PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 22827930-7 2012 Furthermore, pharmacological targeting of mTORC1 with rapamycin also blocked LH/hCG- or forskolin-induced expression of cAMP response element-binding protein (CREB) and steroidogenic enzymes (P450 side-chain cleavage enzyme, 3beta-hydroxysteroid dehydrogenase type 1, and 17alpha-hydroxylase/17,20 lyase) but produced no effect on steroidogenic acute regulatory protein levels. Colforsin 88-97 cAMP responsive element binding protein 1 Homo sapiens 120-157 22827930-7 2012 Furthermore, pharmacological targeting of mTORC1 with rapamycin also blocked LH/hCG- or forskolin-induced expression of cAMP response element-binding protein (CREB) and steroidogenic enzymes (P450 side-chain cleavage enzyme, 3beta-hydroxysteroid dehydrogenase type 1, and 17alpha-hydroxylase/17,20 lyase) but produced no effect on steroidogenic acute regulatory protein levels. Colforsin 88-97 cAMP responsive element binding protein 1 Homo sapiens 159-163 21698527-8 2011 Forskolin (0.05 and 1 mM) acted in synergy with FGF-2 and EGF; however, it caused pronounced donor to donor differences in the increase of cAMP and phospho-CREB levels. Colforsin 0-9 cAMP responsive element binding protein 1 Homo sapiens 156-160 22227470-9 2012 Co-treatment with rolipram and forskolin also enhanced CREB phosphorylation on serine 133 that was inhibited by H-89, PKA inhibitor and cAMP-responsive guanine nucleotide exchange factor 1(Epac1), a Rap GDP exchange factor-mediated Rap1 activity in A172 cells. Colforsin 31-40 cAMP responsive element binding protein 1 Homo sapiens 55-59 22057271-9 2011 Forskolin-stimulated RGS2 mRNA up-regulation is inhibited by CREB sequestration or specific disruption of the CREB-RGS2 promoter interaction, and Ang II-induced CREB phosphorylation and nuclear localization are blocked by iPLA(2)beta pharmacologic inhibition or genetic ablation. Colforsin 0-9 cAMP responsive element binding protein 1 Homo sapiens 61-65 22057271-9 2011 Forskolin-stimulated RGS2 mRNA up-regulation is inhibited by CREB sequestration or specific disruption of the CREB-RGS2 promoter interaction, and Ang II-induced CREB phosphorylation and nuclear localization are blocked by iPLA(2)beta pharmacologic inhibition or genetic ablation. Colforsin 0-9 cAMP responsive element binding protein 1 Homo sapiens 110-119 22057271-9 2011 Forskolin-stimulated RGS2 mRNA up-regulation is inhibited by CREB sequestration or specific disruption of the CREB-RGS2 promoter interaction, and Ang II-induced CREB phosphorylation and nuclear localization are blocked by iPLA(2)beta pharmacologic inhibition or genetic ablation. Colforsin 0-9 cAMP responsive element binding protein 1 Homo sapiens 110-114 22532442-3 2012 Native cellular responses [cAMP elevation, ERK phosphorylation, cAMP responsive element binding (CREB) phosphorylation, and neuritogenesis] and promoter-reporter gene activation after treatment with forskolin, cAMP analogs, and PACAP were measured in Neuroscreen-1 (NS-1) cells, a PC12 variant enabling simultaneous morphological, molecular biological, and biochemical analysis. Colforsin 199-208 cAMP responsive element binding protein 1 Homo sapiens 97-101 22185778-7 2012 The binding of Daxx to CREB correlates with its repressive effect on a CRE-mediated reporter activity induced by forskolin or PKA. Colforsin 113-122 cAMP responsive element binding protein 1 Homo sapiens 23-27 23185487-8 2012 Finally, phosphorylation of cAMP-response element binding protein (CREB) and up-regulation of CREB target genes by GC were inhibited by RCAN1 disruption, and treatment with a cAMP-inducing agent, forskolin, restored the sensitivity to GC in RCAN1-disrupted Nalm-6 cells. Colforsin 196-205 cAMP responsive element binding protein 1 Homo sapiens 67-71 23185487-8 2012 Finally, phosphorylation of cAMP-response element binding protein (CREB) and up-regulation of CREB target genes by GC were inhibited by RCAN1 disruption, and treatment with a cAMP-inducing agent, forskolin, restored the sensitivity to GC in RCAN1-disrupted Nalm-6 cells. Colforsin 196-205 cAMP responsive element binding protein 1 Homo sapiens 94-98 20845474-10 2010 The effects of DETA/NONOate were reversed by forskolin, an activator of CREB signaling. Colforsin 45-54 cAMP responsive element binding protein 1 Homo sapiens 72-76 21344481-6 2011 Similarly, activation of CREB by the adenylate cyclase agonist forskolin failed to induce EphA2 promoter activation. Colforsin 63-72 cAMP responsive element binding protein 1 Homo sapiens 25-29 21075212-10 2011 Moreover, we have also found forskolin, PKA activator, could enhance open chromatin accessibility, by which to expose the CRE and facilitate phosphorylation of CREB, which in turn recruits co-factor CBP and Brg I and then results in a more open chromatin configuration associated with local histone modification, finally heightening RAB25 expression and strengthening its promoter activity. Colforsin 29-38 cAMP responsive element binding protein 1 Homo sapiens 160-164 21035520-4 2011 Forskolin treatment induced a rapid and potent ERK1/2 and p38MAPK phosphorylation; this cascade required PKA-AKAP interactions and led to downstream CREB-1/ATF-1 phosphorylation via ERK1/2-dependent but p38MAPK-independent mechanisms. Colforsin 0-9 cAMP responsive element binding protein 1 Homo sapiens 149-155 21035520-5 2011 Interestingly both p38MAPK and ERK1/2 were involved in forskolin-induced hCG-secretion, suggesting the presence of additional p38MAPK-dependent but CREB-1/ATF-1-independent pathways. Colforsin 55-64 cAMP responsive element binding protein 1 Homo sapiens 148-154 20589829-4 2010 Interestingly, intracellular cAMP elevation upon forskolin pretreatment completely abrogated both ERK1/2 and STAT3 phosphorylation in response to leptin and was accompanied by a consistent CREB phosphorylation. Colforsin 49-58 cAMP responsive element binding protein 1 Homo sapiens 189-193 20589829-6 2010 Importantly, pretreatment with the PKA inhibitor KT-5720 blocked the forskolin-induced CREB phosphorylation and prevented both the inhibition by forskolin of leptin-induced ERK1/2 and STAT3 phosphorylation and the PKA subunits down-regulation