PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 31477569-0 2019 Epigenetic Regulation of Hippocampal Fosb Expression Controls Behavioral Responses to Cocaine. Cocaine 86-93 FBJ osteosarcoma oncogene B Mus musculus 37-41 9294222-0 1997 FosB mutant mice: loss of chronic cocaine induction of Fos-related proteins and heightened sensitivity to cocaine"s psychomotor and rewarding effects. Cocaine 34-41 FBJ osteosarcoma oncogene B Mus musculus 0-4 9294222-6 1997 This deficiency was associated with enhanced behavioral responses to cocaine: fosB mutant mice showed exaggerated locomotor activation in response to initial cocaine exposures as well as robust conditioned place preference to a lower dose of cocaine, compared with wild-type littermates. Cocaine 69-76 FBJ osteosarcoma oncogene B Mus musculus 78-82 9294222-6 1997 This deficiency was associated with enhanced behavioral responses to cocaine: fosB mutant mice showed exaggerated locomotor activation in response to initial cocaine exposures as well as robust conditioned place preference to a lower dose of cocaine, compared with wild-type littermates. Cocaine 158-165 FBJ osteosarcoma oncogene B Mus musculus 78-82 9294222-6 1997 This deficiency was associated with enhanced behavioral responses to cocaine: fosB mutant mice showed exaggerated locomotor activation in response to initial cocaine exposures as well as robust conditioned place preference to a lower dose of cocaine, compared with wild-type littermates. Cocaine 158-165 FBJ osteosarcoma oncogene B Mus musculus 78-82 34785784-5 2022 We focused on miR-1 considering the important role of some of its predicted mRNA targets, Fosb and Npas4, in the effects of cocaine. Cocaine 124-131 FBJ osteosarcoma oncogene B Mus musculus 90-94 33268545-7 2021 To identify whether striatal brain regions are activated in Npas2 mutant females, we measured cocaine-induced DeltaFosB expression. Cocaine 94-101 FBJ osteosarcoma oncogene B Mus musculus 110-119 32742260-0 2020 Cytoplasmic Polyadenylation Element Binding Proteins CPEB1 and CPEB3 Regulate the Translation of FosB and Are Required for Maintaining Addiction-Like Behaviors Induced by Cocaine. Cocaine 171-178 FBJ osteosarcoma oncogene B Mus musculus 97-101 32742260-8 2020 Finally, we found that (1) CPEB is reduced in transgenic mice following cocaine injections and that (2) FosB, known for its contribution to establishing the addictive phenotype, when its expression in the striatum is increased by drug administration, is a novel target of CPEBs molecules. Cocaine 72-79 FBJ osteosarcoma oncogene B Mus musculus 104-108 31568187-6 2019 Our results showed that cocaine exposure significantly decreased both Crem and Fosb methylation in the prefrontal cortex of progenitor mice, while similar patterns of methylation were replicated in the brains of drug-naive non-fostered offspring mice but reversed by postnatal fostering. Cocaine 24-31 FBJ osteosarcoma oncogene B Mus musculus 79-83 31568187-8 2019 Our data provide some evidence that indirect exposure to cocaine may cause marked epigenetic changes within the cortical networks of drug-naive descendants and that mediation by Crem/Fosb signalling in this brain region may be beneficial, while early postnatal fostering may further engineer molecular switching that may predispose the individual to future risky behaviours as well as accumulative potential to developing cognitive impairment later in life. Cocaine 57-64 FBJ osteosarcoma oncogene B Mus musculus 183-187 31705540-9 2020 Furthermore, alterations in glutamatergic excitability (GluA1/GluA2 ratio) and FosB expression were found in the prefrontal cortex and the striatum of alcohol-exposed mice after cocaine-primed reinstatement. Cocaine 179-186 FBJ osteosarcoma oncogene B Mus musculus 80-84 31477569-5 2019 We investigated differences in mouse dorsal and ventral hippocampal DeltaFosB expression in response to chronic cocaine, because these regions appear to regulate distinct cocaine-related behaviors. Cocaine 112-119 FBJ osteosarcoma oncogene B Mus musculus 68-77 31477569-6 2019 We found that cocaine-mediated induction of DeltaFosB was subregion-specific, and that DeltaFosB transcriptional activity in both the dorsal and ventral hippocampus is necessary for cocaine conditioned place preference. Cocaine 14-21 FBJ osteosarcoma oncogene B Mus musculus 44-53 31477569-6 2019 We found that cocaine-mediated induction of DeltaFosB was subregion-specific, and that DeltaFosB transcriptional activity in both the dorsal and ventral hippocampus is necessary for cocaine conditioned place