PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 32815115-5 2020 Furthermore, chronic exposure to nicotine enhanced the PI3K/Akt and ERK/CREB pathways and increased BDNF expression in the DG of CaMKIV null mice. Nicotine 33-41 cAMP responsive element binding protein 1 Mus musculus 72-76 32815115-8 2020 Taken together, we demonstrated that chronic exposure to nicotine rescues depressive-like behavior via alpha7-type nAChR through the activation of both PI3K/Akt and ERK/CREB pathways in CaMKIV null mice. Nicotine 57-65 cAMP responsive element binding protein 1 Mus musculus 169-173 31637050-8 2019 However, Rap1 protein was elevated and CREB phosphorylation was reduced in female nicotine place conditioning mice. Nicotine 82-90 cAMP responsive element binding protein 1 Mus musculus 39-43 27235579-4 2016 Learning in the presence of acute nicotine increases the transcription of mitogen-activated protein kinase 8 (MAPK8, also known as JNK1), likely through a CREB-dependent mechanism. Nicotine 34-42 cAMP responsive element binding protein 1 Mus musculus 155-159 26055203-9 2015 The hippocampal p-CREB/CREB ratio enhanced in ethanol- and ethanol-nicotine induced STD. Nicotine 67-75 cAMP responsive element binding protein 1 Mus musculus 18-22 26055203-15 2015 In addition, cross state-dependent learning between WIN and ethanol or nicotine was associated with the increase of the hippocampal p-CREB/CREB ratio. Nicotine 71-79 cAMP responsive element binding protein 1 Mus musculus 134-138 26055203-15 2015 In addition, cross state-dependent learning between WIN and ethanol or nicotine was associated with the increase of the hippocampal p-CREB/CREB ratio. Nicotine 71-79 cAMP responsive element binding protein 1 Mus musculus 139-143 26055203-9 2015 The hippocampal p-CREB/CREB ratio enhanced in ethanol- and ethanol-nicotine induced STD. Nicotine 67-75 cAMP responsive element binding protein 1 Mus musculus 23-27 23226481-2 2012 The calcium activated protein, calcium/calmodulin-dependent protein kinase IV (CaMKIV) phosphorylates the downstream transcription factor cyclic AMP response element binding protein (CREB), which mediates nicotine responses; however the role of CaMKIV in nicotine dependence is unknown. Nicotine 205-213 cAMP responsive element binding protein 1 Mus musculus 183-187 22086359-0 2012 CREB involvement in the regulation of striatal prodynorphin by nicotine. Nicotine 63-71 cAMP responsive element binding protein 1 Mus musculus 0-4 22086359-2 2012 CREB phosphorylation at Ser133 is enhanced by drugs of abuse, including nicotine. Nicotine 72-80 cAMP responsive element binding protein 1 Mus musculus 0-4 22086359-6 2012 RESULTS: Acute nicotine increased adenylyl cyclase activity, cAMP, and pCREB Ser133 levels in striatum and enhanced CREB binding to CRE elements (DynCREs) of the PD promoter, preferentially DynCRE3. Nicotine 15-23 cAMP responsive element binding protein 1 Mus musculus 72-76 22086359-11 2012 CONCLUSIONS: Our findings suggest that nicotine regulates PD expression in striatum at the transcriptional level and CREB is involved. Nicotine 39-47 cAMP responsive element binding protein 1 Mus musculus 117-121 23226481-2 2012 The calcium activated protein, calcium/calmodulin-dependent protein kinase IV (CaMKIV) phosphorylates the downstream transcription factor cyclic AMP response element binding protein (CREB), which mediates nicotine responses; however the role of CaMKIV in nicotine dependence is unknown. Nicotine 205-213 cAMP responsive element binding protein 1 Mus musculus 138-181 25051446-13 2014 Chronic nicotine treatment enhanced PI-3-kinase activities and increased Akt and glycogen synthase kinase (GSK)-3beta phosphorylation in an nAChR-dependent manner coupled with decreased cAMP response element-binding protein (CREB) phosphorylation. Nicotine 8-16 cAMP responsive element binding protein 1 Mus musculus 186-223 25051446-13 2014 Chronic nicotine treatment enhanced PI-3-kinase activities and increased Akt and glycogen synthase kinase (GSK)-3beta phosphorylation in an nAChR-dependent manner coupled with decreased cAMP response element-binding protein (CREB) phosphorylation. Nicotine 8-16 cAMP responsive element binding protein 1 Mus musculus 225-229 23226481-2 2012 The calcium activated protein, calcium/calmodulin-dependent protein kinase IV (CaMKIV) phosphorylates the downstream transcription factor cyclic AMP response element binding protein (CREB), which mediates nicotine responses; however the role of CaMKIV in nicotine dependence is unknown. Nicotine 255-263 cAMP responsive element binding protein 1 Mus musculus 138-181 23226481-2 2012 The calcium activated protein, calcium/calmodulin-dependent protein kinase IV (CaMKIV) phosphorylates the downstream transcription factor cyclic AMP response element binding protein (CREB), which mediates nicotine responses; however the role of CaMKIV in nicotine dependence is