and

91 lear translocation and binding to endogenous CREB.

92 P increased the phosphorylation of p38, ERK, CREB, and Ser-727 of STAT3 and induced nuclear transloca

93 Furthermore, integrated D1R-ERK-CREB and D2R-Akt-GSK3 pathways in the vHip-mPFC circuit

94 sition increased the activity of the D1R-ERK-CREB pathway in both the vHip and mPFC.

95 gene expression is the transcription factor CREB (cAMP-responsive element binding protein).

96 a the activation of the transcription factor CREB in the injured DRG after peripheral nerve injury.

97 The transcription factor CREB is a predicted upstream regulator of this network a

98 factors converge on the transcription factor CREB, indicating that CREB signaling is a key hub mediat

99 ble domain (KID) of the transcription factor CREB, which interacts with the KIX domain of CREB-bindin

100 pends upon cAMP and the transcription factor CREB.

101 the activation of the transcriptional factor CREB.

102 The transcription factors CREB (cAMP response element binding factor), SRF (serum

103 e specific role of the transcription factors CREB, SRF, and MEF2 in the depression and potentiation c

104 genes regulated by the transcription factors CREB/CREM (cAMP response element-binding protein/modulat

105 MDA receptor (NMDAR) integrity and function, CREB-mediated transcription, and neuronal firing of rela

106 Functional CREB signatures were extracted from the transcriptomes u

107 nd decreased the occupancy of O-GlcNAcylated CREB on the leptin promoter.

108 oding the histone acetyl-transferases (HATs) CREB binding protein (CREBBP) and EP300 are recurrently

109 Our data identify CREB activation via PGE(2) and FGF-2 as a previously unr

110 These results identify CREB modulation as a potential therapy to treat age-rela

111 tes that hippocampal-specific alterations in CREB signaling and synaptic plasticity may underlie cert

112 ic viral injections of AAV-GFP or AAV-CRE in CREB(loxP/loxP) animals, behavioral testing measured anx

113 al cell line HT-22 leading to an increase in CREB phosphorylation.

114 agonist induced only transient increases in CREB phosphorylation and COX-2 expression in amnion fibr

115 EP2 agonist caused long-lasting increases in CREB phosphorylation and COX-2 expression, whereas an EP

116 of several transcription factors, including CREB, ATF2, C/EBP, USF, and NFAT.

117 h activation of signaling pathways including CREB, mTOR, and Src-FAK.

118 RSK1 and MSK2 downstream targets, including CREB and ATF1.

119 tion of p65 at Thr-305 and Ser-319 increased CREB-binding protein (CBP)/p300-dependent activating ace

120 g CREB glycosylation, resulting in increased CREB phosphorylation and leptin promoter occupancy by pC

121 pression, and viral vector-induced increased CREB expression in Crh neurons increased fear expression

122 t kinase-dead U(S)3 (U(S)3-K220A), increases CREB phosphorylation, leading to recruitment of phospho-

123 wever, it has yet to be tested if increasing CREB expression also ameliorates age-related behavioral

124 Indeed, CREB-induced hyperacetylation of chromatin over superenh

125 66-15 although 653-47 alone does not inhibit CREB.

126 rther found that TDP-43 dysfunction inhibits CREB activation and CREB transcriptional output, and res

127 stablishing the causal requirement of intact CREB function specifically within the DG engram during m

128 owever, ApoE-induced synaptogenesis involves CREB activation rather than cFos activation.

129 f AMPK that is relevant to cAMP signaling is CREB; decreased levels of phospho-CREB seem to mediate t

130 in cell growth via inhibition of AKT, NF-kB, CREB and AP-1 activation in DeltaMEGF11 MDA-MB-231 and 4

131 Lastly, CREB-binding protein/p300 acetylated FUS, whereas both s

132 etine treatment could disassociate the MeCP2-CREB-Bdnf promoter IV complex via phosphorylation of MeC

133 ally identified for their role in modulating CREB transcription, the past 5 years has seen an expansi

134 europeptide, at levels capable of modulating CREB signaling in the mouse brain.