induced by the combination of leptin and forskolin. Colforsin 69-78 cAMP responsive element binding protein 1 Homo sapiens 87-91 19416972-4 2009 Chromatin immunoprecipitation and re-chromatin immunoprecipitation assays using selected fragments of the promoter containing the putative REs showed that forskolin and all-trans-RA modulate the formation of complexes between CREB1 and RAR with various co-regulators at the predicted sites. Colforsin 155-164 cAMP responsive element binding protein 1 Homo sapiens 226-231 20053791-0 2010 CREB trans-activation of disruptor of telomeric silencing-1 mediates forskolin inhibition of CTGF transcription in mesangial cells. Colforsin 69-78 cAMP responsive element binding protein 1 Homo sapiens 0-4 20053791-8 2010 Overexpression of CREB enhanced forskolin-stimulated Dot1 promoter activity. Colforsin 32-41 cAMP responsive element binding protein 1 Homo sapiens 18-22 20053791-12 2010 We conclude that forskolin stimulates CREB-mediated trans-activation of the Dot1 gene, which leads to hypermethylation of histone H3K79 at the CTGF promoter, and inhibition of CTGF transcription. Colforsin 17-26 cAMP responsive element binding protein 1 Homo sapiens 38-42 19683536-4 2009 The Cyclin C gene also directly responds to the cAMP activator Forskolin via the transcription factor CREB1 (cAMP response element-binding protein 1), for which we identified four binding sites within the first 2250 bp of its promoter. Colforsin 63-72 cAMP responsive element binding protein 1 Homo sapiens 102-107 19683536-4 2009 The Cyclin C gene also directly responds to the cAMP activator Forskolin via the transcription factor CREB1 (cAMP response element-binding protein 1), for which we identified four binding sites within the first 2250 bp of its promoter. Colforsin 63-72 cAMP responsive element binding protein 1 Homo sapiens 109-148 19416972-5 2009 Interestingly, CREB1 complexes are regulated by all-trans-RA as are RAR complexes by forskolin. Colforsin 85-94 cAMP responsive element binding protein 1 Homo sapiens 15-20 19416972-7 2009 Forskolin and all-trans-RA co-stimulation reduced the binding of CREB1, RAR, and the co-repressor nuclear receptor co-repressor 1 (NCoR1), but enhanced the association of co-activators MED1 and CREB-binding protein (CBP). Colforsin 0-9 cAMP responsive element binding protein 1 Homo sapiens 65-70 18483184-7 2008 Direct cAMP stimulation with forskolin resulted in enhanced human GRP-R promoter activity only in HuTu-80 cells, but not in Caco-2 cells, coinciding with forskolin-induced CREB phosphorylation occurring only in HuTu-80 but not Caco-2 cells. Colforsin 29-38 cAMP responsive element binding protein 1 Homo sapiens 172-176 19385062-3 2009 Forskolin stimulated angiogenesis of human endothelial cells and in vivo neovascularization, which was accompanied by phosphorylation of CREB, ERK, Akt, and endothelial nitric oxide synthase (eNOS) as well as NO production and VEGF expression. Colforsin 0-9 cAMP responsive element binding protein 1 Homo sapiens 137-141 19385062-4 2009 Forskolin-induced CREB phosphorylation, VEGF promoter activity, and VEGF expression were blocked by the PKA inhibitor PKI.Moreover, phosphorylation of ERK by forskolin was inhibited by the MEK inhibitor PD98059, but not PKI. Colforsin 0-9 cAMP responsive element binding protein 1 Homo sapiens 18-22 19385062-4 2009 Forskolin-induced CREB phosphorylation, VEGF promoter activity, and VEGF expression were blocked by the PKA inhibitor PKI.Moreover, phosphorylation of ERK by forskolin was inhibited by the MEK inhibitor PD98059, but not PKI. Colforsin 158-167 cAMP responsive element binding protein 1 Homo sapiens 18-22 19070599-7 2009 Expression of recombinant HDAC8 results in decreased CREB activation and CREB mediated gene transcription in response to forskolin application. Colforsin 121-130 cAMP responsive element binding protein 1 Homo sapiens 73-77 19936037-5 2009 A variety of compounds which affect known members of the CREB pathway were identified as active, including twelve known phosphodiesterase (PDE) inhibitors, and forskolin, a known activator of adenylate cyclase, thus validating the assay"s performance. Colforsin 160-169 cAMP responsive element binding protein 1 Homo sapiens 57-61 18483184-7 2008 Direct cAMP stimulation with forskolin resulted in enhanced human GRP-R promoter activity only in HuTu-80 cells, but not in Caco-2 cells, coinciding with forskolin-induced CREB phosphorylation occurring only in HuTu-80 but not Caco-2 cells. Colforsin 154-163 cAMP responsive element binding protein 1 Homo sapiens 172-176 18372325-4 2008 Forskolin, at threshold concentrations for cAMP production and CREB phosphorylation, induced CRH promoter-driven luciferase activity in 4B cells (EC(50) = 0.7 microm) and CRH primary transcript in hypothalamic neurons (EC(50) = 0.6 microm). Colforsin 0-9 cAMP responsive element binding protein 1 Homo sapiens 63-67 18372325-5 2008 PMA alone failed to activate CRH transcription despite being as effective as forskolin in phosphorylating CREB (Ser133 and Ser121). Colforsin 77-86 cAMP responsive element binding protein 1 Homo sapiens 106-110 18372325-7 2008 Similarly, the calcium/calmodulin-dependent kinase inhibitor, KN-93, enhanced PMA plus forskolin-stimulated CREB phosphorylation and inhibited CRH transcription. Colforsin 87-96 cAMP responsive element binding protein 1 Homo sapiens 108-112 16959941-5 2006 Treatment with 10 microM forskolin or isoproterenol increased cAMP production and cAMP response element binding protein (CREB) phosphorylation in cardiac fibroblasts and inhibited serum- or TGF-beta-stimulated collagen synthesis by 37% or more. Colforsin 25-34 cAMP responsive element binding protein 1 Homo sapiens 82-119 17320350-7 2007 We found that cAMP/PKA/CREB pathway is indeed an important regulator of Smac/DIABLO transcription, since exposure to the cAMP analog 8-CPT-cAMP, the adenylyl cyclase activator forskolin, the inhibitor of phosphodiesterase isobutylmethylxanthine or by hindering PKA activation with H89, regulated the promoter activity, as shown by gene reporter and RT-PCR assays. Colforsin 176-185 cAMP responsive element binding protein 1 Homo sapiens 