Development of gene expression signatures for the A549 cells that overexpressed of FOSB
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PROVIDER: PRJNA438295 | ENA |
REPOSITORIES: ENA
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Project description:Strongly induction of FOSB was observed in a cationic anticancer peptide TP4 treated human A549 lung cancer cell-line, causing obvious cell death. This work aims to address the gene expression profiling upon FOSB overexpression in A549 cell.
2019-02-07 | GSE111827 | GEO
Project description:To examine fosB regulation of neurogenesis, depression and epilepsy, we compared the gene expression profiles of wild type, fosBd/d and fosB-null mice by microarray analysis. Microarray analysis revealed that genes related to neurogenesis, depression and epilepsy are altered in the hippocampus of fosB-null mice.
2013-01-01 | GSE37056 | GEO
Project description:To examine fosB regulation of neurogenesis, depression and epilepsy, we compared the gene expression profiles of wild type, fosBd/d and fosB-null mice by microarray analysis. Microarray analysis revealed that genes related to neurogenesis, depression and epilepsy are altered in the hippocampus of fosB-null mice. Total RNA from the hippocampus of wild-type, fosBd/d and fosB-null mice was prepared using ISOGEN and RNeasy Mini kits. For DNA microarray experiments, total RNA (100ng) was added to poly-A control and treated with WT Expression Kit. cDNA was labeled using WT terminal labeling kit and hybridized with Affymetrix GeneChip Mouse Gene 1.0 ST platform (GPL6246).
2013-01-01 | E-GEOD-37056 | biostudies-arrayexpress
Project description:Gene expression signatures in IRF7 overexpressed 3T3-L1 adipocytes
| PRJNA622292 | ENA
Project description:eGFP-FOSB ChIP-seq on human A549 For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf
2021-03-30 | GSE170613 | GEO
Project description:To identify genes whose expression is regulated by Fosb gene products in microglia, we performed microarray analysis using RNA prepared from wild-type and fosB-null microglial cells. Microarray analysis revealed that expression levels of 6 genes are altered in primary cultured microglial cells prepared from fosB-null mice compared with wild type. fosB+/G mice with a null-mutant allele, fosBG, were established and maintained by backcrossing to C57BL/6J. To yield homozygous mutant mice, fosB+/G (N20 generation) mice were intercrossed. C57BL/6J mice were used as wild-type control.
2014-04-18 | E-GEOD-40714 | biostudies-arrayexpress
Project description:The Fosb gene encodes subunits of the activator protein-1 transcription factor complex. Two mature mRNAs, Fosb and ΔFosb, encoding full-length FOSB and ΔFOSB proteins respectively, are formed by alternative splicing of Fosb mRNA. Fosb products are expressed in several brain regions. Moreover, Fosb-null mice exhibit depressive-like behaviors and adult-onset spontaneous epilepsy, demonstrating important roles in neurological and psychiatric disorders. Study of Fosb products has focused almost exclusively on neurons; their function in glial cells remains to be explored. In this study, we found that microglia express equivalent levels of Fosb and ΔFosb mRNAs to hippocampal neurons and, using microarray analysis, we identified six microglial genes whose expression is dependent on Fosb products. Of these genes, we focused on C5ar1 and C5ar2, which encode receptors for complement C5a. In isolated Fosb-null microglia, chemotactic responsiveness toward the truncated form of C5a was significantly lower than that in wild-type cells. Fosb-null mice were significantly resistant to kainate-induced seizures compared with wild-type mice. C5ar1 mRNA levels and C5aR1 immunoreactivity were increased in wild-type hippocampus 24 hours after kainate administration; however, such induction was significantly reduced in Fosb-null hippocampus. Furthermore, microglial activation after kainate administration was significantly diminished in Fosb-null hippocampus, as shown by significant reductions in CD68 immunoreactivity, morphological change and reduced levels of Il6 and Tnf mRNAs, although no change in the number of Iba-1-positive cells was observed. These findings demonstrate that, under excitotoxicity, Fosb products contribute to a neuroinflammatory response in the hippocampus through regulation of microglial C5ar1 and C5ar2 expression.
2014-04-18 | GSE40714 | GEO
Project description:We examined here the regulation of gene expression in ventral hippocampus neurons that project to nucleus accumbens (vHPC-NAc) by the transcription factor, ΔFosB. The activity of this circuit is critical to stress-induced social withdrawal. ΔFosB regulates the physiology and behavior of this circuit to produce resilience. Circuit-specific translating ribosomal affinity purification (TRAP) was conducted followed by RNASeq. A strain of floxed Fosb mice (the gene that encodes ΔFosB) was crossed with a ribosomal L10-GFP fusion protein line (Rosa26). To target vHPC-NAc neurons, a retrograde recombinant HSV-Cre was injected into NAc to retrogradely drive expression of GFP and knockout the Fosb gene in vHPC-NAc. Bilateral biopsy punches of vHPC containing GFP-labeled projections were collected, pooled, and processed by TRAP followed by 3rd-generation sequencing of actively translating mRNA. We have now identified Fosb-regulated gene expression in a specific hippocampal-to-accumbens circuit that is important for resilience to stress-induced social withdrawal.
2020-06-30 | GSE137283 | GEO
Project description:Mast cells are innate immune cells that play a crucial role in numerous physiological processes across tissues by releasing pre-stored and newly synthesized mediators in response to stimuli, an activity largely driven by changes in gene expression. Given their widespread influence, dysfunction in mast cells can contribute to a variety of pathologies including allergies, long COVID, and autoimmune and neuroinflammatory disorders. Despite this, the specific transcriptional mechanisms that control mast cell mediator release remain poorly understood, significantly hindering the development of effective therapeutic strategies. We found that the two proteins encoded by the transcription factor FosB, FOSB and the highly stable variant ΔFOSB, are robustly expressed upon stimulation in both murine and human mast cell progenitors. Motivated by these findings, we generated a novel mouse model with targeted ablation of FosB gene expression specifically in mast cells (MC FosB- ) by crossing a mast cell-specific Cre reporter line (Mcpt5-Cre) with a Cre-dependent floxed FosB mouse lines. We found that mast cell progenitors derived from MC FosB- mice, compared to wild types (WT), exhibit baseline increased histamine content and vesicle numbers. Additionally, they show enhanced calcium mobilization, degranulation, and histamine release following allergy-related IgE-mediated stimulation, along with heightened IL-6 release in response to infection-like LPS stimulation. In vivo experiments with IgE- mediated and LPS challenges revealed that MC FosB- mice experience greater drops in body temperature, heightened activation of tissue-resident mast cells, and increased release of pro-inflammatory mediators compared to their WT counterparts. These findings suggest that FosB products play a crucial regulatory role in moderating stimulus-induced mast cell activation in response to both IgE and LPS stimuli. Lastly, by integrating CUT&RUN and RNAseq data, we identified several genes targeted by ΔFOSB that could mediate these observed effects, including Mir155hg, CLCF1, DUSP4, and Trib1. Together, this study provides the first evidence that FOSB/ΔFOSB modulate mast cell functions and provides a new possible target for therapeutic interventions aimed at ameliorating mast cell-related diseases.
2025-01-14 | GSE286256 | GEO
Project description:To study the effect of transcription factor GFI1 on lung cancer cells, we overexpressed GFI1 in A549 cells and performed RNA-seq. Moreover, control and GFI1-expressing A549 cells that were forced into suspension for 48hrs were used performed RNA-seq.
2022-09-14 | GSE165307 | GEO