CREB1 Mouse Monoclonal Antibody
- Known as:
- CREB1 Mouse Monoclonal Antibody
- Catalog number:
- BIN-001385-M01
- Product Quantity:
- 0.1mg
- Category:
- -
- Supplier:
- Zyagen
- Gene target:
- CREB1 Mouse Monoclonal Antibody
Related genes to: CREB1 Mouse Monoclonal Antibody
- Gene:
- CREB1 NIH gene
- Name:
- cAMP responsive element binding protein 1
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 2q33.3
- Locus Type:
- gene with protein product
- Date approved:
- 1990-02-05
- Date modifiied:
- 2016-10-05
Related products to: CREB1 Mouse Monoclonal Antibody
Related articles to: CREB1 Mouse Monoclonal Antibody
- Gulf War Illness (GWI) is a chronic neuroimmune condition affecting veterans of the 1990-91 Gulf War. Current treatments primarily target symptom relief, and the biological mechanisms underlying GWI remain poorly understood. Using a validated mouse model of Gulf War Illness (GWI) combining corticosterone (CORT) and diisopropyl fluorophosphate (DFP) exposure to induce stress- and toxicant-related neuroimmune priming, we examined how prior exposure alters molecular responses to a subsequent immune challenge. Male mice were exposed to CORT and DFP with repeated intermittent CORT, followed by lipopolysaccharide (LPS) or saline to assess transcriptional and epigenetic changes in brain and blood. We analysed transcript abundance, chromatin accessibility, and DNA methylation in the hippocampus, frontal cortex, and blood at 6 h, 12 h and 24hrs after LPS challenge (3-4 mice per group). We identified widespread transcriptional changes and dynamic chromatin accessibility following LPS exposure, with DNA methylation modifications that persisted in the hippocampus and blood. Thirty-three genes, including , , , and , were differentially expressed and methylated in both hippocampus and blood across all time points. These genes clustered in immune- and glial-related pathways. Transcription factor analysis revealed enrichment of NF-κB, CREB1, EGR1, JUN, and MYC binding motifs in regions with differential methylation. Our findings identify novel candidate biomarkers in peripheral blood that reflect brain molecular changes, providing a new framework for elucidating the long-term epigenetic impacts of stress and toxicant exposure in GWI. - Source: PubMed
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Sasaki AKelly K AMichalovicz L TAshbrook D GWijenayake SO'Callaghan J PMcGowan P O - Biological sex regulates fundamental neurobiology, as well as the etiology and prevalence of neuropsychiatric disorders. Cyclin-dependent kinase 5 (Cdk5) is a neuronally enriched kinase that regulates synaptic plasticity, neuronal homeostasis, and hippocampal-dependent memory. While Cdk5 protein activity is necessary and sufficient to promote memory in male rodents, its role in females and its gene regulation in either sex remain poorly understood. In males, Cdk5 protein inhibition impairs fear memory. We previously showed that fear conditioning activates gene expression and increases permissive chromatin acetylation in male, but not female hippocampus. We hypothesize that gene repression would impair fear memory in males. We developed an excitatory neuron-specific, CRISPR/dCas9-HDAC3 epigenetic editing tool to target histone acetylation at the endogenous Cdk5 promoter. This strategy reduced histone acetylation and decreased Cdk5 mRNA, protein, and kinase activity in both sexes. Interestingly, repression in hippocampal neurons impaired fear and spatial memory in both male and female mice. Targeted deacetylation also evicted the transcription factor CREB1 from the Cdk5 promoter, revealing a link between histone acetylation and Cdk5 transcriptional activation. These findings demonstrate that acetylation in neurons is necessary for hippocampal memory in both sexes, providing new insight into sex-specific epigenetic regulation of memory. - Source: PubMed
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