135 polysaccharide that activates a specific MSK/CREB-dependent anti-inflammatory and repair gene signatu

136 slocation of transcription factors NFkappaB, CREB, and NFAT1.

137 and transcriptional activation of NFkappaB, CREB and NFAT1.

138 ndings establish that targeting IL1beta-NFKB/CREB-Wnt signalling should be considered for adjuvant th

139 response to TLR4 agonists, neither MSKs nor CREB are required for IL-10 production in these cells.

140 es AMPK to selectively induce EP300, but not CREB-binding protein (CBP).

141 for sustained activity of Erk1/2 and nuclear CREB phosphorylation, and increased transcription of a B

142 ng pathway that ultimately increases nuclear CREB phosphorylation and, in most cases, expression of i

143 for increased phosphorylation of the nuclear CREB transcription factor and expression of c-Fos induce

144 Finally, pharmacological activation of CREB in the female Mecp2 heterozygous mice rescued sever

145 ion of CREB or pharmacological activation of CREB signaling in those forebrain neurons rescued the ph

146 f the CREB-responsive gene and activation of CREB target gene expression.

147 strocyte exposed to well-known activators of CREB-dependent transcription as well as publicly availab

148 tion analyses reveal constitutive binding of CREB to target gene promoters in the absence of neuronal

149 t the P-motif provides integrated control of CREB-H function, coupling intercompartmental transport i

150 Deletion of CREB in the ventral, but not dorsal, hippocampus resulte

151 One such mechanism is deregulation of CREB-regulated transcriptional coactivators (CRTCs).

152 CREB, which interacts with the KIX domain of CREB-binding protein upon phosphorylation.

153 2+) elevations and prolonged the duration of CREB activation to more than 24 h in the visual cortex.

154 This study examines the effects of CREB deletion specifically in the ventral or dorsal hipp

155 nsfer to block the transcription function of CREB, SRF, and MEF2 in the visual cortex, and measured v

156 consolidation, and identify a novel group of CREB target genes involved in the encoding of long-term

157 nism is the Nr4a family of genes, a group of CREB-dependent nuclear orphan receptors that have previo

158 inhibition of PI3K enhanced the induction of CREB and STAT3 phosphorylation and COX-2 expression by P

159 RTC1) is required for efficient induction of CREB target genes during neuronal activity.

160 Knockdown of CREB with antisense oligodeoxynucleotide against CREB re

161 ound a significant reduction in the level of CREB and phosphorylated CREB in forebrain neurons differ

162 uclear co-activator binding domain (NCBD) of CREB-binding protein, each forming three well-defined al

163 Importantly, overexpression of CREB or pharmacological activation of CREB signaling in

164 ed RANKL+/-TNF-stimulated phosphorylation of CREB and expression of c-fos in BMMs (p < 0.01), culmina

165 sional cortex by reducing phosphorylation of CREB and PSD95 proteins after TBI.

166 ccurred with no effect on phosphorylation of CREB in D1 dopaminoceptive neurons of NAc.

167 Phosphorylation of CREB protein prevents its interaction with a coactivator

168 trated that RvD2 enhanced phosphorylation of CREB, ERK1/2, and STAT3 in WT but not DRV2-KO macrophage

169 2) hyperactivation to the phosphorylation of CREB-binding protein (CBP).

170 mediated by induction of phosphorylation of CREB.

171 t genes are induced following recruitment of CREB and its coactivators to promoter proximal binding s

172 g nucleosome-free regions for recruitment of CREB to beta cell-specific enhancers.

173 ndent and was mediated by the recruitment of CREB to its responsive element in the IL-10 promoter.

