ライフサイエンスコーパス: CREB

1 CREB is activated following phosphorylation at a conserv

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

3 CREB overexpression in aged animals ameliorated the long

4 CREB phosphorylation also proceeds with slow, sigmoid ki

5 CREB phosphorylation was blocked by p38 inhibitors and i

6 CREB protein was elevated in TRAF3(-/-) B cells, without

7 CREB signaling is dysfunctional in the brains of mouse m

8 CREB, hepatocyte specific (CREBH) is a liver-enriched, e

9 CREB-binding protein (CBP) and p300 are highly homologou

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

11 CREB-mediated transcriptional activity was increased in

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

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

14 ent extracellular regulated kinase (ERK)1/2, CREB phosphorylation, and CB1 internalization following

15 with decreased cAMP-PKA-CREB and cAMP-ERK1/2-CREB signaling and neuroplasticity.

16 study uncovers a TET1/GFI1/EZH2/SIN3A/miR-22/CREB-MYC signalling circuit and thereby provides insight

17 In the same allele, we engineered a CREB-luciferase reporter transgene for noninvasive biolu

18 trocyte-neuron lactate shuttle, leading to a CREB-dependent increase in astrocytic glucose metabolism

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

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

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

22 These extracellular cues activate CREB through phosphorylation at Ser133 by various protei

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

24 otein (CBP) and its paralog p300 to activate CREB-dependent gene transcription.

25 of importin, which is required for activated CREB to get into the nucleus.

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

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

28 sponsive element binding protein activation (CREB activation) and identified 2 potential CREB-binding

29 fferent types of transcriptional activators: CREB/ATF-type Atf1, C(2)H(2)zinc finger-type Rst2, and C

30 or), and VP16-XlCreb1 (constitutively active CREB) would break the all-or-none concordance.

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

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

33 Furthermore, activation of an EGFR-PI3K-Akt-CREB signaling pathway mediated YAP gene expression and

34 and kidney through reduced VEGFR2/PKC-alpha/CREB signaling.

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

36 REB), activating transcription factor-1, and CREB-induced CRE modulator proteins in kidney nuclear pr

37 tional regulation of IL-10 by HIF-1alpha and CREB is critical for activation of Mvarphis by IFN-gamma

38 additional cell signaling pathways, AKT and CREB phosphorylation.

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

40 proliferation by regulating Calcineurin and CREB-regulated transcriptional co-activator (Crtc).

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

42 ng protein from up-regulating the CTNNB1 and CREB proteins and their target genes, indicating that WN

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

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

45 hosphorylation of target proteins (HSP27 and CREB) associated with intimal hyperplasia.

46 tively inactivated CRMP2, APC, S6 kinase and CREB.

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

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

49 phosphorylation of NF-kappaB, ERK, p38, and CREB in mouse bone marrow-derived DCs compared with sing

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

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

52 led to increased phosphorylation of p65 and CREB.

53 PLA2alpha/prostaglandin/cAMP/PKA pathway and CREB phosphorylation that coordinately regulate immediat

54 , MAPK-activated protein kinase 2, rpS6, and CREB phosphorylation in fetal Tbet(+)CD4(+) T cells, CD8

55 tutive neuronal COX-2 expression via Sp1 and CREB protein-dependent transcriptional mechanisms.

56 ibitors of PKC, p38, ERK, CaMKII, STAT3, and CREB partially blocked the activation of HAS2 expression

57 (ROS) production via activation of TGR5 and CREB.

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

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

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

61 ellular regulators and roles of CRTCs beyond CREB.

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

63 by inhibiting cAMP response element binding (CREB) protein and AKT phosphorylation, respectively.

64 CTNNB1) and cAMP responsive element binding (CREB) protein levels to decreaseviaa glycogen synthase k

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

66 Here, we show that both CREB and its activated form pCREB-Ser(133) (pCREB) are r

67 In honeybee brains, CREB-dependent genes are regulated in an age-dependent m

68 excitation-transcription coupling caused by CREB (cyclic adenosine monophosphate-responsive element-

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

70 -1a cells in bacterial sepsis is mediated by CREB and the identification of CREB in B-1a cells reveal

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

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

73 tion, such as the MAP kinases, MKPs, CaMKII, CREB, Fyn, and Tau.