preference. Cocaine 182-189 FBJ osteosarcoma oncogene B Mus musculus 87-96 31477569-7 2019 Further, we characterize changes in histone modifications at the FosB promoter in hippocampus in response to chronic cocaine and found that locus-specific epigenetic modification is essential for FosB induction and multiple hippocampus-dependent behaviors, including cocaine place preference. Cocaine 117-124 FBJ osteosarcoma oncogene B Mus musculus 65-69 31477569-7 2019 Further, we characterize changes in histone modifications at the FosB promoter in hippocampus in response to chronic cocaine and found that locus-specific epigenetic modification is essential for FosB induction and multiple hippocampus-dependent behaviors, including cocaine place preference. Cocaine 267-274 FBJ osteosarcoma oncogene B Mus musculus 65-69 31477569-8 2019 Collectively, these findings suggest that exposure to cocaine induces histone modification at the hippocampal FosB gene promoter to cause DeltaFosB induction critical for cocaine-related learning.SIGNIFICANCE STATEMENT Although cocaine addiction is driven in part by the formation of indelible associations between the drug and the environment, paraphernalia, and circumstances of use, and although this type of associative learning is dependent upon changes in gene expression in a brain region called the hippocampus, the mechanisms by which cocaine alters hippocampal gene expression to drive formation of these associations is poorly understood. Cocaine 54-61 FBJ osteosarcoma oncogene B Mus musculus 110-114 31477569-8 2019 Collectively, these findings suggest that exposure to cocaine induces histone modification at the hippocampal FosB gene promoter to cause DeltaFosB induction critical for cocaine-related learning.SIGNIFICANCE STATEMENT Although cocaine addiction is driven in part by the formation of indelible associations between the drug and the environment, paraphernalia, and circumstances of use, and although this type of associative learning is dependent upon changes in gene expression in a brain region called the hippocampus, the mechanisms by which cocaine alters hippocampal gene expression to drive formation of these associations is poorly understood. Cocaine 54-61 FBJ osteosarcoma oncogene B Mus musculus 138-147 31477569-8 2019 Collectively, these findings suggest that exposure to cocaine induces histone modification at the hippocampal FosB gene promoter to cause DeltaFosB induction critical for cocaine-related learning.SIGNIFICANCE STATEMENT Although cocaine addiction is driven in part by the formation of indelible associations between the drug and the environment, paraphernalia, and circumstances of use, and although this type of associative learning is dependent upon changes in gene expression in a brain region called the hippocampus, the mechanisms by which cocaine alters hippocampal gene expression to drive formation of these associations is poorly understood. Cocaine 171-178 FBJ osteosarcoma oncogene B Mus musculus 110-114 31477569-8 2019 Collectively, these findings suggest that exposure to cocaine induces histone modification at the hippocampal FosB gene promoter to cause DeltaFosB induction critical for cocaine-related learning.SIGNIFICANCE STATEMENT Although cocaine addiction is driven in part by the formation of indelible associations between the drug and the environment, paraphernalia, and circumstances of use, and although this type of associative learning is dependent upon changes in gene expression in a brain region called the hippocampus, the mechanisms by which cocaine alters hippocampal gene expression to drive formation of these associations is poorly understood. Cocaine 171-178 FBJ osteosarcoma oncogene B Mus musculus 138-147 31477569-8 2019 Collectively, these findings suggest that exposure to cocaine induces histone modification at the hippocampal FosB gene promoter to cause DeltaFosB induction critical for cocaine-related learning.SIGNIFICANCE STATEMENT Although cocaine addiction is driven in part by the formation of indelible associations between the drug and the environment, paraphernalia, and circumstances of use, and although this type of associative learning is dependent upon changes in gene expression in a brain region called the hippocampus, the mechanisms by which cocaine alters hippocampal gene expression to drive formation of these associations is poorly understood. Cocaine 171-178 FBJ osteosarcoma oncogene B Mus musculus 110-114 31477569-8 2019 Collectively, these findings suggest that exposure to cocaine induces histone modification at the hippocampal