unknown. Nicotine 255-263 cAMP responsive element binding protein 1 Mus musculus 183-187 23226481-3 2012 Given the proposed role of CaMKIV in CREB activation, we hypothesized that CaMKIV might be a crucial molecular component in the development of nicotine dependence. Nicotine 143-151 cAMP responsive element binding protein 1 Mus musculus 37-41 19212318-0 2009 Nucleus accumbens CREB activity is necessary for nicotine conditioned place preference. Nicotine 49-57 cAMP responsive element binding protein 1 Mus musculus 18-22 21232579-0 2011 Alterations in BDNF and phospho-CREB levels following chronic oral nicotine treatment and its withdrawal in dopaminergic brain areas of mice. Nicotine 67-75 cAMP responsive element binding protein 1 Mus musculus 32-36 21232579-10 2011 In conclusion, the current results suggest the involvement of BDNF- and CREB-related neuronal processes in nicotine-induced neurochemical, behavioural, and neuroplastic changes in dopaminergic neurocircuits. Nicotine 107-115 cAMP responsive element binding protein 1 Mus musculus 72-76 21113126-4 2011 Nicotine-mediated RyR2 upregulation was driven by CREB, and caused a long-lasting reinforcement of Ca2+ signalling via the process of Ca2+-induced Ca2+ release. Nicotine 0-8 cAMP responsive element binding protein 1 Mus musculus 50-54 19212318-3 2009 Previous studies have implicated nucleus accumbens (NAc) CREB activity in the modulation of cocaine and morphine reward, and have shown that nicotine conditioned place preference (CPP) is associated with NAc CREB activation. Nicotine 141-149 cAMP responsive element binding protein 1 Mus musculus 57-61 19212318-3 2009 Previous studies have implicated nucleus accumbens (NAc) CREB activity in the modulation of cocaine and morphine reward, and have shown that nicotine conditioned place preference (CPP) is associated with NAc CREB activation. Nicotine 141-149 cAMP responsive element binding protein 1 Mus musculus 208-212 19212318-8 2009 Taken together, these studies identify the NAc shell as a brain region where CREB activity is essential for nicotine CPP. Nicotine 108-116 cAMP responsive element binding protein 1 Mus musculus 77-81 12614343-0 2003 In vivo nicotine treatment regulates mesocorticolimbic CREB and ERK signaling in C57Bl/6J mice. Nicotine 8-16 cAMP responsive element binding protein 1 Mus musculus 55-59 18713928-5 2008 To demonstrate that nicotine reduced nociceptive input in this model, the lumbar spinal cords of a subgroup of these mice were stained for the phosphorylated form if CREB. Nicotine 20-28 cAMP responsive element binding protein 1 Mus musculus 166-170 15953421-0 2005 Mu-opioid receptor and CREB activation are required for nicotine reward. Nicotine 56-64 cAMP responsive element binding protein 1 Mus musculus 23-27 15953421-2 2005 Exposure to an environment previously associated with rewarding properties of nicotine results in an increase of CREB phosphorylation similar to that seen following nicotine administration, and this response is absent in MOR(-/-) mice. Nicotine 78-86 cAMP responsive element binding protein 1 Mus musculus 113-117 15953421-5 2005 However, this effect, along with rewarding properties of nicotine, is blocked in mice with a targeted disruption in the CREB gene. Nicotine 57-65 cAMP responsive element binding protein 1 Mus musculus 120-124 15953421-6 2005 Together, pharmacologic and genetic manipulations indicate that phosphorylation of CREB and upregulation of functional MORs are required for nicotine-conditioned reward. Nicotine 141-149 cAMP responsive element binding protein 1 Mus musculus 83-87 12614343-4 2003 CREB phosphorylation was reduced in the nucleus accumbens following chronic nicotine, consistent with previous reports that decreased accumbens CREB activity increases drug reinforcement. Nicotine 76-84 cAMP responsive element binding protein 1 Mus musculus 0-4 12614343-4 2003 CREB phosphorylation was reduced in the nucleus accumbens following chronic nicotine, consistent with previous reports that decreased accumbens CREB activity increases drug reinforcement. Nicotine 76-84 cAMP responsive element binding protein 1 Mus musculus 144-148 12614343-5 2003 In contrast, CREB phosphorylation was increased in the prefrontal cortex following chronic nicotine exposure and in the ventral tegmental area during nicotine withdrawal. Nicotine 91-99 cAMP responsive element binding protein 1 Mus musculus 13-17 12614343-5 2003 In contrast, CREB phosphorylation was increased in the prefrontal cortex following chronic nicotine exposure and in the ventral tegmental area during nicotine withdrawal. Nicotine 150-158 cAMP responsive element binding protein 1 Mus musculus 13-17 12614343-8 2003 Overall, these results support a role for ERK and CREB activity in neural plasticity associated with nicotine dependence. Nicotine 101-109 cAMP responsive element binding protein 1 Mus musculus 50-54