23-27 17325033-5 2007 Induction of CREB phosphorylation with forskolin or 6bnz-cAMP mimics TGFbeta"s inhibitory effect on cyclin A expression. Colforsin 39-48 cAMP responsive element binding protein 1 Homo sapiens 13-17 17152074-0 2007 Upregulation of AKT1 protein expression in forskolin-stimulated macrophage: evidence from ChIP analysis that CREB binds to and activates the AKT1 promoter. Colforsin 43-52 cAMP responsive element binding protein 1 Homo sapiens 109-113 17152074-1 2007 Recently, we reported that silencing CREB gene expression by RNAi significantly attenuates forskolin-induced activation of Akt1. Colforsin 91-100 cAMP responsive element binding protein 1 Homo sapiens 37-41 17152074-7 2007 Forskolin-dependent Akt1 synthesis was abolished by pretreating the cells with CREB-directed dsRNA as demonstrated at both the message and protein level, as well as by determining the synthesis of [(35)S]-labeled Akt1 protein. Colforsin 0-9 cAMP responsive element binding protein 1 Homo sapiens 79-83 17152074-11 2007 In conclusion, we show here for the first time transcriptional upregulation of Akt1 by CREB, based upon Akt1 protein synthesis and its modulation by transitional and translational inhibitors in forskolin-stimulated cells, Akt1 protein. Colforsin 194-203 cAMP responsive element binding protein 1 Homo sapiens 87-91 17235686-4 2007 Addition of forskolin, a known inducer of intracellular c-AMP and of oligodendrocyte differentiation, also stimulated CREB phosphorylation in a p38 kinase dependent way. Colforsin 12-21 cAMP responsive element binding protein 1 Homo sapiens 118-122 18024890-8 2007 Using [35S]GTPgammaS and reporter gene assays, we found that A5 is able to constitutively couple to alpha i-type G-proteins in transfected cells, and that this interaction is able to inhibit forskolin-triggered cAMP response element-binding protein (CREB) activation. Colforsin 191-200 cAMP responsive element binding protein 1 Homo sapiens 211-248 18024890-8 2007 Using [35S]GTPgammaS and reporter gene assays, we found that A5 is able to constitutively couple to alpha i-type G-proteins in transfected cells, and that this interaction is able to inhibit forskolin-triggered cAMP response element-binding protein (CREB) activation. Colforsin 191-200 cAMP responsive element binding protein 1 Homo sapiens 250-254 17289845-7 2007 Mutagenesis of the CRE or overexpression of a dominant-negative CREB reduced forskolin-induced promoter activation. Colforsin 77-86 cAMP responsive element binding protein 1 Homo sapiens 64-68 16959941-5 2006 Treatment with 10 microM forskolin or isoproterenol increased cAMP production and cAMP response element binding protein (CREB) phosphorylation in cardiac fibroblasts and inhibited serum- or TGF-beta-stimulated collagen synthesis by 37% or more. Colforsin 25-34 cAMP responsive element binding protein 1 Homo sapiens 121-125 16172130-0 2005 Coordinate regulation of forskolin-induced cellular proliferation in macrophages by protein kinase A/cAMP-response element-binding protein (CREB) and Epac1-Rap1 signaling: effects of silencing CREB gene expression on Akt activation. Colforsin 25-34 cAMP responsive element binding protein 1 Homo sapiens 99-138 16483570-5 2006 Furthermore, the importance of CREB activation is strengthened by experiments with CREB mutants, treatment with forskolin, and in situ analysis of P-CREB status in cells transfected with Tax or its nonprotecting M47 mutant. Colforsin 112-121 cAMP responsive element binding protein 1 Homo sapiens 31-35 16678346-6 2006 However, NAMDA enhanced the activation of ERK and CREB in the presence of forskolin (1.7-fold increase for pCREB, 2.1-fold increase for pERK2, p<0.05 from forskolin). Colforsin 74-83 cAMP responsive element binding protein 1 Homo sapiens 50-54 16678346-6 2006 However, NAMDA enhanced the activation of ERK and CREB in the presence of forskolin (1.7-fold increase for pCREB, 2.1-fold increase for pERK2, p<0.05 from forskolin). Colforsin 158-167 cAMP responsive element binding protein 1 Homo sapiens 50-54 16678346-9 2006 The data showed that NAMDA enhances forskolin-induced ERK-CREB activation and potentiates forskolin-induced resistance to apoptosis. Colforsin 36-45 cAMP responsive element binding protein 1 Homo sapiens 58-62 16443828-5 2006 Ectopic expression of ICER or induction of endogenous ICER with the cAMP agonists forskolin and prostaglandin E2 resulted in the formation of ICER-containing complexes, including an ICER:CREB heterodimer to the AP-1/CRE-like site and inhibition of MIP-1beta promoter activity. Colforsin 82-91 cAMP responsive element binding protein 1 Homo sapiens 187-191 16449647-8 2006 Activation of the CREB transcriptional factor by forskolin dramatically promoted the expression of PEN-2 mRNA and protein, whereas the other components of the gamma-secretase complex remained unaffected. Colforsin 49-58 cAMP responsive element binding protein 1 Homo sapiens 18-22 16172130-0 2005 Coordinate regulation of forskolin-induced cellular proliferation in macrophages by protein kinase A/cAMP-response element-binding protein (CREB) and Epac1-Rap1 signaling: effects of silencing CREB gene expression on Akt activation. Colforsin 25-34 cAMP responsive element binding protein 1 Homo sapiens 140-144 16172130-7 2005 Silencing of CREB gene expression by RNA interference prior to forskolin treatment not only decreased CREB protein and its phosphorylation at Ser-133, but also phosphorylation of Akt at Ser-473, and Thr-308. Colforsin 63-72 cAMP responsive element binding protein 1 Homo sapiens 13-17 16079300-7 2005 Although expression of protein kinase A (PKA) and cAMP-stimulated PKA activity were similar in both the normal and diseased cell types, forskolin- and PGE(2)-stimulated cAMP response element-binding protein (CREB) phosphorylation was decreased in the diseased cell lines compared with the normal cells. Colforsin 136-145 cAMP responsive element binding protein 1 Homo sapiens 169-206 15984930-6 2005 Forskolin increased PiC promoter activity via the CREB site. Colforsin 0-9 cAMP responsive element binding protein 1 Homo sapiens 50-54 16079300-7 2005 Although expression of protein kinase A (PKA) and cAMP-stimulated PKA activity were similar in both the normal and diseased cell types, forskolin- and PGE(2)-stimulated cAMP response element-binding protein (CREB) phosphorylation was decreased in the diseased cell lines compared with the normal cells. Colforsin 136-145 cAMP responsive element binding protein 1 Homo sapiens 208-212 15871998-11 2005 Moreover, a sequence in the pre-S2 region is responsible for further transcriptional induction via CREB activators such as PKA and forskolin. Colforsin 131-140 cAMP responsive element binding protein 1 Homo sapiens 99-103 15691881-8 2005 Furthermore, chromatin immunoprecipitation showed that the combination of androgen and forskolin increased phosphorylated CREB occupancy, which was accompanied by histone acetylation, at the putative cAMP responsive element located in the 5" upstream regulatory region of the PSA gene. Colforsin 87-96 cAMP responsive element binding protein 1 Homo sapiens 122-126 15596846-9 2005 Furthermore, BILF1 is able to inhibit forskolin-triggered CREB activation via stimulation of endogenous G proteins in a pertussis toxin-sensitive manner, verifying that BILF1 signals constitutively through Galphai. Colforsin 38-47 cAMP responsive element binding protein 1 Homo sapiens 58-62 15082775-9 2004 Several of the CREB targets were altered in their expression by treatment with forskolin; interestingly, both induced and repressed genes were found. Colforsin 79-88 cAMP responsive element binding protein 1 Homo sapiens 15-19 15340044-7 2004 Treatment with forskolin, an activator of adenylyl cyclase, restored both CREB-1 and pCREB-1 levels; this resulted in the restoration of CRE-binding, CRE-reporter activity, and CREB-1 and RFC mRNA levels. Colforsin 15-24 cAMP responsive element binding protein 1 Homo sapiens 74-80 15340044-7 2004 Treatment with forskolin, an activator of adenylyl cyclase, restored both CREB-1 and pCREB-1 levels; this resulted in the restoration of CRE-binding, CRE-reporter activity, and CREB-1 and RFC mRNA levels. Colforsin 15-24 cAMP responsive element binding protein 1 Homo sapiens 177-191 15302573-5 2004 Treatment with forskolin, an activator of CREB, significantly attenuated cytochrome c release and Bax translocation in response of serum deprivation. Colforsin 15-24 cAMP responsive element binding protein 1 Homo sapiens 42-46 15302573-6 2004 In analogy to forskolin treatment, Tax expression results in sustained phosphorylation of CREB at Ser(133) during serum starvation. Colforsin 14-23 cAMP responsive element binding protein 1 Homo sapiens 90-94 15030385-0 2004 KCl and forskolin synergistically up-regulate cholecystokinin gene expression via coordinate activation of CREB and the co-activator CBP. Colforsin 8-17 cAMP responsive element binding protein 1 Homo sapiens 107-111 15020218-5 2004 Dexras1 decreased forskolin-stimulated CREB activation (P < 0.01) and this activity was also inhibited by co-expression of RGS4. Colforsin 18-27 cAMP responsive element binding protein 1 Homo sapiens 39-43 15030385-6 2004 Moreover GAL4-CREB-DIEDML, which mediates the phosphorylation-independent binding of CBP, and the C-terminal domain of CBP was synergistically activated by forskolin and KCl. Colforsin 156-165 cAMP responsive element binding protein 1 Homo sapiens 14-18 15030385-3 2004 Here, we report that KCl and forskolin synergistically increase CCK gene transcription via protein kinase A (PKA) and extracellular signal-regulated kinase (ERK) signalling pathways, activating cAMP response element-binding protein (CREB) associated with the CRE(- 80) element of the CCK promoter. Colforsin 29-38 cAMP responsive element binding protein 1 Homo sapiens 194-231 15030385-3 2004 Here, we report that KCl and forskolin synergistically increase CCK gene transcription via protein kinase A (PKA) and extracellular signal-regulated kinase (ERK) signalling pathways, activating cAMP response element-binding protein (CREB) associated with the CRE(- 80) element of the CCK promoter. Colforsin 29-38 cAMP responsive element binding protein 1 Homo sapiens 233-237 12529429-5 2003 However, a brief treatment with forskolin, which is effective for short-term potentiation and which could also activate CREB, was not sufficient to induce long-term potentiation of resealing. Colforsin 32-41 cAMP responsive element binding protein 1 Homo sapiens 120-124 12743114-5 2003 Treatment with forskolin, an adenylyl cyclase activator, increased that activation-associated phosphorylation of CREB, which was prolonged by tTG overexpression. Colforsin 15-24 cAMP responsive element binding protein 1 Homo sapiens 113-117 12956721-5 2003 Moreover, phospho-CREB1-specific immunoreactivity is increased significantly in protein extracts of the CNS by forskolin, an activator of adenylate cyclase. Colforsin 111-120 cAMP responsive element binding protein 1 Homo sapiens 18-23 12956721-6 2003 The forskolin-induced increase in phospho-CREB1 immunoreactivity is localized to the nuclei of CNS neurons, some of which have an important role in the formation of LTM. Colforsin 4-13 cAMP responsive element binding protein 1 Homo sapiens 42-47 12210727-7 2002 The levels of phosphorylated CRE (Ser133) binding protein-1 (CREB-1) increased rapidly, sevenfold at 30 min, and reached 10-fold at 4 h following forskolin treatment. Colforsin 146-155 cAMP responsive element binding protein 1 Homo sapiens 61-67 12114266-9 2002 We further provide evidence that CRH signaling can be mimicked by activation of cAMP/PKA/CREB using forskolin in primary human microvascular endothelial cells. Colforsin 100-109 cAMP responsive element binding protein 1 Homo sapiens 89-93 11579131-6 2001 Conversely, overexpression of active GSK3 beta to 3.5-fold the normal levels completely blocked increases in CREB DNA binding activity induced by epidermal growth factor, insulin-like growth factor-1, forskolin, and cyclic AMP. Colforsin 201-210 cAMP responsive element binding protein 1 Homo sapiens 109-113 10903915-4 2000 We demonstrated here that intracellular localization of these redox molecules differ from each other and that the redox molecules differentially regulate NF-kappaB, AP-1, and CREB activation induced by TNFalpha, PMA, and forskolin