FosB gene promoter to cause DeltaFosB induction critical for cocaine-related learning.SIGNIFICANCE STATEMENT Although cocaine addiction is driven in part by the formation of indelible associations between the drug and the environment, paraphernalia, and circumstances of use, and although this type of associative learning is dependent upon changes in gene expression in a brain region called the hippocampus, the mechanisms by which cocaine alters hippocampal gene expression to drive formation of these associations is poorly understood. Cocaine 171-178 FBJ osteosarcoma oncogene B Mus musculus 138-147 31477569-8 2019 Collectively, these findings suggest that exposure to cocaine induces histone modification at the hippocampal FosB gene promoter to cause DeltaFosB induction critical for cocaine-related learning.SIGNIFICANCE STATEMENT Although cocaine addiction is driven in part by the formation of indelible associations between the drug and the environment, paraphernalia, and circumstances of use, and although this type of associative learning is dependent upon changes in gene expression in a brain region called the hippocampus, the mechanisms by which cocaine alters hippocampal gene expression to drive formation of these associations is poorly understood. Cocaine 171-178 FBJ osteosarcoma oncogene B Mus musculus 110-114 31477569-8 2019 Collectively, these findings suggest that exposure to cocaine induces histone modification at the hippocampal FosB gene promoter to cause DeltaFosB induction critical for cocaine-related learning.SIGNIFICANCE STATEMENT Although cocaine addiction is driven in part by the formation of indelible associations between the drug and the environment, paraphernalia, and circumstances of use, and although this type of associative learning is dependent upon changes in gene expression in a brain region called the hippocampus, the mechanisms by which cocaine alters hippocampal gene expression to drive formation of these associations is poorly understood. Cocaine 171-178 FBJ osteosarcoma oncogene B Mus musculus 138-147 31477569-9 2019 Here, we demonstrate that chronic cocaine engages locus-specific changes in the epigenetic profile of the FosB gene in the hippocampus, and that these alterations are required for cocaine-dependent gene expression and cocaine-environment associations. Cocaine 34-41 FBJ osteosarcoma oncogene B Mus musculus 106-110 31477569-9 2019 Here, we demonstrate that chronic cocaine engages locus-specific changes in the epigenetic profile of the FosB gene in the hippocampus, and that these alterations are required for cocaine-dependent gene expression and cocaine-environment associations. Cocaine 180-187 FBJ osteosarcoma oncogene B Mus musculus 106-110 31477569-9 2019 Here, we demonstrate that chronic cocaine engages locus-specific changes in the epigenetic profile of the FosB gene in the hippocampus, and that these alterations are required for cocaine-dependent gene expression and cocaine-environment associations. Cocaine 180-187 FBJ osteosarcoma oncogene B Mus musculus 106-110 31043484-6 2019 RNA sequencing revealed five genes upregulated in cocaine relative to food self-administering mice: Fosb, Npas4, Vgf, Nptx2, and Pmepa1, which reflect known and novel cocaine plasticity-associated genes. Cocaine 50-57 FBJ osteosarcoma oncogene B Mus musculus 100-104 20720536-9 2010 In contrast, acute and repeated cocaine administrations induced hypomethylation and decreased binding of MeCP2 at the fosB promoter, and these are associated with transcriptional upregulation of fosB in NAc. Cocaine 32-39 FBJ osteosarcoma oncogene B Mus musculus 118-122 29740282-9 2018 Immediate early gene (IEG) expression (cFos and FosB) induced by repeated cocaine injections was significantly increased in the forebrain of M4R-D1RCre mice, whereas it remained normal in the M4R-ChATCre mice. Cocaine 74-81 FBJ osteosarcoma oncogene B Mus musculus 48-52 28963688-9 2018 Furthermore, our data delineate the molecular response of Crem and Fosb to oral cocaine in group-housed mice and demonstrates differential regulation of activities within the substrate brain regions studied. Cocaine 80-87 FBJ osteosarcoma oncogene B Mus musculus 67-71 22049069-7 2011 Nicotine primed the response to cocaine by enhancing its ability to induce transcriptional activation of the FosB gene through inhibition of histone deacetylase, which caused global histone acetylation in the striatum. Cocaine 32-39 FBJ osteosarcoma oncogene B Mus musculus 109-113 30963104-0 2019 Fosb Induction in Nucleus Accumbens by Cocaine Is Regulated by