Ask about this productRelated genes to: FOSL1 antibody
- Gene:
- FOSL1 NIH gene
- Name:
- FOS like 1, AP-1 transcription factor subunit
- Previous symbol:
- -
- Synonyms:
- fra-1
- Chromosome:
- 11q13.1
- Locus Type:
- gene with protein product
- Date approved:
- 2000-12-04
- Date modifiied:
- 2016-10-05
Related products to: FOSL1 antibody
Related articles to: FOSL1 antibody
- Mechanotransduction, i.e., the conversion of mechanical cues into biochemical signals, is essential for bone development, remodeling, and adaptation. Although mechanical loading is known to regulate osteoblast function and bone homeostasis, dissecting the early and sustained mechanotransductive responses at the microscale remains challenging due to limitations of existing in vitro models. Here, we report the development and application of a mechanostimulation system comprising a polypyrrole (PPy)-based wire actuator that expands and contracts (4 μm in radius) upon electrical actuation and enables precise, localized micromechanical stimulation of a small number of cells within standard culture formats. Using this system, we applied short-term (30 min) cyclic (Cyc30) or static (Stat30), as well as prolonged (120 min) cyclic (Cyc120) stimulations to two osteoblast-like cells (MC3T3-E1 or KUSA-A1). Subsequent transcriptomic profiling and computational network analyses revealed that Cyc30 was not capable of inducing significant changes in mRNA expression, suggesting cellular adaptation to short-term cyclic loading. In contrast, Stat30 induced the upregulation of Fos, Btg2, Egr1, and Fosl1, all known genes associated with mechanotransduction, supporting the validity and reproducibility of our experimental mechanostimulation system. Notably, two long non-coding RNAs (B930036N10Rik and 5430431A17Rik) were identified for the first time as being upregulated in response to Stat30 stimuli. Among the differentially expressed genes (DEGs) upregulated by Cyc120 stimuli, Hmox1, a stress-inducible enzyme known for its roles in maintaining cellular homeostasis and promoting survival, was the only DEG repeatedly observed across the Cyc30/Cyc120 and Stat30/Cyc120 comparisons in both cell types, potentially emerging as a key stress-response gene under prolonged mechanical loading. Collectively, these results establish the PPy-based microactuator as a powerful tool for microscale mechanobiology, and provide molecular insight into immediate-early responsive transcriptional programs underlying osteoblastic mechanoadaptation conserved across different cell types. - Source: PubMed
Publication date: 2026/04/30
Chen JiaminOrtega-Santos Amaia BHayano SatoruWang ZiyiMartinez Jose GHara Emilio SatoshiJager Edwin W HKamioka Hiroshi - Pancreatic intraepithelial neoplasia (PanIN) is common in healthy individuals, but can progress to invasive pancreatic ductal adenocarcinoma (PDAC). PanIN cells spread non-invasively throughout pancreatic ducts, while PDAC is defined by the ability to exit ducts and invade the parenchyma. Using high-resolution spatial transcriptomics, we identify a conserved epithelial program, MP10 that marks invasive cancer cells across human PDAC and is activated during PanIN-to-PDAC progression in mice. MP10 resembles the re-epithelialization program of wound-edge keratinocytes, including hemidesmosome components, integrins, and metabolic genes required for keratinocyte migration. Rare PanIN cells spontaneously activate MP10 while also triggering tumor suppressor genes (TSGs), which keep the incipient malignant cells in check. TSG loss unleashes these cells to invade the parenchyma, driven by the wound-induced transcription factor FOSL1. MP10-expressing cancer cells induce nearby CAFs into a wound-like CTHRC1 state, which in turn promote neoplastic MP10 through EGFR activation, forming a wound-like loop that underlies invasive PDAC. - Source: PubMed
Publication date: 2026/04/30
Zhuo MeilianLi YongZhang YifengYang ChenluZou DiXu WenhaoHan JingWang SaisaiDeng HaohaoPan XuDun RuikangHe RuizheShi YihongHan XianlinZhang TaipingWang WeibinDai MenghuaXu QiangLiu LuluWang WenzeLiu YuanhaoLiu MingyangDeng ZiqingZhao YupeiWu WenmingPeng JunyaChen MoDavid Charles J - Ovarian carcinoma is a difficult-to-treat cancer. It is often resistant to chemotherapy and targeted therapy. The 5-year survival rates of patients with advanced tumors are usually below 40%. Immunotherapy represents an emerging treatment option. We investigated the prognostic significance of the oncogenic transcription factor AP-1, formed by the dimerization of FOS and JUN family members. - Source: PubMed