and by expression of signaling intermediate kinases, NIK, MEKK, and PKA in HEK293 cells. Colforsin 221-230 cAMP responsive element binding protein 1 Homo sapiens 175-179 11514056-8 2001 Although progesterone did not alter the amount of CRE-binding protein (CREB), which is a main transcriptional factor bound to CRE(s) on hCGalpha promoter, progesterone abolished forskolin-induced CREB phosphorylation. Colforsin 178-187 cAMP responsive element binding protein 1 Homo sapiens 50-69 11514056-8 2001 Although progesterone did not alter the amount of CRE-binding protein (CREB), which is a main transcriptional factor bound to CRE(s) on hCGalpha promoter, progesterone abolished forskolin-induced CREB phosphorylation. Colforsin 178-187 cAMP responsive element binding protein 1 Homo sapiens 71-75 11514056-8 2001 Although progesterone did not alter the amount of CRE-binding protein (CREB), which is a main transcriptional factor bound to CRE(s) on hCGalpha promoter, progesterone abolished forskolin-induced CREB phosphorylation. Colforsin 178-187 cAMP responsive element binding protein 1 Homo sapiens 196-200 11445280-0 2001 Pairing of forskolin and KCl increases differentiation of immortalized hippocampal neurons in a CREB Serine 133 phosphorylation-dependent and extracellular-regulated protein kinase-independent manner. Colforsin 11-20 cAMP responsive element binding protein 1 Homo sapiens 96-100 11445280-2 2001 Using an immortalized hippocampal cell line, HiB5, we have tried a pairing of forskolin with KCl depolarization, which acts as an ERK and CREB kinase activator in hippocampal neurons, to investigate if an activation of ERK and phosphorylation of CREB at the critical regulatory site, serine 133 might be coupled in differentiation. Colforsin 78-87 cAMP responsive element binding protein 1 Homo sapiens 138-142 11526505-7 2001 In contrast, treatment with forskolin, an activator of adenylyl cyclase, led to phosphorylation of CREB and ATF-1 and activation of COX-2 promoter. Colforsin 28-37 cAMP responsive element binding protein 1 Homo sapiens 99-103 10804193-7 2000 Moreover, at 14 DIV, but not at 7 DIV, NMDA receptor stimulation induced a dephosphorylation of CREB that previously had been phosphorylated by KCl depolarization or forskolin, suggesting an NMDA receptor-dependent activation of a CREB phosphatase. Colforsin 166-175 cAMP responsive element binding protein 1 Homo sapiens 96-100 10803591-9 2000 A-CREB, a dominant negative inhibitor of CREB, completely inhibited forskolin induction of the hD2 promoter. Colforsin 68-77 cAMP responsive element binding protein 1 Homo sapiens 2-6 10803591-9 2000 A-CREB, a dominant negative inhibitor of CREB, completely inhibited forskolin induction of the hD2 promoter. Colforsin 68-77 cAMP responsive element binding protein 1 Homo sapiens 41-45 10777769-7 2000 However, incubation of slices with forskolin, an activator of the cAMP-dependent protein kinase (PKA) cascade, did result in increases in active ERK and cAMP response element-binding protein (CREB) phosphorylation in area CA3. Colforsin 35-44 cAMP responsive element binding protein 1 Homo sapiens 153-190 10777769-7 2000 However, incubation of slices with forskolin, an activator of the cAMP-dependent protein kinase (PKA) cascade, did result in increases in active ERK and cAMP response element-binding protein (CREB) phosphorylation in area CA3. Colforsin 35-44 cAMP responsive element binding protein 1 Homo sapiens 192-196 9774641-7 1998 In cells treated with both heregulin and forskolin there was a sustained accumulation of phospho-CREB, which was not observed in cells treated with either agent alone. Colforsin 41-50 cAMP responsive element binding protein 1 Homo sapiens 97-101 10319317-5 1999 Binding of CREB to a fragment of the hCRH promoter containing a canonical, functional cAMP response element was absent in untreated cells, but was specifically induced after activation of the protein kinase A pathway with forskolin. Colforsin 222-231 cAMP responsive element binding protein 1 Homo sapiens 11-15 9492053-14 1998 Phosphorylated CREB was increased by forskolin treatment, an effect that was blocked by a PKA-inhibitor. Colforsin 37-46 cAMP responsive element binding protein 1 Homo sapiens 15-19 9802424-14 1998 Pretreatment with CREB antisense, but not the sense oligodeoxynucleotides, inhibited forskolin-, thapsigargin- and NPY-stimulated luciferase activity. Colforsin 85-94 cAMP responsive element binding protein 1 Homo sapiens 18-22 9352075-2 1997 Isoproterenol, forskolin, and CPS-cAMP markedly stimulated the phosphorylation of CREB in parotid acinar cells, and PKA inhibitors H-8 and H-89 dose-dependently inhibited it. Colforsin 15-24 cAMP responsive element binding protein 1 Homo sapiens 82-86 1325813-7 1992 The AAV inverted terminal repeat (ITR) region immediately upstream of the p5 promoter appears to have an enhancer effect and the promoter also contains a CREB site which confers a response to forskolin. Colforsin 192-201 cAMP responsive element binding protein 1 Homo sapiens 154-158 9068120-8 1997 Application of the D1 agonist SKF 38393, or direct stimulation of adenylyl cyclase with forskolin, also resulted in the phosphorylation of CREB and the induction of c-fos in striatal neurons. Colforsin 88-97 cAMP responsive element binding protein 1 Homo sapiens 139-143 7699994-9 1994 Evidence suggests that forskolin-responsive signal transduction pathways may lead cyclic AMP responsive element (CRE) binding protein (CREB) to act on a CRE at -222 in the proximal REN promoter DNA. Colforsin 23-32 cAMP responsive element binding protein 1 Homo sapiens 135-139 7827622-6 1994 Cells stimulated with forskolin responded with a robust time- and dose-dependent increase in nuclear phospho-CREB immunoreactivity (P-CREB-ir), confirming that activation of this transcription factor occurred through the cyclic AMP-PKA pathway. Colforsin 22-31 cAMP responsive element binding protein 1 Homo sapiens 109-113 7827622-6 1994 Cells stimulated with forskolin responded with a robust time- and dose-dependent increase in nuclear phospho-CREB immunoreactivity (P-CREB-ir), confirming that activation of this transcription factor occurred