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Analyzing CREB binding motif and sites in the mouse lens epithelial cells alpha-TN4 overexpressing Vector, WT-CREB, S133A-CREB, R314A-CREB and S133A/R314A –CREB.

ABSTRACT: Transcription factor CREB regulates lens Epithelial-Mesenchymal Transition（EMT）in both S133 phosphorylation dependent and independent manners. We found that S133A-CREB can activate lens EMT, while R314A-CREB attenuated it. To understand the mechanism by which S133A-CREB and R314A-CREB modulates EMT gene expression. ChIP assay using CREB antibody in the in the mouse lens epithelial cells alpha-TN4 overexpressing Vector, WT-CREB, S133A-CREB, R314A-CREB and S133A/R314A-CREB, and ChIP-seq was conducted on the ChIP DNA. We found that WT-CREB, S133A-CREB as well as R314A-CREB binds to the promoter regions of mesenchymal genes, and S133A-CREB retained canonical CREB binding motif, while R314A-CREB exhibited shifted binding motif preference to ATF1.

ORGANISM(S): Mus musculus

PROVIDER: GSE276462 | GEO | 2025/02/05

REPOSITORIES: GEO

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Using RNA-seq to analyze gene expression in the mouse lens epithelial cells alpha-TN4 overexpressing Vector, WT-CREB, KCREB, R314A-CREB, S133A-CREB, S133A-KCREB and S133A/R314A -CREB before and after TGFβ treatment

Project description:CREB regulates lens EMT in both S133 phosphorylation dependent and independent manners. We found that S133A-CREB activated, while R314A-CREB attenuated lens mesenchymal marker gene Fn1 and Snail2. To better understand the mechanism by which S133A and R314A mutations modulate EMT gene expression. RNA-seq on the alpha-TN4 overexpressing Vector, WT-CREB, KCREB, R314A-CREB, S133A-CREB, S133A-KCREB and S133A/R314A -CREB before and after TGFβ treatment.

2025-02-05 | GSE276922 | GEO

Heterochromatin assembly and transcriptome repression by Set1 in coordination with a class II histone deacetylase

2014-12-12 | GSE63301 | GEO

Epigenome analysis of intracranial mesenchymal tumors with FET-CREB fusions

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Transcription profiling of fetal lung from wild type and CREB knock-out mice

Project description:The cAMP response element binding protein (Creb) is a member of a leucine zipper transcription factor family that regulates gene expression primarily in response to the intracellular cAMP signalling pathway. Previous studies have shown Creb1-null mice suffer respiratory failure with lung atelectasis and a large reduction in Sftpd mRNA. Using a new line of Creb1-null mice we have further investigated Creb function in the developing mouse lung, focussing on differentiation of the airway epithelium. The lungs of Creb1-null fetal mice showed normal respiratory development until E17.5 when proximal and distal airways fail to inflate. Subsequent ultrastructural analysis of the lungs of E17.5 Creb1-null fetal mice revealed a defect in AEC differentiation with a reduction in proportions of type-II AECs and in particular, a very large reduction in type-I AECs. Furthermore, immunostaining for the proximal epithelial cell markers Scgb1a1 (also known as CC10) (Clara cells), Foxj1 (Ciliated cells), and CGRP (Neuroendocrine cells) showed delayed or defective proximal epithelial differentiation in Creb1-null fetal lungs. Quantitative real time PCR (qRT-PCR) analysis at E17.5 in Creb1-null fetal lungs showed differential expression of mRNAs for Creb/Atf1 subfamily members, surfactant-associated proteins, type-I AEC markers and proximal epithelial markers. Furthermore, whole-genome microarray analysis at E17.5 in Creb1-null fetal lungs has provided novel genes which will prove useful to further investigate Creb-mediated signalling in lung development. Together these results demonstrate that Creb plays a key role in determining cell lineages and differentiation of the developing lung epithelium.