174 tion with KIX, the disordered pKID region of CREB protein is central in the transcription of cAMP res

175 In this study, we tested the role of CREB, SRF, and MEF2 in ocular dominance plasticity (ODP)

176 asive evidence towards the distinct roles of CREB within the dorsal and ventral hippocampus separatel

177 Dark rearing increased the sensitivity of CREB activity to Ca(2+) elevations and prolonged the dur

178 rs to chronically image in vivo signaling of CREB, an activity-dependent transcription factor importa

179 Transfection of CREB in HEK293 cells together with the kinase demonstrat

180 phosphorylation and nuclear translocation of CREB.

181 ateral pre-motor cortex, and upregulation of CREB and DLK signaling.

182 ion was closely associated with NF-kappaB or CREB motifs.

183 of co-activator complexes containing p300 or CREB-binding protein (CBP), and increased acetylation of

184 phorylation but not cyclic AMP production or CREB phosphorylation.

185 st this hypothesis, we virally overexpressed CREB in CA1 of dorsal hippocampus.

186 Concurrently, cells overexpressing CREB in aged animals had reduced post-burst afterhyperpo

187 n of CRFR1-GFP cells with phosphorylated (p) CREB.

188 ylated NF-kappaB (p-NF-kappaB), MARCO, and p-CREB were measured with western blot and RNAseq.

189 ed a significantly higher concentration of p-CREB in granulomas.

190 developed granulomas, while expression of p-CREB was not changed.

191 ion through the inhibition of the cAMP/PKA/p-CREB pathway, or by blocking adenosine signaling downstr

192 pho-cAMP response element-binding protein (p-CREB), and cAMP response element (CRE)-Luc, or PDGF-indu

193 ects of alpha-MSH were blocked by specific p-CREB inhibition.

194 p300/CREB binding protein associated factor (PCAF/KAT2B) and

195 bitor of the protein acetyltransferases p300/CREB-binding protein (CBP).

196 Our results further suggest that p300/CREB-binding protein-mediated transcription factor acety

197 of the histone acetyltransferase paralogues CREB-binding protein (CBP) and E1A-binding protein P300

198 orylation, leading to recruitment of phospho-CREB (pCREB) to the promoter of the CREB-responsive gene

199 gnaling is CREB; decreased levels of phospho-CREB seem to mediate the observed effects of metformin o

200 yperglycemia promoted phospho-p65 or phospho-CREB and CBP bindings and RNA polymerase II recruitment

201 CREB activity (phosphorylated CREB) was also increased by DHA and EPA but not by SA.

202 tion in the level of CREB and phosphorylated CREB in forebrain neurons differentiated from MECP2(T158

203 eurotrophic factor (BNDF) and phosphorylated CREB, both in young (3-week-old) and adult ( 7-month-old

204 inase demonstrated that HIPK2 phosphorylated CREB at Ser271 but not Ser133; likewise, PKA phosphoryla

205 but not Ser133; likewise, PKA phosphorylated CREB at Ser133 but not Ser271, suggesting two distinct C

206 known as PA1) cooperates with phosphorylated CREB and ligand-activated glucocorticoid receptor to dir

207 cellular gene expression by phosphorylating CREB at Ser133 and by promoting the dephosphorylation of

208 In some cases, for example Dopamine-PKA-CREB and GABA-PKC-CREB signaling pathways, the biotypes

209 tes sAC which in turn activates the cAMP/PKA/CREB axis.

210 phospho-ERK activation, independently of PKA/CREB signaling.SIGNIFICANCE STATEMENT ERK phosphorylatio

211 , for example Dopamine-PKA-CREB and GABA-PKC-CREB signaling pathways, the biotypes were oppositely dy

212 Previously, we identified 666-15 as a potent CREB inhibitor.

213 To probe CREB-Zfp189 interactions, we employ CRISPR-mediated locu

214 ersed cAMP response element-binding protein (CREB) activation and activity-regulated cytoskeleton-ass

215 elial cAMP response element-binding protein (CREB) activation and subsequent synthesis and secretion

216 ive cAMP-responsive element-binding protein (CREB) and a cluster termed C24-DS2 binding the vitamin D

217 tors, cAMP-response element-binding protein (CREB) and heat-shock factor-4a (HSF-4a) facilitated the

218 on of CAMP response element binding protein (CREB) and PSD95 after TBI.