Dawood MonaOoko EdnahEfferth ThomasBoulos Joelle C - Viral myocarditis (VM) is a cardiac inflammatory condition caused by viral infection and serves as a critical precursor to life-threatening complications, such as dilated cardiomyopathy and heart failure. Coxsackievirus B3 (CVB3), a predominant etiological agent of VM, lacks targeted therapeutic interventions despite ongoing antiviral development. Mitophagy is a selective mitochondrial quality control mechanism mediated by PINK1. It has two key roles: maintaining mitochondrial homeostasis and regulating innate antiviral immunity. Here, we employed single-cell RNA sequencing to reveal a significant correlation between impaired mitophagy and cardiomyocyte pathology in CVB3-induced myocarditis. We demonstrated that CVB3 infection suppresses PINK1-dependent mitophagy, while the attenuation of PINK1 reciprocally enhances CVB3 replication. Mechanistically, CVB3 non-structural protein 3C promotes the degradation of mitochondrial antiviral signaling protein (MAVS). MAVS interacts with PINK1 to form a regulatory loop: PINK1 deficiency boosts MAVS reduction, which further promotes viral replication and worsens myocardial injury. Furthermore, we identify the transcription factor FOSL1 as a novel negative regulator of PINK1 transcription through direct promoter binding. Collectively, these findings show that the 3C/FOSL1/PINK1/MAVS signaling axis is a key mechanism in CVB3 pathogenesis. We propose innovative therapeutic targets for viral myocarditis through restoration of mitochondrial homeostasis and modulation of host-virus interactions. - Source: PubMed
Publication date: 2026/04/26
Liu TingjunWan AoXu YinhaiLu HongxiangXie YiweiWu HanWang JiangWang HuaHao TingtingZhang YonggenXu JinfengShen HongxingLi Shibao - The inflammation-intestinal metaplasia (IM)-carcinoma cascade has been proposed as a framework for gastric cancer (GC) development, yet the cell-level heterogeneity and microenvironmental remodeling underlying this progression remain poorly characterized. Here, we constructed a single-cell transcriptomic atlas by integrating scRNA-seq data from chronic gastritis (superficial, CGS), IM, cancer-adjacent, and tumor tissues through a unified analytical pipeline. Seven major cell lineages were resolved. Relative to CGS, IM and GC tissues exhibited a progressive contraction of epithelial compartments accompanied by expansion of immune and stromal populations. Copy number variation (CNV) inference identified two tumor-restricted malignant epithelial subgroups-one biased toward differentiation and the other enriched for inflammatory and epithelial-mesenchymal transition (EMT) signatures-as well as putative proto-malignant intermediates that coexisted with phenotypically normal epithelium. Cell-cell communication analysis indicated broadly augmented crosstalk between epithelial cells and T cells, myeloid cells, and fibroblasts, with prominent involvement of a CD44-extracellular matrix (ECM) axis. Pseudotime trajectory analysis placed malignant epithelium at late positions along gastric and pyloric mucosal cell differentiation backbones, coinciding with increasing CNV burden and enrichment of stem-like transcriptional programs. Gene regulatory network analysis revealed coordinated activity of lineage-specification modules (HNF4/CDX, NR1H4/ESRRA), proliferative regulons (MYC/TFDP1), and inflammatory/EMT-associated programs (FOSL1/REL/NF-κB). In independent cohorts, elevated expression of several malignant-epithelium-associated transcription factors-including HNF4A, KLF3, FOSL1, TCF7L2, BCL3, RELB, ONECUT2, and MAF-correlated with unfavorable overall survival. Collectively, these findings provide single-cell-resolution evidence consistent with the proposed three-stage model of gastric carcinogenesis and highlight candidate transcriptional regulators warranting further investigation as potential early-detection biomarkers. - Source: PubMed
Publication date: 2026/04/22
Li XiulanGuo MengqiWen YunhanLong Bo