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

75 a(2+)-dependent NFATc1 expression via CaMKIV/CREB during inflammatory osteoclastogenesis in the prese

76 CBP (CREB (cAMP responsive element binding protein) binding p

77 ade of the transcriptional coactivators CBP (CREB binding protein) and p300 as an alternative approac

78 he binding epitopes in the ZZ domain of CBP (CREB-binding protein) and SUMO1 using NMR spectroscopy.

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

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

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

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

83 presence of its transcriptional coactivator, CREB-binding protein (CBP).

84 association with transcription coactivators CREB-binding protein (CBP) and its paralog p300 to activ

85 The transcriptional coactivators CREB-binding protein (CBP) and p300 undergo a particular

86 Similarly, the transcription cofactors CREB-binding protein (CBP) and p300 are reduced in the p

87 of GsD in the liver results in constitutive CREB activity and hyperglycemia.

88 In contrast, CREB deletion in the dorsal hippocampus resulted in lear

89 ty evolved as a tunable mechanism to control CREB transcriptional output and promote metabolic homeos

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

91 MP-responsive element-binding protein (CREB)/CREB-regulated transcription coactivator (CRTC) activati

92 signaling pathway, thereby facilitating CRTC/CREB-mediated transcription.

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

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

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

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

97 ucleus, which appears required for efficient CREB phosphorylation and gene transcription.

98 -wide transcriptional analysis of C. elegans CREB mutants.

99 lear translocation and binding to endogenous CREB.

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

101 n factor c-myb to the cotranscription factor CREB binding protein (CBP).

102 ith the activity of the transcription factor CREB (cAMP-response element binding protein).

103 ession was regulated by transcription factor CREB (cAMP-response element-binding protein) and silenci

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

105 creased activity of the transcription factor CREB in HIF-1alpha-deficient Mvarphis drove IL-10 produc

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

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

108 Basal binding of the transcription factors CREB and Sp1 to the native neuronal COX-2 promoter was c

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

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

111 harmacologically relevant concentrations for CREB inhibition.

112 Functional CREB signatures were extracted from the transcriptomes u

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

114 there might be a role for neuronal honeybee CREB (Apis mellifera CREB, or AmCREB) in the bee's divis

115 However, CREB transcription is upregulated by both clade B and C

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

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

118 of the ATM/CK cluster potentiated bursts in CREB-mediated transcription by promoting recruitment of

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

120 thout change in mRNA, but with a decrease in CREB ubiquitination.

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

122 be involved in GC differentiation including CREB, ss-catenin, AKT, p42/44 MAPK, GAB2, GSK-3ss, FOXO1

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

124 rther augmented by nicotine due to increased CREB phosphorylation and thereby increases the risk for

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

126 on and/or overactivation of CREB, indicating CREB as a potential cancer drug target.

127 e, we report that VZV infection also induced CREB phosphorylation in fibroblasts and that XX-650-23,

128 activator in IFN signaling, thereby inducing CREB-binding protein downregulation in EBV-transformed B

129 sphorylation of the ATM/CK cluster inhibited CREB-mediated gene expression, DNA binding activity and

130 at 666-15 was fairly selective in inhibiting CREB.

131 APP-CTF accumulation initiates CREB signaling cascade through an association of APP-CTF

132 hermore, we found that miR-188 expression is CREB-dependent.

133 re associated with nearby activation of MAPK/CREB signalling, a marker of epileptic activity, in supe

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

135 e for neuronal honeybee CREB (Apis mellifera CREB, or AmCREB) in the bee's division of labor.

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

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

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

139 Notably, CREB, a factor involved in the regulation of several cel

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

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

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

143 al release of endothelin-1 and activation of CREB.

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

145 o be composed of the enzymatic activities of CREB-binding protein (CBP) and SMARCAD1, which belongs t

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

147 olished promoter activity and the binding of CREB, confirming the importance of this region and of it

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

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

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

151 rdered nuclear coactivator binding domain of CREB binding protein (UniProt CBP_MOUSE P45481 ), residu

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

153 athway that HDAC2 and TSP1 act downstream of CREB activation in beta-adrenergic signaling to promote

154 tients, indicating additional dysfunction of CREB signaling in AD.

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

156 ely abrogated by a dominant-negative form of CREB.