through the cyclic AMP-PKA pathway. Colforsin 22-31 cAMP responsive element binding protein 1 Homo sapiens 134-138 7827622-7 1994 Maximal stimulation was achieved within 15 min and persisted for up to 1 h. Treatment with melatonin alone did not alter basal P-CREB-ir levels, yet melatonin inhibited the forskolin-induced increase in P-CREB-ir in a dose-dependent manner (IC50 of between 10(-10) M and 10(-8) M melatonin when tested against 1 microM forskolin). Colforsin 173-182 cAMP responsive element binding protein 1 Homo sapiens 205-209 9219156-5 1997 The addition of isoproterenol or forskolin further enhanced the stimulatory effect of pRSV/ CREB on the expression of pOGH (ANG N-1498/+18). Colforsin 33-42 cAMP responsive element binding protein 1 Homo sapiens 92-96 8625901-10 1996 The observation that S133A-CREB completely blocked the response to FSK or Q227L-alpha(S) of a Pit-1 promoter containing a mutated site PitB1 implies that the binding sites for Pit-1 and CREB account for all of the response elements for FSK or alpha(S) in the Pit-1 promoter. Colforsin 67-70 cAMP responsive element binding protein 1 Homo sapiens 27-31 8625901-10 1996 The observation that S133A-CREB completely blocked the response to FSK or Q227L-alpha(S) of a Pit-1 promoter containing a mutated site PitB1 implies that the binding sites for Pit-1 and CREB account for all of the response elements for FSK or alpha(S) in the Pit-1 promoter. Colforsin 67-70 cAMP responsive element binding protein 1 Homo sapiens 186-190 8625901-10 1996 The observation that S133A-CREB completely blocked the response to FSK or Q227L-alpha(S) of a Pit-1 promoter containing a mutated site PitB1 implies that the binding sites for Pit-1 and CREB account for all of the response elements for FSK or alpha(S) in the Pit-1 promoter. Colforsin 236-239 cAMP responsive element binding protein 1 Homo sapiens 27-31 8625901-10 1996 The observation that S133A-CREB completely blocked the response to FSK or Q227L-alpha(S) of a Pit-1 promoter containing a mutated site PitB1 implies that the binding sites for Pit-1 and CREB account for all of the response elements for FSK or alpha(S) in the Pit-1 promoter. Colforsin 236-239 cAMP responsive element binding protein 1 Homo sapiens 186-190 8382684-6 1993 The relatively low affinity and/or a restricted binding specificity of the VL30 CREs made it possible to detect forskolin-induced binding of CREB- and Jun-related proteins to these sequences. Colforsin 112-121 cAMP responsive element binding protein 1 Homo sapiens 141-145 1534852-3 1992 Experiments with oligonucleotides with mutations in the imperfect palindrome demonstrated that one TGAC motif is necessary and sufficient for both the binding of the CREB-related factor and transcriptional activity in response to forskolin in a human T-cell line, Jurkat. Colforsin 230-239 cAMP responsive element binding protein 1 Homo sapiens 166-170 1534852-4 1992 We also found that binding of the CREB-like factor to the 21-bp core element was enhanced by treatment with TPA, with little effect on transcriptional activity; in contrast, forskolin and p40tax did not facilitate binding, though they enhanced transcription. Colforsin 174-183 cAMP responsive element binding protein 1 Homo sapiens 34-38 34373489-5 2021 In line, we observed increased differentiation in CGNPs treated with Forskolin, Bmp6 and Bmp12 (Gdf7), which induce CREB phosphorylation. Colforsin 69-78 cAMP responsive element binding protein 1 Homo sapiens 116-120 1324879-6 1992 These data suggest that forskolin upregulates HLA class II molecules by means of the interaction between CRE and cAMP responsible element binding protein (CREB). Colforsin 24-33 cAMP responsive element binding protein 1 Homo sapiens 113-153 1324879-6 1992 These data suggest that forskolin upregulates HLA class II molecules by means of the interaction between CRE and cAMP responsible element binding protein (CREB). Colforsin 24-33 cAMP responsive element binding protein 1 Homo sapiens 155-159 34741086-5 2021 Here we provide evidence that PER2 acts as a co-factor of CREB to facilitate the formation of a transactivation complex on the CRE element of the Per1 gene regulatory region in response to light or forskolin. Colforsin 198-207 cAMP responsive element binding protein 1 Homo sapiens 58-62 34741086-6 2021 Using in vitro and in vivo approaches, we show that PER2 modulates the interaction between CREB and its co-regulator CRTC1 to support complex formation only after a light or forskolin stimulus. Colforsin 174-183 cAMP responsive element binding protein 1 Homo sapiens 91-95 34401899-6 2021 Furthermore, pretreatment with cAMP activator forskolin or protein kinase A (PKA) activator 8-bromo-cAMP blocked the inhibition of melatonin on CREB phosphorylation and testosterone synthesis. Colforsin 46-55 cAMP responsive element binding protein 1 Homo sapiens 144-148 34803425-8 2021 Increased CREB phosphorylation and protein kinase A (PKA) activity induced by FSK were also mitigated in the presence of Rf. Colforsin 78-81 cAMP responsive element binding protein 1 Homo sapiens 10-14 30972626-5 2019 CREB reporter luc-gene assay indicated that coexpressed delta1R significantly reduced the potency of the D2R-like agonist quinpirole to inhibit via D2R activation the forskolin induced increase of the CREB signal. Colforsin 167-176 cAMP responsive element binding protein 1 Homo sapiens 0-4 34199197-5 2021 The activation of cAMP/PKA/CREB signaling was observed in organ of Corti primary cells treated with FSK, especially in supporting cells. Colforsin 100-103 cAMP responsive element binding protein 1 Homo sapiens 27-31 34199197-6 2021 Co-treatment with gap junction enhancers such as all-trans retinoic acid (ATRA) and quinoline showed potentiating effects with FSK on cell survival via activation of cAMP/PKA/CREB. Colforsin 127-130 cAMP responsive element binding protein 1 Homo sapiens 175-179 30972626-6 2019 In contrast, the addition of 100 nM cocaine was found to markedly increase the quinpirole potency to inhibit the forskolin-induced increase of the CREB signal in the D2R-delta1R cells. Colforsin 113-122 cAMP responsive element binding protein 1 Homo sapiens 147-151 31863152-7 