Ask about this productRelated genes to: FGF8 protein
- Gene:
- FGF8 NIH gene
- Name:
- fibroblast growth factor 8
- Previous symbol:
- -
- Synonyms:
- AIGF
- Chromosome:
- 10q24.32
- Locus Type:
- gene with protein product
- Date approved:
- 1995-08-15
- Date modifiied:
- 2016-10-05
Related products to: FGF8 protein
Related articles to: FGF8 protein
- Birds and mammals exhibit extraordinary facial diversity, reflecting adaptations to distinct ecological niches and feeding strategies. While core face-building developmental programs are conserved and orchestrated by interactions between ectodermal organizers and the underlying mesenchyme, mechanisms driving facial shape variation remain poorly understood. Here, we integrate single-cell transcriptomic and chromatin accessibility profiling of mouse and chicken developing face to construct a comparative regulatory map. Although both ectodermal and mesenchymal populations display distinct regulatory features in each species, the mesenchyme exhibits markedly greater divergence, pointing to its central role in shaping facial morphology. We further reveal unexpected molecular complexity in the main face-shaping organizer, including a mouse-specific expression domain. At key morphogen loci (, , and ), conserved and lineage-specific enhancers exhibit spatially restricted activity patterns that mirror divergent signaling domains. These findings demonstrate how cis-regulatory evolution modulates conserved developmental programs to generate morphological novelty, providing a valuable resource for studying vertebrate facial evolution. - Source: PubMed
Publication date: 2026/05/06
Kyomen StellaSeton Louk W GCook Laura EEscamilla-Vega ElioMurillo-Rincón Andrea PJacobsen AlexanderDamatac AmorFortmann-Grote CarstenFuss JaninaVisel AxelKaucká Markéta - Precise spatiotemporal regulation of epithelial-mesenchymal interactions is fundamental to craniofacial morphogenesis. Fibroblast Growth Factor 8 (FGF8) is a pivotal signaling molecule in early mandibular development; however, its stage-specific regulatory mechanisms remain poorly understood. In this study, we demonstrate that Fgf8 and its receptors exhibit a dynamic, declining expression profile in the mouse mandibular arch between embryonic days 9 (E9) and E11. Using organ and micromass culture systems, we identify a critical developmental window at E10 during which FGF8 exerts a dual effect: it promotes mesenchymal cell expansion while simultaneously suppressing chondrogenic differentiation in a dose-dependent manner. Interestingly, by E11, mandibular cells undergo an autonomous transcriptional shift, reduced proliferative capacity, and show downregulation of proliferation-related gene sets, leading to resistance to FGF8-induced proliferation and chondrogenic inhibition. Mechanistically, we show that FGF8 specifically activates the ERK signaling pathway within the responsive E10 window. Pharmacological inhibition of MEK/ERK signaling successfully rescues the suppressed chondrogenic differentiation, identifying ERK as the key mediator of FGF8-induced chondrogenic inhibition at this stage. Together, our findings reveal that FGF8 acts as a stage-specific regulator that coordinates the transition from cell proliferation to chondrogenic commitment during early Meckel's cartilage development via the ERK pathway. - Source: PubMed
Publication date: 2026/05/02
Qi HeTerao FumieAl Akel DiyaaYoshizaki KeigoTakahashi Ichiro - Oocyte maturation defect (OMD) is a rare cause of female infertility characterized by the persistent arrest of oocytes at immature stages. While biallelic PATL2 variants have been associated with OMD, the underlying molecular mechanisms remain unclear. This study aimed to identify novel PATL2 variants in OMD patients and investigate their functional consequences using a Patl2 knockout (KO) mouse model. - Source: PubMed
Publication date: 2026/04/30