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

158 s mediated by CREB and the identification of CREB in B-1a cells reveals a potential avenue for treatm

159 REB is therefore regarded as an indicator of CREB-dependent transcriptional activation.

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

161 monstrate that pharmacological inhibition of CREB is well-tolerated in vivo and indicate that such in

162 regulates B-cell survival via inhibition of CREB stability, information highly relevant to the role

163 y identified 666-15 as a potent inhibitor of CREB with efficacious anti-cancer activity both in vitro

164 Knockdown of CREB significantly decreased TDCA-induced increase in NO

165 Knockdown of CREB with antisense oligodeoxynucleotide against CREB re

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

167 othesize that the IC display a high level of CREB-dependent transcription that might be related to ne

168 he fourth intrinsically disordered linker of CREB-binding protein (CBP).

169 or noninvasive bioluminescence monitoring of CREB activity.

170 sent overexpression and/or overactivation of CREB, indicating CREB as a potential cancer drug target.

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

172 Conversely, overexpression of CREB significantly increased TDCA-induced TM increase.

173 However, overexpression of CREB, which increases excitability of AcbSh neurons, enh

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

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

176 Here we show that phosphorylation of CREB on a conserved cluster of Ser residues (the ATM/CK

177 Phosphorylation of CREB protein prevents its interaction with a coactivator

178 mice revealed facilitated phosphorylation of CREB, decreased binding to DISC1, and upregulation of DI

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

180 ese results further support the potential of CREB as a valuable cancer drug target.

181 Thus, processes of CREB activation and p300/CBP binding are important for V

182 Ethanol exposure blocked the recruitment of CREB and its coactivator CRTC2 to gluconeogenic promoter

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

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

185 , reveals a previously unappreciated role of CREB signaling in RTT pathogenesis, and identifies a pot

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

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

188 se element-binding protein) and silencing of CREB resulted in reduced expression of MCL-1 and increas

189 tion of MYC and YAP through stabilization of CREB.

190 a reduction in the phosphorylation status of CREB (pCREB).

191 Y, which we show here is a direct target of CREB and Crtc.

192 findings, Mcl-1, an antiapoptotic target of CREB-mediated transcription, was increased in the absenc

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

194 phosphorylation and nuclear translocation of CREB.

195 of candidate enhancer regions using data on CREB-binding protein co-factor binding or ATAC-seq chrom

196 logic or genetic inhibition of EGFR, Akt, or CREB blunted YAP expression in response to high-glucose

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

198 f the homologous Kat3 co-activators, p300 or CREB-binding protein, differentially regulates maintenan

199 phorylation but not cyclic AMP production or CREB phosphorylation.

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

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

202 taining also revealed higher expression of P-CREB in Pkd2(-/) (WS25);Pde1a(-/-), Pkd2(-) (/WS25);Pde1

203 (Ser133) cAMP-responsive binding protein (P-CREB), activating transcription factor-1, and CREB-induc

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

205 tivity of the histone acetyltransferase p300/CREB-binding protein (CBP) in regulating promoter-proxim

206 directly modulate the signaling pathway p38-CREB in DCs, thereby impairing cytokine production and i

207 We found that Crtc and its binding partner CREB enhance energy homeostasis by stimulating the expre

208 ve to survival inhibition with pharmacologic CREB inhibitor.

209 IV, protecting against saturation of phospho-CREB in the face of higher firing rates and bigger Ca(2+

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

211 from mice expressing a non-phosphorylatable CREB allele failed to attenuate gluconeogenic genes in r

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

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

214 and HIPK1 and HIPK3, directly phosphorylated CREB.

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

216 or-alpha levels and increased phosphorylated CREB levels after TBI, suggesting that this drug inhibit

217 An increase of phosphorylated CREB is therefore regarded as an indicator of CREB-depen

218 together, specific binding of phosphorylated CREB to the G allele-carrying promoter enhances MMP7 gen

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

220 y identified inhibitor of the phosphorylated-CREB (pCREB) interaction with p300/CBP, restricted cell-

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

222 eficits, accompanied with decreased cAMP-PKA-CREB and cAMP-ERK1/2-CREB signaling and neuroplasticity.

223 racts with adenylate cyclase, activating PKA/CREB, and inhibiting GSK-3.

224 eceptors, and their downstream effectors PKA/CREB and DAG/IP3.