2020 Sequestration of transcription co-activators CBP/p300, known to bind both CREB and Smad3, may limit betahCG production, since CBP/p300 inhibitor C646 significantly restricted its forskolin-induced upregulation. Colforsin 179-188 cAMP responsive element binding protein 1 Homo sapiens 74-78 31863152-12 2020 Smad3 inhibitor SIS3 interferes with forskolin-induced CREB signaling. Colforsin 37-46 cAMP responsive element binding protein 1 Homo sapiens 55-59 30972626-5 2019 CREB reporter luc-gene assay indicated that coexpressed delta1R significantly reduced the potency of the D2R-like agonist quinpirole to inhibit via D2R activation the forskolin induced increase of the CREB signal. Colforsin 167-176 cAMP responsive element binding protein 1 Homo sapiens 201-205 26398148-7 2015 A further luciferase reporter assay demonstrated that CREB phosphorylation on ser133 was responsible for forskolin-induced inhibition of TNFAIP1 expression. Colforsin 105-114 cAMP responsive element binding protein 1 Homo sapiens 54-58 30610963-10 2019 AEA reduced intracellular cAMP levels in trophoblasts by 75% at 1 h, and completely inhibited forskolin-induced phosphorylation of the cAMP response element binding protein (CREB). Colforsin 94-103 cAMP responsive element binding protein 1 Homo sapiens 135-172 30610963-10 2019 AEA reduced intracellular cAMP levels in trophoblasts by 75% at 1 h, and completely inhibited forskolin-induced phosphorylation of the cAMP response element binding protein (CREB). Colforsin 94-103 cAMP responsive element binding protein 1 Homo sapiens 174-178 29197151-4 2018 The role of CREB was further confirmed by the observation that forskolin, a strong activator of CREB phosphorylation/activity, increased CacyBP/SIP gene promoter activity. Colforsin 63-72 cAMP responsive element binding protein 1 Homo sapiens 12-16 29197151-4 2018 The role of CREB was further confirmed by the observation that forskolin, a strong activator of CREB phosphorylation/activity, increased CacyBP/SIP gene promoter activity. Colforsin 63-72 cAMP responsive element binding protein 1 Homo sapiens 96-100 27470212-3 2016 When the cells were grown at low density (70% confluence), FSK was capable of stimulating cAMP responsive element binding (CREB) phosphorylation, a marker for FSK-stimulated PKA activation, and resulted in a significant increase of NER activity compared to control treatment. Colforsin 59-62 cAMP responsive element binding protein 1 Homo sapiens 90-121 27470212-3 2016 When the cells were grown at low density (70% confluence), FSK was capable of stimulating cAMP responsive element binding (CREB) phosphorylation, a marker for FSK-stimulated PKA activation, and resulted in a significant increase of NER activity compared to control treatment. Colforsin 59-62 cAMP responsive element binding protein 1 Homo sapiens 123-127 27470212-3 2016 When the cells were grown at low density (70% confluence), FSK was capable of stimulating cAMP responsive element binding (CREB) phosphorylation, a marker for FSK-stimulated PKA activation, and resulted in a significant increase of NER activity compared to control treatment. Colforsin 159-162 cAMP responsive element binding protein 1 Homo sapiens 123-127 27388056-8 2016 In forskolin-stimulated human hepatoma cells, these alkaloids suppressed the expression of a reporter gene under the control of cAMP response element and also prevented increases in the endogenous levels of phosphorylated CREB and PEPCK mRNA expression. Colforsin 3-12 cAMP responsive element binding protein 1 Homo sapiens 222-226 27284327-8 2016 Crucially, the results of western blot analyses suggested that PTH (1-34) treatment and, to a greater degree, PTH (1-34) plus forskolin treatment caused an increase in phosphorylated cAMP response element binding protein (p-CREB) expression, but the effect of PTH on p-CREB expression was blocked by H-89. Colforsin 126-135 cAMP responsive element binding protein 1 Homo sapiens 269-273 30359971-13 2018 C2C12 myotubes treated with forskolin also increased endogenous CREB and PGC-1alpha binding. Colforsin 28-37 cAMP responsive element binding protein 1 Homo sapiens 64-68 29050254-6 2017 Interestingly, agents that increase the intracellular cAMP level and the phosphorylation of CREB (e.g., adrenergic receptor agonist, forskolin, and cAMP analogues) upregulated the expression of Nm23-H1/2 in HEK293 cells and several cancer cell lines including A549, HeLa, MDA-MB-231, and MDA-MB-435s cells. Colforsin 133-142 cAMP responsive element binding protein 1 Homo sapiens 92-96 27891679-13 2017 Using Western blotting analysis, forskolin, through AC3 activation, caused phosphorylation of CREB, but not ERK. Colforsin 33-42 cAMP responsive element binding protein 1 Homo sapiens 94-98 28276525-7 2017 Moreover, forskolin phase-shifted Bmal1 transcriptional rhythm with a type-0 phase response curve, in accordance with long-lasting CREB phosphorylation levels after forskolin exposure. Colforsin 10-19 cAMP responsive element binding protein 1 Homo sapiens 131-135 27284327-8 2016 Crucially, the results of western blot analyses suggested that PTH (1-34) treatment and, to a greater degree, PTH (1-34) plus forskolin treatment caused an increase in phosphorylated cAMP response element binding protein (p-CREB) expression, but the effect of PTH on p-CREB expression was blocked by H-89. Colforsin 126-135 cAMP responsive element binding protein 1 Homo sapiens 224-228 26797246-3 2016 cAMP induced by forskolin+IBMX or GLP-1 caused increased expression of miR-212/miR-132, and elevated phosphorylation of cAMP-response-element-binding-protein (CREB)/Activating-transcription-factor-1 (ATF1) and Salt-Inducible-Kinases (SIKs). Colforsin 16-25 cAMP responsive element binding protein 1 Homo sapiens 120-157 26797246-3 2016 cAMP induced by forskolin+IBMX or GLP-1 caused increased expression of miR-212/miR-132, and elevated phosphorylation of cAMP-response-element-binding-protein (CREB)/Activating-transcription-factor-1 (ATF1) and Salt-Inducible-Kinases (SIKs). Colforsin 16-25 cAMP responsive element binding protein 1 Homo sapiens 159-163 25961543-4 2015 Forskolin significantly increased cAMP levels and the expression