About: FOSL2 is a research topic. Over the lifetime, 11 publications have been published within this topic receiving 228 citations. The topic is also known as: Fos-Related Antigen & FRA-2.
TL;DR: It is demonstrated here that transcription factor COUP-TF-interacting protein 1 (CTIP1/BCL11A; hereafter CTIP1) is highly expressed in the developing murine epidermis and appears to play a role in EPB establishment via direct or indirect regulation of a subset of genes encoding proteins involved in epidermal differentiation and lipid metabolism.
Abstract: The epidermal permeability barrier (EPB) prevents organisms from dehydration and infection. The transcriptional regulation of EPB development is poorly understood. We demonstrate here that transcription factor COUP-TF-interacting protein 1 (CTIP1/BCL11A; hereafter CTIP1) is highly expressed in the developing murine epidermis. Germline deletion of Ctip1 (Ctip1 -/-) results in EPB defects accompanied by compromised epidermal differentiation, drastic reduction in profilaggrin processing, reduced lamellar bodies in granular layers and significantly altered lipid composition. Transcriptional profiling of Ctip1 -/- embryonic skin identified altered expression of genes encoding lipid-metabolism enzymes, skin barrier-associated transcription factors and junctional proteins. CTIP1 was observed to interact with genomic elements within the regulatory region of the gene encoding the differentiation-associated gene, Fos-related antigen2 (Fosl2) and lipid-metabolism-related gene, Fatty acid elongase 4 (Elvol4), and the expression of both was altered in Ctip1 -/- mice. CTIP1 appears to play a role in EPB establishment of via direct or indirect regulation of a subset of genes encoding proteins involved in epidermal differentiation and lipid metabolism. These results identify potential, CTIP1-regulated avenues for treatment of skin disorders involving EBP defects.
TL;DR: Novel, functional FRA-2 targets are identified across the genome through expression profile analysis in a knockdown transgenic rat, providing functional insight into selective genomic targeting by Fra-2, highlighting discordance between predicted and actual targets.
TL;DR: In this article, the global gene expression effects on mammary epithelium of bexarotene, gefitinib, and celecoxib were analyzed in light of their effectiveness as chemopreventive agents.
Abstract: Genetically engineered mouse cancer models are among the most useful tools for testing the in vivo effectiveness of the various chemopreventive approaches. The p53-null mouse model of mammary carcinogenesis was previously characterized by us at the cellular, molecular, and pathologic levels. In a companion article, Medina et al. analyzed the efficacy of bexarotene, gefitinib, and celecoxib as chemopreventive agents in the same model. Here we report the global gene expression effects on mammary epithelium of such compounds, analyzing the data in light of their effectiveness as chemopreventive agents. SAGE was used to profile the transcriptome of p53-null mammary epithelium obtained from mice treated with each compound versus controls. This information was also compared with SAGE data from p53-null mouse mammary tumors. Gene expression changes induced by the chemopreventive treatments revealed a common core of 87 affected genes across treatments (P < 0.05). The effective compounds, bexarotene and gefitinib, may exert their chemopreventive activity, at least in part, by affecting a set of 34 genes related to specific cellular pathways. The gene expression signature revealed various genes previously described to be associated with breast cancer, such as the activator protein-1 complex member Fos-like antigen 2 (Fosl2), early growth response 1 (Egr1), gelsolin (Gsn), and tumor protein translationally controlled 1 (Tpt1), among others. The concerted modulation of many of these transcripts before malignant transformation seems to be conducive to predominantly decrease cell proliferation. This study has revealed candidate key pathways that can be experimentally tested in the same model system and may constitute novel targets for future translational research.
TL;DR: The study reveals the ability to assess time-dependent changes in gene expression patterns in NRCMs associated with CG exposure and suggests that there are multiple deregulated pathways associated with cardiomyocyte death after CG exposure, including JAK/Stat signaling, IL-9 signaling and Nur77 signaling.
TL;DR: The Fosl2 gene was mapped using a polymorphic microsatellite localized in the promoter region of the gene and the following pair of primers allows amplification of this micros satellite.
Abstract: Species: Mouse Locus name: Fos like antigen 2 [1]. Locus symbol: Fosl2 Map position: cen-ll6-2.5 (0.3-8.7)-Fos12-15 (8.0-24.7)-D5Nds2 for a 95% confidence interval. Method o f mapping: 80 in terspeci f ic backcross progeny: (AKUxPWK) x AKU [2]. Allele detection: Fosl2 gene was mapped using a polymorphic microsatellite localized in the promoter region of the gene [1]. The following pair of primers allows amplification of this microsatellite: