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CREB ChIP-chip and HaloCHIP-chip experiments

ABSTRACT: Regulation of gene expression is essential for normal development and cellular growth. Transcriptional events are tightly controlled both spatially and temporally by specific DNA-protein interactions. In this study we finely map the genome-wide targets of the CREB protein across all known and predicted human promoters, and characterize the functional consequences of a subset of these binding events using high-throughput reporter assays. To measure CREB binding, we used HaloCHIP, an antibody-free alternative to the ChIP method that utilizes the HaloTag fusion protein, and also high-throughput promoter-luciferase reporter assays, which provide rapid and quantitative screening of promoters for transcriptional activation or repression in living cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE18347 | GEO | 2009/10/01

SECONDARY ACCESSION(S): PRJNA118157

REPOSITORIES: GEO

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CREB ChIP-chip and HaloCHIP-chip experiments

Project description:Regulation of gene expression is essential for normal development and cellular growth. Transcriptional events are tightly controlled both spatially and temporally by specific DNA-protein interactions. In this study we finely map the genome-wide targets of the CREB protein across all known and predicted human promoters, and characterize the functional consequences of a subset of these binding events using high-throughput reporter assays. To measure CREB binding, we used HaloCHIP, an antibody-free alternative to the ChIP method that utilizes the HaloTag fusion protein, and also high-throughput promoter-luciferase reporter assays, which provide rapid and quantitative screening of promoters for transcriptional activation or repression in living cells. CREB ChIP-chip two biologcal replicates. HaloCHIP-chip three biological replicates with and without Forskolin

2010-05-22 | E-GEOD-18347 | biostudies-arrayexpress

ChIp-Chip using RNAP II, CREB C/EBPb and cJun antibody in undifferentiated or differentiated keratinocytes (ChIP-Chip)

Project description:Combinatorial recruitment of CREB, C/EBPb and Jun determines activation of promoters upon keratinocyte differentiation Chromatin immunoprecipitation (ChIP) of RNAP II, CREB C/EBPb and cJun in undifferentiated or differentiated keratinocytes demonstrate recruitment of RNAP II to promoters bound by combination of specific transcription factors comparison of undifferentiated and differentated keratinocytes

2013-07-01 | E-GEOD-48381 | biostudies-arrayexpress

HIV-1 gp120 impairs spatial memory through CREB

Project description:HIV-associated neurocognitive disorders (HAND) remain an unsolved problem that persists despite using antiretroviral therapy. We have obtained data showing that HIV-gp120 protein contributes to neurodegeneration through metabolic reprogramming. This led to decreased ATP levels, lower mitochondrial DNA copy numbers, and loss of mitochondria cristae, all-important for mitochondrial biogenesis. gp120 protein also disrupted mitochondrial movement and synaptic plasticity. Searching for the mechanisms involved, we found that gp120 alters the cyclic AMP response element-binding protein (CREB) phosphorylation on serine residue 133 necessary for its function as a transcription factor. Since CREB regulates the promoters of PGC1 and BDNF genes, we found that CREB dephosphorylation causes PGC1 and BDNF loss of functions. Our data was validated in vitro and in vivo. The negative effect of gp120 was alleviated in cells and animals in the presence of rolipram that inhibits the phosphodiesterase protein 4 (PDE4) and restores CREB phosphorylation. We concluded that HIV-gp120 protein contributes to HAND via inhibition of CREB protein function.

2022-06-09 | PXD031891 | Pride

ChIp-Chip using RNAP II, CREB C/EBPb and cJun antibody in undifferentiated or differentiated keratinocytes (ChIP-Chip)

2013-07-01 | GSE48381 | GEO

ChIp-Chip using RNAP II, CREB C/EBPb and cJun antibody in undifferentiated or differentiated keratinocytes (expression)

Project description:Combinatorial recruitment of CREB, C/EBPb and Jun determines activation of promoters upon keratinocyte differentiation Chromatin immunoprecipitation (ChIP) of RNAP II, CREB C/EBPb and cJun in undifferentiated or differentiated keratinocytes demonstrate recruitment of RNAP II to promoters bound by combination of specific transcription factors. Analysis of mRNA expression data from contrl keratinocytes or keratinovtyes where binding of transcription factors is disrupted demonstrate functional requirements for ceratin class of promoters

2013-07-01 | GSE48382 | GEO

Chromatin immunoprecipitation of human cell lines to identify cAMP-response element binding protein (CREB) binding sites.

Project description:Hormones and nutrients often induce genetic programs via signaling pathways that interface with gene-specific activators. Activation of the cAMP pathway, for example, stimulates cellular gene expression by means of the PKA-mediated phosphorylation of cAMP-response element binding protein (CREB) at Ser-133. Here, we use genome-wide approaches to characterize target genes that are regulated by CREB in different cellular contexts. CREB was found to occupy approximately 4,000 promoter sites in vivo, depending on the presence and methylation state of consensus cAMP response elements near the promoter. The profiles for CREB occupancy were very similar in different human tissues, and exposure to a cAMP agonist stimulated CREB phosphorylation over a majority of these sites. Only a small proportion of CREB target genes was induced by cAMP in any cell type, however, due in part to the preferential recruitment of the coactivator CREB-binding protein to those promoters. These results indicate that CREB phosphorylation alone is not a reliable predictor of target gene activation and that additional CREB regulatory partners are required for recruitment of the transcriptional apparatus to the promoter.