of PKA, p-CREB and AQP3. Colforsin 0-9 cAMP responsive element binding protein 1 Homo sapiens 75-79 25488359-5 2015 Nobiletin treatment effectively decreased ET plus SCF-induced Raf-1, MEK and ERK1/2 phosphorylation and also downregulated the forskolin-induced phosphorylation of CREB. Colforsin 127-136 cAMP responsive element binding protein 1 Homo sapiens 164-168 25928058-6 2015 In addition, CREB phosphorylation and C/EBPbeta expression induced by 3-isobutyl-1-methylxanthine (IBMX) and forskolin were also attenuated by berberine. Colforsin 109-118 cAMP responsive element binding protein 1 Homo sapiens 13-17 25597433-6 2015 Specifically, aspartate/glutamate carrier gene expression is induced via CREB by forskolin while it is inhibited by the PKA inhibitor, H89. Colforsin 81-90 cAMP responsive element binding protein 1 Homo sapiens 73-77 25951193-5 2015 Forskolin treatment and PKA expression activate the ITM2A promoter confirming that ITM2A expression is dependent on the PKA-CREB pathway. Colforsin 0-9 cAMP responsive element binding protein 1 Homo sapiens 124-128 25175744-6 2014 cAMP-responsive element binding protein (CREB) was proven to be the key transcription factor which regulated the FUR P1 promoter during forskolin-induced BeWo cell fusion, and two critical cAMP-responsive elements (CREs) in the P1 promoter were further identified. Colforsin 136-145 cAMP responsive element binding protein 1 Homo sapiens 0-39 24819468-5 2014 CREB phosphorylation was stimulated by TSH and forskolin in TAD-2 cells. Colforsin 47-56 cAMP responsive element binding protein 1 Homo sapiens 0-4 26632189-2 2015 We found a compound that inhibited forskolin-induced cAMP response element (CRE)-dependent transcription, the interaction between the kinase-inducible domain (KID) and the interacting domain (KIX), and endogenous CREB phosphorylation. Colforsin 35-44 cAMP responsive element binding protein 1 Homo sapiens 213-217 25175744-6 2014 cAMP-responsive element binding protein (CREB) was proven to be the key transcription factor which regulated the FUR P1 promoter during forskolin-induced BeWo cell fusion, and two critical cAMP-responsive elements (CREs) in the P1 promoter were further identified. Colforsin 136-145 cAMP responsive element binding protein 1 Homo sapiens 41-45 25175744-7 2014 Finally, we showed that CREB mediated endogenous furin activation and that CREB siRNA attenuated forskolin-induced furin expression and cell fusion in BeWo cells. Colforsin 97-106 cAMP responsive element binding protein 1 Homo sapiens 75-79 24041570-6 2014 The Hspa1a expression was augmented by TNF-alpha (tumor necrosis factor-alpha) and forskolin in NF-kappaB and CREB-dependent manners, respectively. Colforsin 83-92 cAMP responsive element binding protein 1 Homo sapiens 110-114 24701590-7 2014 The results show that Ht31, but not the control peptide Ht31-P, reduced forskolin-stimulated Ser133 phosphorylation of A-kinase substrate CREB, reduced alpha2C-AR mRNA levels, reduced cell surface translocated receptors, and attenuated agonist-triggered receptor functional responses. Colforsin 72-81 cAMP responsive element binding protein 1 Homo sapiens 138-142 24694916-8 2014 (3) After different concentration of forskolin treated 2 hours, the expression of total CREB had no significant difference among them(P > 0.05). Colforsin 37-46 cAMP responsive element binding protein 1 Homo sapiens 88-92 24694916-18 2014 (6) p-CREB and AQP3 protein expression were significantly lower in 5 micromol/L forskolin combined 10 micromol/L H-89 incubating 2 hours group when compared with 5 micromol/L forskolin, but higher than that in 10 micromol/L H-89 treated group (P < 0.05). Colforsin 80-89 cAMP responsive element binding protein 1 Homo sapiens 6-10 24694916-9 2014 While the expression of cAMP level, PKA activity, p-CREB and AQP3 protein were significantly changed, which were higher in 2.5 micromol/L, 5 micromol/L, 50 micromol/L forskolin group when compared with 0 micromol/L (P < 0.05). Colforsin 167-176 cAMP responsive element binding protein 1 Homo sapiens 52-56 23624386-5 2013 The CREB reporter gene assay indicated that the neurotensin receptor agonist JMV 449 markedly reduced the potency of the D2R like agonist quinpirole to inhibit the forskolin induced increase of the CREB signal. Colforsin 164-173 cAMP responsive element binding protein 1 Homo sapiens 4-8 23636431-5 2013 In contrast, the forskolin-induced phosphorylation of CREB was not down-regulated by arenarol. Colforsin 17-26 cAMP responsive element binding protein 1 Homo sapiens 54-58 23624386-5 2013 The CREB reporter gene assay indicated that the neurotensin receptor agonist JMV 449 markedly reduced the potency of the D2R like agonist quinpirole to inhibit the forskolin induced increase of the CREB signal. Colforsin 164-173 cAMP responsive element binding protein 1 Homo sapiens 198-202 23454521-8 2013 The forskolin-stimulated adenylate cyclase/cAMP cascade was evaluated by ELISA or western blotting of brain-derived neurotrophic factor (BDNF) and the phosphorylation of cAMP response element binding protein (CREB). Colforsin 4-13 cAMP responsive element binding protein 1 Homo sapiens 170-207 23454521-8 2013 The forskolin-stimulated adenylate cyclase/cAMP cascade was evaluated by ELISA or western blotting of brain-derived neurotrophic factor (BDNF) and the phosphorylation of cAMP response element binding protein (CREB). Colforsin 4-13 cAMP responsive element binding protein 1 Homo sapiens 209-213 23454521-10 2013 Photoactivation of optoMOR decreased the Ca(2+) influx and inhibited the forskolin-induced cAMP generation, activation of CREB, and BDNF levels in optoMOR-expressing cells similar to the activation of native mu-opioid receptor by DAMGO. Colforsin 73-82 cAMP responsive element binding protein 1 Homo sapiens 122-126 23220584-5 2013 The early response to fasting can be explained by a canonical PKA-CREB-CRTC2 signaling pathway because: i) CIDEC expression was induced by forskolin, ii) Fsp27 promoter activity was increased by CREB, and iii) Fsp27 expression was upregulated in the liver of Sirt1 knockout animals. Colforsin 139-148 cAMP responsive element binding protein 1 Homo sapiens 66-70