219 ctors cAMP-response element binding protein (CREB) and signal transducer and activator of transcripti

220 ate (cAMP) response element-binding protein (CREB) family transcription factors within their native c

221 of cAMP-responsive element-binding protein (CREB) for induction of Ralpha2 expression, they neverthe

222 tor cAMP-responsive element-binding protein (CREB) is essential for a wide range of brain processes.

223 ndent cAMP response element binding protein (CREB) phosphorylation.

224 Cyclic AMP-response element-binding protein (CREB) plays key transcriptional roles in cell metabolism

225 f the cAMP response element-binding protein (CREB) signaling pathway.

226 (ERK)-cAMP-response element binding protein (CREB) signaling, as well as DA D2 receptor (D2R) and pro

227 eased cAMP response element-binding protein (CREB) signalling responses in adaptive immune cell types

228 et of cAMP response element-binding protein (CREB) that is activated by beta-adrenergic signaling.

229 actor cAMP response element-binding protein (CREB) to enhance the expression of proteins essential fo

230 f the cAMP response element-binding protein (CREB) transcription factor significantly slows Caenorhab

231 a(2+)/cAMP response element-binding protein (CREB) transcription factor.

232 f the cAMP response element binding protein (CREB), a transcriptional factor involved with learning a

233 3), CAMP-responsive element-binding protein (CREB), and brain-derived neurotropic factor (BDNF) by up

234 -kB), cAMP response element-binding protein (CREB), and glucocorticoid receptor (GR).

235 cule, cAMP-response element binding protein (CREB), which serves as a pivotal transcription factor fo

236 on of cAMP response element-binding protein (CREB), which, in turn, increased BDNF expression.

237 duced cAMP response element-binding protein (CREB)-binding protein (CBP)-mediated H3K9/14 hyperacetyl

238 on of cAMP response element-binding protein (CREB)-insulin receptor substrate 2 (Irs-2), and increase

239 ophosphate response element binding protein (CREB)-regulated transcription coactivator 1 (CRTC1) by a

240 tein, cAMP response element binding protein (CREB)-regulated transcription coactivator-1, Jacob, nucl

241 a(2+)/cAMP response element binding protein (CREB).

242 K and cAMP response element-binding protein (CREB).

243 antagonist, RP-cAMPs did not block n-3 PUFA CREB activation.

244 ated that extinction associates with reduced CREB expression, and viral vector-induced increased CREB

245 orter assays revealed that E2F3 up-regulates CREB expression and that Tat interferes with this up-reg

246 ers the CREB transcription factor to repress CREB-reporter gene activity.

247 mory enhancement by HDAC inhibitors requires CREB-CBP interaction and Nr4a gene function, these data

248 ty before postnatal ethanol exposure rescued CREB activation, Arc, chromatin remodeling and Rac1 expr

249 Ser271 CREB axis is a new arsenic-responsive CREB activation mechanism in parallel with the PKA-phosp

250 d CREB transcriptional output, and restoring CREB signaling rescues defects in dendritic branching.

251 Additionally, mutations in the second CREB-pKID/c-Myb-binding pocket of the KIX domain moderat

252 nism in parallel with the PKA-phospho-Ser133 CREB axis.

253 esults suggest that the HIPK2-phospho-Ser271 CREB axis is a new arsenic-responsive CREB activation me

254 Phospho-Ser271 CREB showed facilitated interaction with the TFIID subun

255 Simultaneous imaging of the red-shifted CREB sensor and GCaMP permitted exploration of how exper

256 ation (NF-kB) and beta-adrenergic signaling (CREB) and by decreased activity of GR-related TFs (P's <

257 esponsive element binding protein signaling [CREB]).