2006-05-09 | E-WMIT-11 | biostudies-arrayexpress

Zfp189 Mediates Stress Resilience Through a CREB-Regulated Transcriptional Network in Prefrontal Cortex

Project description:Stress resilience involves numerous brain-wide transcriptional changes. Determining the organization and orchestration of these transcriptional events may reveal novel antidepressant targets, but this remains unexplored. Here, we characterize the resilient transcriptome with co-expression analysis and identify a single transcriptionally-active uniquely-resilient gene network. Zfp189, a previously unstudied zinc finger protein, is the top network key driver and its overexpression in prefrontal cortical (PFC) neurons preferentially activates this network, alters neuronal activity and promotes behavioral resilience. CREB, which binds Zfp189, is the top upstream regulator of this network. To probe CREB-Zfp189 interactions as a network regulatory mechanism, we employ CRISPR-mediated locus-specific transcriptional reprogramming to direct CREB selectively to the Zfp189 promoter. This single molecular interaction in PFC neurons recapitulates the pro-resilient Zfp189-dependent downstream effects on gene network activity, electrophysiology and behavior. These findings reveal an essential role for Zfp189 and a CREB-Zfp189 regulatory axis in mediating a central transcriptional network of resilience.

2019-08-22 | GSE118317 | GEO

Integrative genomic analysis of CREB defines a critical role for transcription factor networks in mediating the fed/fasted switch in liver [ChIP-seq]

Project description:Metabolic homeostasis in mammals critically depends on the regulation of fasting-induced genes by CREB in the liver. Previous genome-wide analysis has shown that only a small percentage of CREB target genes are induced in response to fasting-associated signaling pathways. The precise molecular mechanisms by which CREB specifically targets these genes in response to alternating hormonal cues remain to be elucidated. We performed chromatin immunoprecipitation coupled to high-throughput sequencing of CREB in livers from both fasted and re-fed mice. In order to quantitatively compare the extent of CREB-DNA interactions genome-wide between these two physiological conditions we developed a novel, robust analysis method, termed the M-bM-^@M-^Xsingle sample independenceM-bM-^@M-^Y (SSI) test that greatly reduced the number of false positive peaks. We found that CREB remains constitutively bound to its target genes in the liver regardless of the metabolic state. Integration of the CREB cistrome with expression microarrays of fasted and re-fed mouse livers and ChIP-seq data for additional transcription factors revealed that the gene expression switches between the fasted and fed states are associated with co-localization of additional transcription factors at CREB sites. Our results support a model in which CREB is constitutively bound to thousands of potential target genes and combinatorial interactions between DNA-binding factors are necessary to achieve the specific transcriptional response of the liver to fasting. Furthermore, our genome-wide analysis identifies thousands of novel CREB target genes in liver, including a previously unknown role for CREB in regulating ER stress genes in response to nutrient influx. CREB ChIP-seq was performed on mouse liver from fasted and re-fed mice, using 5 separate biological replicates for each condition. GR and C/EBP(beta) ChIP-seq were performed as single replicates on ad-lib fed mice.

2013-05-01 | E-GEOD-45674 | biostudies-arrayexpress

CREB Controls Cortical Circuit Plasticity and Functional Recovery after Stroke

Project description:Treatments that stimulate neuronal excitability enhance motor performance after stroke.cAMP-response-element binding protein (CREB) is a transcription factor that plays a key rolein neuronal excitability. Increasing the levels of CREB with a viral vector in a small pool ofmotor neurons enhances motor recovery after stroke, while blocking CREB signaling preventsstroke recovery. Silencing CREB-transfected neurons in the peri-infarct region with thehM4di-DREADD blocks motor recovery. Reversing this inhibition allows recovery to continue,demonstrating that it is possible to turn off and on stroke recovery by manipulating theactivity of CREB-transfected neurons. CREB transfection enhances re-mapping of injuredsomatosensory and motor circuits, and induces the formation of new connections withinthese circuits. CREB is a central molecular node in the circuit responses after stroke that leadto recovery from motor deficits.

2018-06-08 | GSE115527 | GEO

proteins pulled down by CREB, part 2

Project description:Hepatocarcinoma is the third leading cause of death in cancer in the world. In recent years, research on CREB in hepatocellular carcinoma has become a hotspot, so our research group wants to use the mass spectrometry analysis what proteins can bind with CREB, and then explore the links between CREB and hepatocellular carcinoma.

2019-11-08 | PXD008261 | Pride

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