2009-04-30 | E-MEXP-1295 | biostudies-arrayexpress

Heterochromatin assembly and transcriptome repression by Set1 in coordination with a class II histone deacetylase

Project description:Gene expression profiling of S. pombe set1/COMPASS/H3K4 mutants, atf1 and set1 atf1 deletion mutants, set1 clr3 deletion mutants; ChIP-chip tiling microarray profiling of S. pombe Set1, Atf1, H3K4me3 in wt/atf1 deletion mutants, H3K9me2 in wt/set1 clr3 deletion mutants Custom Agilent 60mer microarrays were used to assay gene expression in set1/COMPASS mutants in combination with atf1 and clr3 mutants, and to profile genome-wide binding of Set1, Atf1, H3K4me3 and H3K9me2 in S. pombe cells (two-color mutant vs. wildtype, ChIP vs. input experiments).

2014-12-12 | E-GEOD-63301 | biostudies-arrayexpress

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

Targeted activation of CREB in reactive astrocytes is neuroprotective in focal acute cortical injury.

Project description:Transcriptome profiling of mice overexpressing a constitutively active form of CREB in astrocytes (VP16-CREB) vs WT mice, both in normal conditions and after a focal cryolesion (C) in the parietal cortex. Goal is to determine which astrocytic genes are responsible for the neuroprotection we observed in VP16-CREB mice after injury.

2016-04-27 | GSE68187 | GEO

Transcription profiling of mouse transgenics expressing A-CREB to investigate basal and kainate-induced gene expression in A-CREB mouse hippocampi

Project description:The cAMP responsive element binding protein (CREB) pathway has been involved in two major cascades of gene expression regulating neuronal function. The first one presents CREB as a critical component of the molecular switch that control longlasting forms of neuronal plasticity and learning. The second one relates CREB to neuronal survival and protection. To investigate the role of CREB-dependent gene expression in neuronal plasticity and survival in vivo, we generated bitransgenic mice expressing A-CREB, an artificial peptide with strong and broad inhibitory effect on the CREB family, in forebrain neurons in a regulatable manner. The expression of ACREB in hippocampal neurons impaired L-LTP, reduced intrinsic excitability and the susceptibility to induced seizures, and altered both basal and activity-driven gene expression. In the long-term, the chronic inhibition of CREB function caused severe loss of neurons in the CA1 subfield as well as in other brain regions. Our experiments confirmed previous findings in CREB deficient mutants and revealed new aspects of CREB-dependent gene expression in the hippocampus supporting a dual role for CREB-dependent gene expression regulating intrinsic and synaptic plasticity and promoting neuronal survival. manufacturer's protocol. Experiment Overall Design: Each sample contained total RNA from the hippocampi of a group of 3-4 three weeks old mice. We obtained duplicate samples for each experimental condition (in total 14 WT and 20 A-CREB mice where used in this experiment). Mouse Genome 430 2.0 genechips were hybridized, stained, washed and screened for quality according to the manufacturer's protocol.

2009-01-17 | E-GEOD-14320 | biostudies-arrayexpress

Expression Profile of CREB knockdown in Myeloid Leukemia Cells

Project description:Background. The cAMP Response Element Binding Protein, CREB, is a transcription factor that regulates cell proliferation, differentiation, and survival in several model systems, including neuronal and hematopoietic cells. We demonstrated that CREB is overexpressed in acute myeloid and leukemia cells compared to normal hematopoietic stem cells. CREB knockdown inhibits leukemic cell proliferation in vitro and in vivo, but does not affect long-term hematopoietic reconstitution. Therefore, we propose CREB to be a potential target for therapy. To understand downstream pathways regulating CREB, we performed expression profiling with RNA from the K562 myeloid leukemia cell line. Results. By combining our expression data from CREB knockdown cells with prior ChIP data on CREB binding we were able to identify a list of putative CREB regulated genes. We performed extensive analyses on the top genes in this list as high confidence CREB targets. We found that this list is enriched for genes involved in cancer, and unexpectedly, highly enriched for histone genes. Furthermore, histone genes regulated by CREB were more likely to be specifically expressed in hematopoietic lineages. The transcription factor Elk-1 was upregulated in response to CREB deletion. Conclusions. We have identified a high confidence list of CREB targets in K562 cells. These genes allow us to begin to understand the mechanisms by which CREB contributes to acute leukemia. In particular, we speculate that the regulation of histone genes may play an important role in this process, by possibly altering the regulation of DNA replication during the cell cycle.

2008-08-30 | GSE12056 | 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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