258 receptor of CD4(+) T cells, leading to SP1, CREB, and GATA1 activation and SOCS3 expression.

259 mechanisms regulating induction of specific CREB/CRTC1-dependent genes during neuronal activity rema

260 Induction of Zfp189 with site-specific CREB is pro-resilient, whereas suppressing Zfp189 expres

261 gonist-induced cAMP formation and subsequent CREB and G-protein-dependent ERK1/2 phosphorylation, in

262 F production induced by n-3 PUFA, suggesting CREB dependence.

263 Targeting CREB is a promising strategy to develop potential cancer

264 We conclude that CREB and STAT3 are the key transcription factors respons

265 We found that CREB stimulates the expression of pancreatic beta cell-s

266 We found that CREB, SRF, and MEF2 are all required for ODP, but have d

267 Our results indicate that CREB acts downstream of the transforming growth factor b

268 e transcription factor CREB, indicating that CREB signaling is a key hub mediating integration of syn

269 -dependent BDNF mRNA induction and show that CREB family transcription factors are the main regulator

270 We show that CREB family transcription factors, together with the coa

271 These findings suggest that CREB, within CeA Crh neurons, may function as a molecula

272 Therefore, our study suggests that CREB and PSD95 are novel substrates of PERK, so inhibiti

273 The CREB-dependence and cAMP independence of this process su

274 nd neuronal dendritic growth mediated by the CREB transcription factor.

275 However, the CREB specific inhibitor (666-15) diminished BDNF and GDN

276 Selective inhibitors of the CREB binding protein (CREBBP)/EP300 bromodomains are req

277 epolarization-induced phosphorylation of the CREB nuclear transcription factor, which stimulates the

278 U(S)3 thus acts as an upstream kinase of the CREB signaling pathway to regulate the transcription fun

279 ated its binding to another IDP, NCBD of the CREB-binding protein.

280 Further, mutation of the CREB-CBP interaction domain reduces Nr4a promoter acetyl

281 and attenuated in mice with mutation of the CREB-CBP interaction domain.

282 show that learning-induced expression of the CREB-regulated nuclear receptor gene Nr4a2 is selectivel

283 phospho-CREB (pCREB) to the promoter of the CREB-responsive gene and activation of CREB target gene

284 nt gene transcription upon activation of the CREB/CRTC1 signaling pathway in neurons.

285 o regulate the transcription function of the CREB/Meq heterodimer, which targets cellular and viral g

286 molecule 11 (653-47) that can potentiate the CREB inhibitory activity of 666-15 although 653-47 alone

287 ed expression of diffuse mHtt sequesters the CREB transcription factor to repress CREB-reporter gene

288 upregulation of Nurr1 expression through the CREB signaling pathway.

289 are enriched for pathways that signal to the CREB transcription factor.

290 presence of an E2F3-binding site within the CREB promoter, which we validated with ChIP and transien

291 9 treatment or feeding, SHP recruits LSD1 to CREB-bound autophagy genes, including Tfeb, resulting in

292 clic-AMP response-binding protein (pCREB) to CREB ratio in the hippocampus and medial prefrontal cort

293 The histone acetyl transferases CREB-binding protein (CBP) and its paralog p300 play a c

294 s the human promoter responsive to BDNF-TrkB-CREB signaling, whereas the rat ortholog is unresponsive

295 Ubiquitous CREB target genes are induced following recruitment of C

296 We further demonstrated that, upon CREB activation, HDAC2 represses thrombospondin-1 (TSP1)

297 the production of cAMP in islets, which via CREB mediated pathways results in the down-regulation of

298 n of all the major BDNF transcripts, whereas CREB itself directly binds only to BDNF promoter IV, is

299 istinct pattern of gene expression, in which CREB-dependent transcription features prominently (P = 6

300 ed gene array between cells transfected with CREB alone and CREB plus HIPK2 over empty vector-transfe