225 Elevated PKA/CREB activity in healthy flies produces patterns of slee

226 We were curious whether aberrations in PKA/CREB signaling were responsible for our early-onset slee

227 (CREB activation) and identified 2 potential CREB-binding sites in the mouse leptin promoter region.

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

229 duced cAMP-response-element binding protein (CREB) activation, a critical pathway involved in learnin

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

231 lates CAMP response element binding protein (CREB) and PSD95 directly at the S129 and T19 residues, r

232 ative cAMP response element binding protein (CREB) and was eliminated by mutating the CRE-binding sit

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

234 lator cAMP response element binding protein (CREB) in both mouse and human B cells.

235 actor cAMP response element-binding protein (CREB) in young adult rodents facilitates cognition, and

236 cAMP response element binding protein (CREB) is a key regulator of glucose metabolism and synap

237 cAMP-response element binding protein (CREB) is a nuclear transcription factor activated by mul

238 cyclic AMP response element binding protein (CREB) is a primary hub of activity-driven genetic progra

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

240 of cAMP-responsive element-binding protein (CREB) is strongly decreased in prefrontal cortex of Nf1(

241 eased cAMP response element binding protein (CREB) phosphorylation in FLO-1 cells.

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

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

244 Cyclic-AMP response element-binding protein (CREB) signaling has a critical role in the formation of

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

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

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

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

249 ctor, cAMP response element-binding protein (CREB), and by an inhibitor of importin, which is require

250 on of cAMP-response element-binding protein (CREB), the cAMP-regulated transcription factor involved

251 of cAMP-responsive element binding protein (CREB), the transcription factor that represses leptin tr

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

253 cyclic-AMP response element-binding protein (CREB)-binding protein (CBP) and p300, which activate tra

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

255 o the cAMP response element binding protein (CREB)-binding protein reveals that the pLxIS motif also

256 vator cAMP response element binding protein (CREB)-cAMP-regulated transcription coactivator (Crtc) ha

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

258 P-PKA-cAMP response element-binding protein (CREB).

259 clic AMP-responsive element-binding protein (CREB)/CREB-regulated transcription coactivator (CRTC) ac

260 N-beta promoter and its coactivator protein (CREB-binding protein).

261 Rats received CREB or control virus, before undergoing water maze trai

262 of a 5-HT6 receptor inverse agonist reduces CREB phosphorylation in prefrontal cortex of WT mice but

263 e2 (CK2) positively and negatively regulates CREB-mediated transcription in a signal dependent manner

264 on resistance in Drosophila by up-regulating CREB target gene expression in neurons, although the und

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

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

267 Restoring CREB activity and silencing PTPN22 enhanced NSTEMI patie

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

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

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

271 and region-dependent alterations of several CREB target genes that are well-known markers of neuropl

272 esponsive element binding protein signaling [CREB]).

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

274 miR-BART16 directly targets CREB-binding protein, a key transcriptional coactivator

275 damage may depend on the activation of TGR5, CREB and NOX5-S.

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

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

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

279 r's disease (AD), and evidence suggests that CREB signaling may be disrupted in human AD brains as we

280 s demonstrate how cross-coupling between the CREB/CRTC and JAK/STAT pathways contributes to BM homeos

281 3 bound to its transcriptional cofactor, the CREB-binding protein.

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

283 ranscription by promoting recruitment of the CREB coactivator, cAMP-regulated transcriptional coactiv

284 of Brd4 and BrdT, and the KIX domain of the CREB-binding protein) using commercially available fluor

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

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

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

288 RTC1, FLT3 and MYCBP, and thus represses the CREB and MYC pathways.

289 lity of HIPK1 and HIPK2 proteins, leading to CREB activation via Ser271 phosphorylation.

290 9 treatment or feeding, SHP recruits LSD1 to CREB-bound autophagy genes, including Tfeb, resulting in

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

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

293 oy a novel CaMK-dependent pathway to trigger CREB phosphorylation and gene expression.

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

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

296 restricted cell-cell spread of VZV in vitro CREB phosphorylation did not require the viral open read

297 emory deficits in fear conditioning, whereas CREB deletion in the ventral hippocampus showed an enhan

298 rovide a tool to explore novel means whereby CREB impinges on brain functions requiring adaptive, lon

299 TRAF3 and enhanced Mcl-1 was suppressed with CREB inhibition.

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