Ask about this productRelated genes to: FGF17 protein
- Gene:
- FGF17 NIH gene
- Name:
- fibroblast growth factor 17
- Previous symbol:
- -
- Synonyms:
- FGF-13
- Chromosome:
- 8p21.3
- Locus Type:
- gene with protein product
- Date approved:
- 1998-12-22
- Date modifiied:
- 2014-11-19
Related products to: FGF17 protein
Related articles to: FGF17 protein
- To assess the susceptibility to seizures, expression of fibroblast growth factor 17 (Fgf17) in rats with Cortical dysplasia (CD), and its effect on hippocampal neurons. - Source: PubMed
Liu TiantianLiu HengfangJia Yanjie - Fibroblast growth factor 17 (FGF17) is implicated in neurodevelopment and synaptic function, yet its role in motivation remains unclear. This study compared serum FGF17 levels (measured using ELISA) between 74 patients with major depressive disorder (MDD) and 72 healthy controls (HCs), and examined its relationship with negative symptoms measured by the Motivation and Pleasure (MAP) and Expression (EXP) subscales of the Clinical Assessment Interview for Negative Symptoms (CAINS). Compared to HCs, patients with MDD exhibited lower FGF17 levels. Within the MDD group, serum FGF17 showed small to modest negative correlations with the ratings of the MAP and EXP scores. Moreover, multiple linear regression showed that FGF17 was a potential predictor of these scores after FDR correction. These preliminary findings suggest that reduced peripheral FGF17 levels are associated with motivational deficits in patients with MDD, warranting further investigation into its role in the neurobiology of "negative-like" symptoms in this clinical group. - Source: PubMed
Publication date: 2026/04/07
Zhu ZhenhuaYin XuyuanHuang JiaWang YiQi QiWang PeijieLui Simon S YHui LiChan Raymond C K - Polycystic ovary syndrome (PCOS), one of the most common endocrine and reproductive disorders in women of reproductive age, is frequently complicated by insulin resistance (IR), which affects 50%–80% of PCOS patients and is strongly associated with an increased risk of early pregnancy loss. Evidence suggests that IR may contribute to this risk by impairing endometrial function, a notion supported by observed functional improvements following metformin treatment. While previous studies have provided clues regarding PCOS with IR (PCOS-IR) at the ovarian miRNA and endometrial protein levels, the understanding of the upstream transcriptomic events regulating these pathways remains limited. We performed RNA-Seq on endometrial tissues from PCOS-IR and PCOS without IR (PCOS-NIR), thereby identifying 339 common differentially expressed genes (DEGs) using DESeq2 and Limma. Functional enrichment analysis revealed that DESeq2-identified genes primarily participated in cellular signaling, metabolic regulation, and immune-related pathways. Further weighted gene co-expression network analysis (WGCNA) identified gene modules highly correlated with the PCOS-IR phenotype. Integrating multi-step strategies, including random forest analysis and STRING interaction networks, ultimately identified FGF17, AKT3, and IRS4 as key candidate genes. Quantitative real-time PCR (qRT-PCR) confirmed that FGF17 mRNA expression was significantly downregulated in the endometrium of the PCOS-IR group. This finding suggests that FGF17 may play a pivotal role in PCOS-IR-related endometrial dysfunction, with promise as a therapeutic target to improve reproductive outcomes in patients. These results provide important theoretical support for subsequent mechanistic exploration and clinical intervention. - Source: PubMed
Publication date: 2026/03/16
Wang YingyingZhang HongqingHui YijieZhang YajuanShan Hongying - The reprogramming of glutamine metabolism holds a pivotal position in the energy provision and biosynthesis of tumors. However, the regulatory mechanism of this phenomenon in non-small cell lung cancer (NSCLC) is still not well-understood. NSCLC is a type of malignancy that has a high incidence and mortality rate globally. There is an urgent need to elucidate the role of glutamine metabolism in its pathological mechanism. This clarification may provide theoretical guidance for developing new therapeutic approaches. - Source: PubMed
Publication date: 2026/01/02
Kong QinghuaWang XiaoyanDing Wei - The role of FGF is the least understood of the morphogens driving mammalian gastrulation. Here, we have investigated FGF function in a 2D gastruloid model for human gastrulation. We observed a ring of FGF-dependent ERK activity that closely follows the emergence of primitive streak (PS)-like cells but expands further inward. This ERK activity pattern depends on localized activation of basolateral FGF receptor 1 (FGFR1) by endogenous FGF gradients and is required for PS-like differentiation, with loss of PS-like cells upon FGF receptor inhibition rescued by direct ERK activation. Single cell transcriptome analysis confirmed that, among the ligands, FGF2 is broadly expressed, FGF8 is transiently expressed during PS-like differentiation and FGF4/17 are specifically expressed in PS-like cells - similar to the human and monkey embryo but different from the mouse. FGF4 knockdown greatly reduced PS-like differentiation, while FGF17 knockdown primarily affected subsequent mesoderm differentiation. FGF8 expression was spatially and temporally displaced from PS markers and FGF4 expression, while knockdown expanded PS-like cells, suggesting FGF8 may limit PS-like differentiation. Thus, we have identified a previously unreported role for FGF-dependent ERK signaling in 2D gastruloids and possibly the human embryo, where FGF4 and FGF17 signal through basolateral FGFR1 to induce PS-like cells and derivatives, potentially restricted by FGF8. - Source: PubMed
Publication date: 2026/02/09
Jo KyoungLiu Zong-YuanPatel GauriYu ZhiyuanYao LiAngTeague SethJohnson CraigSpence JasonHeemskerk Idse