Ask about this productRelated genes to: FGF4 protein
- Gene:
- FGF4 NIH gene
- Name:
- fibroblast growth factor 4
- Previous symbol:
- HSTF1
- Synonyms:
- K-FGF, HBGF-4, HST, HST-1, KFGF
- Chromosome:
- 11q13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1988-04-20
- Date modifiied:
- 2014-11-19
Related products to: FGF4 protein
Related articles to: FGF4 protein
- - Source: PubMed
Publication date: 2026/04/20
Wu QiaoyunChen YueweiYao XintongRen SiqiangXie HanLi SisiYing XinwangWang Xueqiang - Do certain killer-cell immunoglobulin-like receptor (KIR) polymorphisms of uterine natural killer (uNK) cells contribute to early pregnancy losses, and if so, how? - Source: PubMed
Publication date: 2026/04/13
Cuadrado-Torroglosa IsabelPalomar AndreaQuiñonero AliciaGarcia-Velasco Juan AAlecsandru DianaDomínguez Francisco - Anaplastic lymphoma kinase () rearrangement has been identified in approximately 1% of lung squamous cell carcinomas (LUSCCs). Due to its rarity, the efficacy of anaplastic lymphoma kinase-tyrosine kinase inhibitors in the treatment of -positive LUSCCs is poorly characterized. - Source: PubMed
Publication date: 2026/03/24
Li ShengshuDu XiaosongZhang XinxinMa HaixiaYang YanliLi YuanWei QinChen YanLi HongweiBu PengLiu DujuanHan SongyanChen Deyi - X-chromosome inactivation (XCI) balances gene expression between sexes in mammals and is essential to female development. XCI initiation strictly relies on the upregulation of long noncoding RNA Xist upon differentiation. Despite the co-occurrence and tight correlation between XCI and differentiation, master coordinators to synchronize XCI and differentiation remain ill-defined. Here, we report that FGF4, an autocrine differentiation-prompting stimulus, is essential for Xist upregulation and XCI initiation in mouse embryonic stem cells (ESCs). Either Fgf4 deficiency or FGFR blocking results in failure of Xist upregulation and XCI initiation. Mechanistically, FGF4 initiates XCI in a MEK/ERK-dependent manner, via two parallel but opposing pathways: i)FGF4 phosphorylates and activates YY1, a robust transcription activator of Xist, and ii) FGF4 facilitates decline of pluripotency factors Prdm14, Nanog and Rex1, resolving Xist repression. Together, we show how FGF4 comprehensively orchestrates XCI and ESC differentiation, and ensures XCI initiation by coordinating two opposing regulators that directly influence Xist transcription. The FGF-ERK-YY1 axis also constitutes a missing link between ubiquitously expressed Yy1 and its functional activation responsible for Xist upregulation and XCI initiation. - Source: PubMed
Publication date: 2026/03/25
Ma LizhuFu WeiAn LeiYang QianyingHai RuiqiXi GuangyinWang YinjuanLiu JuanZhang ChaoFu YaoZhang ZhenniWang XiaodongTian Jianhui - Myelin debris accumulation after spinal cord injury (SCI) drives persistent neuroinflammation, lysosomal dysfunction, and lipid overload in macrophages, ultimately impairing tissue repair. Here, we identify fibroblast growth factor 4 (FGF4) as a previously unrecognized regulator of macrophage-mediated myelin debris clearance. Endogenous FGF4 transiently increased in the early phase of SCI but rapidly declined. Using in vitro models, we demonstrate that exogenous FGF4 markedly enhances myelin debris phagocytosis through activation of the FGFR1-PI3K/AKT signaling pathway, leading to upregulation of Clec10a, a C-type lectin receptor not previously linked to myelin debris processing. Silencing Clec10a significantly mitigated the phagocytic and neuroprotective benefits of FGF4, supporting Clec10a as an important mediator of this response. D-GalNAc competitive inhibition assays showed that Clec10a does not rely on the conserved carbohydrate-recognition domain to bind to myelin debris. FGF4 enhanced the maturation and degradative efficiency of the endolysosomal system, driving internalized myelin debris through Rab5 early endosomes, Rab7 late endosomes, and Lamp1 lysosomes, where CTSD-mediated proteolysis was restored. This correction of lysosomal dysfunction was accompanied by reduced lysosomal membrane permeabilization. In vivo administration of FGF4 enhanced myelin debris clearance and alleviated lipid accumulation at the injury site, accompanied by attenuation of NLRP3 inflammasome activity and a shift in macrophage phenotypes toward a reparative state. Together, our results identify FGF4 as a previously unrecognized regulator of macrophage phagosome maturation and lysosomal function after spinal cord injury, linking FGFR1–PI3K/AKT signaling to Clec10a-mediated intracellular processing of internalized myelin debris and inflammation resolution. - Source: PubMed
Publication date: 2026/02/23
Lu WenjieJiang MinghaoZhuang JunyuSong JiahuiZhou ChengZhou YangboZhu ZhongweiWu AiminSheng SunrenZhu SipinWang Zhouguang