Human FOS Like Antigen 1 ELISA, FOSL1
- Known as:
- Human FOS Like Antigen 1 Enzyme-linked immunosorbent assay test, FOSL1
- Catalog number:
- E01F0013
- Product Quantity:
- 96 Tests/kit
- Category:
- -
- Supplier:
- BGene
- Gene target:
- Human FOS Like Antigen 1 ELISA FOSL1
Related genes to: Human FOS Like Antigen 1 ELISA, FOSL1
- 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: Human FOS Like Antigen 1 ELISA, FOSL1
Related articles to: Human FOS Like Antigen 1 ELISA, FOSL1
- The perioperative period represents a critical window in cancer management, during which anesthetic choice may influence tumor biology. Sevoflurane, a volatile anesthetic widely used in neurosurgery, has been shown to modulate gene expression in glioblastoma (GBM). This study aimed to identify novel biomarkers in GBM and to investigate their functional roles and prognostic significance, thereby exploring the potential impact of this common perioperative agent on tumor behavior and patient outcomes. - Source: PubMed
Publication date: 2026/05/22
Tang RuiChen HuYan YaLei Xiaofeng - Objective To investigate the heterogeneity characteristics of cancer-associated fibroblasts (CAF) in acral melanoma (AM) and their functional roles in the tumor microenvironment (TME), providing a theoretical basis for developing effective therapeutic strategies. Methods The single-cell RNA sequencing data used in this study were previously generated by our research group and have been deposited in the HRA001804 dataset of the National Genomics Data Center (NGDC). Five AM patient samples were selected from this dataset for analysis, including 4 primary tumor samples (PL1, PL2, PL4, PL5) and 1 lymph node metastasis sample (LG2). Bioinformatics methods including unsupervised clustering, pseudotime trajectory analysis, transcription factor regulatory network analysis, and cell-cell communication analysis were used for data mining. Results Three subtypes of CAF were identified from 41 960 high-quality cells: immunomodulatory CAF (iCAF), myofibroblastic CAF (mCAF), and proliferative CAF (pCAF). Pseudotime trajectory analysis demonstrated that mCAF were located at the initiation of differentiation, while iCAF and pCAF were distributed in distinct terminal branches. FOS-like 1, AP-1 transcription factor subunit (FOSL1) was identified as a key transcription factor regulating the differentiation of CAF into pCAF, and its co-expression modules were enriched in the P53 signal pathway, AP-1 transcription factor network, and MYC-mediated cell proliferation pathways. Cell communication analysis revealed an interaction network centered on iCAF, with critical pathways including CSPG4-(ITGA2+ITGB1), GDF15-TGFBR2, LGALS9-CD45/CD44, and CD70-CD27 signal pathways. Conclusion CAF in AM exhibits high heterogeneity, with FOSL1 playing a key regulatory role in CAF differentiation. CAF participates in tumor microenvironment regulation through complex intercellular communication networks. These findings provide important insights into understanding the biological characteristics of acral melanoma and developing targeted therapeutic strategies. - Source: PubMed
Du ZhiminRao WeiWang YilinFeng JingyiZhao Hua - Inflammatory bowel diseases (IBD), including ulcerative colitis and Crohn's disease, are chronic inflammatory disorders of the gastrointestinal tract associated with epithelial barrier dysfunction, dysregulated immune responses, and an increased risk of cancer. Persistent inflammation is a key driver of IBD-associated tumorigenesis, yet the transcriptional regulators linking inflammatory signaling to epithelial transformation remain incompletely defined. FOSL1 (FOS-like antigen 1), a member of the activator protein-1 (AP-1) transcription factor family, has emerged as a critical mediator at the intersection of inflammation, epithelial homeostasis, and cancer progression. FOSL1 is induced by pro-inflammatory pathways commonly activated in IBD, including MAPK/ERK, NF-κB, and cytokine signaling, and regulates gene programs involved in cell proliferation, migration, barrier integrity, immune modulation, and survival. Accumulating evidence demonstrates that FOSL1 expression is elevated in inflamed intestinal mucosa and in IBD-associated malignancies, where it contributes to epithelial dysfunction, chronic inflammation, tumor initiation, metastasis, angiogenesis, and therapeutic resistance. Moreover, FOSL1-driven transcriptional networks show mechanistic overlap between IBD-associated colorectal cancer (CRC) and other inflammation-linked gastrointestinal cancers, such as pancreatic ductal adenocarcinoma (PDAC). In this review, we summarize current knowledge on the regulation and function of FOSL1 in intestinal inflammation and IBD-associated cancers, highlight its context-dependent roles in epithelial and immune compartments, and discuss emerging therapeutic strategies aimed at indirectly targeting FOSL1 signaling pathways. - Source: PubMed
Publication date: 2026/04/27
Rilee Grace JRadhakrishnan Senthil KYang Guang-YuLi Jiong - Diabetic foot ulcer (DFU), a condition marked by high rates of recurrence, amputation, and mortality, represents one of the major challenges in diabetes management. RNA-binding proteins (RBPs) are pivotal for post-transcriptional regulation in diabetic complications. However, the aberrantly expressed RBP genes and their regulatory mechanisms in DFU remain unclear. This study aimed to investigate the potential functions and molecular interactions of YWHAZ, a dysregulated RBP identified in DFU tissues. - Source: PubMed
Publication date: 2026/05/07
Zha TianjianYao JunjieWang HaoCao QiangZhang JianChen ZhaoWang Jie - Biliary atresia (BA) is a life-threatening paediatric liver disease, characterized by bile duct obstruction, progressive inflammation and fibrosis. Treatment options are limited, often necessitating surgery or liver transplantation to prevent irreversible liver damage. Prednisolone has shown promise in treating BA; however, there is currently no consensus on its effectiveness, and the mechanism of action remains unknown. We investigated the effects of prednisolone in a BA model induced by Rhesus Rotavirus (RRV). Liver samples were collected from day-21 and day-28 post-RRV infected mice injected with PBS or steroid, and subjected to single-cell RNA sequencing (scRNA-seq) and immunohistochemistry. We identified subpopulations of hepatic stellate cells (HSCs) and macrophages that serve as key effectors of prednisolone-mediated disease amelioration. Prednisolone treatment at 28-days post RRV-infection suppressed pro-inflammatory Ly6c-high macrophages, increased immunosuppressive M2 Kupffer cells, and promoted deactivation of HSCs into the quiescent state. Computational reconstruction of HSC differentiation pathways revealed that the Nr3c1-Klf7 gene regulatory network (GRN) modulates the transition of HSCs between quiescence and activation, and we show that HSCs differentiate into three myofibroblasts (MyoFbs) subpopulations, each exhibiting different pathogenic potential. We identified a pro-inflammatory MyoFB subpopulation (MFB-2) characterized by the Fosl1-Hnf1b GRN. MFB-2 secretes elevated levels of macrophage-activating cytokines, exhibits resistance to apoptotic signals, and displayed impaired responsiveness to prednisolone. The HSC and MyoFb subtypes were also identified in BA patient livers with highly conserved gene expression and functional profiles, supporting their importance in BA progression. Prednisolone treatment transforms the liver immune-mesenchymal niche from an inflammatory to regenerative state in BA and modulation of GRNs in HSCs plays a pivotal role. - Source: PubMed
Publication date: 2026/05/19
Blakeley Paul DLiu FangranWu ZhongluanTang Clara S MTam Paul K HWong Kenneth K HLui Vincent C HChung Patrick H Y