E2F3a. Cocaine 39-46 FBJ osteosarcoma oncogene B Mus musculus 0-4 30963104-2 2019 In this study, we find a novel regulatory role for the transcription factor E2F3, recently implicated in transcriptional regulation by cocaine, in controlling DeltaFosB induction in the mouse nucleus accumbens (NAc) following cocaine administration. Cocaine 135-142 FBJ osteosarcoma oncogene B Mus musculus 159-168 30963104-2 2019 In this study, we find a novel regulatory role for the transcription factor E2F3, recently implicated in transcriptional regulation by cocaine, in controlling DeltaFosB induction in the mouse nucleus accumbens (NAc) following cocaine administration. Cocaine 226-233 FBJ osteosarcoma oncogene B Mus musculus 159-168 30803445-7 2019 Therefore, we suggest spinophilin fulfills an essential role in cocaine-induced behavioral sensitization, likely via ERK1/2 phosphorylation and induction of c-Fos and FosB in the striatum, a mechanism that may underlie specific processes in cocaine addiction. Cocaine 64-71 FBJ osteosarcoma oncogene B Mus musculus 168-172 28963688-2 2018 However, the functional consequences of regulated expression patterns of Fosb and Crem (cAMP response element modulator) in both brain regions in response to volitional intake of cocaine in social environment is yet to be explored. Cocaine 179-186 FBJ osteosarcoma oncogene B Mus musculus 73-77 28963688-7 2018 These changes were accompanied by hypomethylation or hypermethylation in the promoters of Fosb and Crem genes in the PFC and HPC of the cocaine-experienced mice, respectively. Cocaine 136-143 FBJ osteosarcoma oncogene B Mus musculus 90-94 20720536-9 2010 In contrast, acute and repeated cocaine administrations induced hypomethylation and decreased binding of MeCP2 at the fosB promoter, and these are associated with transcriptional upregulation of fosB in NAc. Cocaine 32-39 FBJ osteosarcoma oncogene B Mus musculus 195-199 19890265-1 2010 Previous studies show that (1) two members of fos family transcription factors, c-Fos and FosB, are induced in frontal brain regions by methamphetamine; (2) null mutation of c-Fos exacerbates methamphetamine-induced neurotoxicity; and (3) null mutation of FosB enhances behavioral responses to cocaine. Cocaine 294-301 FBJ osteosarcoma oncogene B Mus musculus 90-94 17468183-3 2007 Previous rodent studies have shown that many addictive substances and stressful stimuli increase the expression of the transcription factor FosB in limbic and associated regions and that the protein products of fosB contribute to certain behavioral effects of cocaine and morphine. Cocaine 260-267 FBJ osteosarcoma oncogene B Mus musculus 140-144 19446794-9 2009 Finally, we found corresponding changes in ERK1/2 activation and in accumulation of FosB/DeltaFosB, a well-characterized marker for long-term responses to cocaine, in MSN from these animals. Cocaine 155-162 FBJ osteosarcoma oncogene B Mus musculus 84-88 17468183-3 2007 Previous rodent studies have shown that many addictive substances and stressful stimuli increase the expression of the transcription factor FosB in limbic and associated regions and that the protein products of fosB contribute to certain behavioral effects of cocaine and morphine. Cocaine 260-267 FBJ osteosarcoma oncogene B Mus musculus 211-215 16263220-2 2006 It has also been shown that extracellular signal-regulated kinase activation can regulate cocaine-induced expression of c-Fos and FosB, two possible components of activator protein 1. Cocaine 90-97 FBJ osteosarcoma oncogene B Mus musculus 130-134 16380431-0 2005 CREB-binding protein controls response to cocaine by acetylating histones at the fosB promoter in the mouse striatum. Cocaine 42-49 FBJ osteosarcoma oncogene B Mus musculus 81-85 16380431-3 2005 Here, we show that histone acetylation by the cAMP-response element binding protein (CREB)-binding protein (CBP) mediates sensitivity to cocaine by regulating expression of the fosB gene and its splice variant, DeltafosB, a transcription factor previously implicated in addiction. Cocaine 137-144 FBJ osteosarcoma oncogene B Mus musculus 177-181 16380431-5 2005 We show that mutant mice that lack one allele of the CBP gene and have normal levels of fosB expression are less sensitive to chronic (10-day) administration of cocaine than are wild-type mice. Cocaine 161-168 FBJ osteosarcoma oncogene B Mus musculus 88-92 15056714-8 2004 Moreover, ERK activation mediates acute cocaine-induced expression of Fos family genes, including c-fos, fosB and fra2. Cocaine 40-47 FBJ osteosarcoma oncogene B Mus musculus 105-109