Yu LiWang LinPan BaishenWang BeiliDong XiGuo WeiChe Qi - Limited targeted agents are approved for pediatric sarcomas. Tyrosine kinase (TK) inhibitors (TKi) have shown clinical efficacy in some, but not all, young patients with sarcoma. A major obstacle preventing further advances and clinical implementation is the lack of predictive response biomarkers to guide TK-targeted treatments. TK-activating fusions or mutations are rare in these patients. RNA overexpression of TKs is a frequent feature. The unresolved question is when upregulated TK expression is associated with kinase activation and signaling dependence. We explored the TK molecular landscape of 107 patients with sarcoma from the ZERO Childhood Cancer Precision Medicine Program (ZERO) using whole-genome and -transcriptome sequencing. Phosphoproteomic analyses of tyrosine phosphorylation (pY) and functional in vitro and in vivo assays were performed in cell lines and patient-derived xenografts (PDX). Our analysis shows that although novel genomic driver lesions are rare, when present they are therapeutically actionable as exemplified by a novel LSM1-FGFR1 fusion identified in a patient with osteosarcoma. We further show that in certain contexts, TK RNA expression can indicate TK pathway activity and predict TKi sensitivity. We highlight the utility of FGFR inhibitors in PAX3-FOXO1 fusion-positive rhabdomyosarcomas (FP-RMS) characterized by high FGFR4 and FGF8 RNA expression levels and FGFR4 activation (FGFR4_pY). We demonstrate marked tumor growth inhibition in all FP-RMS PDXs treated with single-agent FGF401 (FGFR4-specific inhibitor) and single-agent lenvatinib (multikinase FGFR inhibitor) and report a clinical response to lenvatinib in a patient with relapsed metastatic FP-RMS. Altogether, we identified new patients with sarcoma who may benefit from FGFR inhibitors, most notably FP-RMS via FGFR4/FGF8 coexpression. - Source: PubMed
Publication date: 2026/04/27
Fordham Ashleigh MBrown Lauren MMayoh ChelseaSalib AliceBarger Zara AWong MarieLim Kam Sian Terry C CHu ChangyuanXie JinhanGunther KateTrebilcock PeterTerry Rachael LBarahona PauletteAjuyah PamelaSherstyuk AlexandraAvila AnicaCadiz RoxannePerkins Callum MGifford Andrew JMao JieDolman M Emmy MZhao AndreaO'Regan Luke PGorgels DanielLau Loretta M SZiegler David SHaber MichelleTyrrell VanessaLock Richard BCowley Mark JNicholls WayneDaly Roger JEkert Paul GFleuren Emmy D G - Temporomandibular joint osteoarthritis (TMJOA) is recognized as one of the most important oral-maxillofacial degenerative diseases, and affects a large group of the population worldwide. The progression of TMJOA is accompanied by an imbalance of cytokines in the joint cavity and a slow but long-lasting degradation of the joint tissues. FGF8, an important member of the fibroblast growth factor family, has been shown to be up-regulated in the cavities of osteoarthritis joints. However, its role in TMJOA progression remains unclear. Here, we established a mouse TMJOA model by using unilateral anterior crossbite (UAC), and investigated the role of FGF8 on the changes in condylar cartilage in the progress of TMJOA by using adeno-associated virus carrying FGF8 gene. We found that FGF8 accelerated the cartilage deterioration during TMJOA progression. FGF8 overexpression partially impaired the mature phenotype of chondrocytes by decreasing the expression of collagen type II (COL2A1) and aggrecan, and exacerbated chondrocyte hypertrophy by increasing the expression of collagen type X (COL10A1), matrix metallopeptidase 13 (MMP13) and a disintegrin and metalloproteinase with thrombospondin 5 (ADAMTS5). FGF8 promotes chondrocyte cytokine perturbation by up-regulating the expression profiles of inflammatory factors, chemotactic factors and interferons and down-regulating the expression of growth factors via the transcription factor JunB. Furthermore, FGF8-mediated JunB facilitates chondrocyte hypertrophy by binding to the promoters of Col10α1 and Mmp13. These results help understand the importance of FGF8 in the progression of TMJOA and provide cues for potential therapeutic strategies for osteoarthritis. - Source: PubMed
Publication date: 2026/04/15
Chen HaoranFeng ShuoLi ChengLiu YongtaoXue ChengXie JingZuo Tao