Ask about this productRelated genes to: FGF16 antibody
- Gene:
- FGF16 NIH gene
- Name:
- fibroblast growth factor 16
- Previous symbol:
- MF4
- Synonyms:
- -
- Chromosome:
- Xq21.1
- Locus Type:
- gene with protein product
- Date approved:
- 1998-12-22
- Date modifiied:
- 2014-11-19
Related products to: FGF16 antibody
Related articles to: FGF16 antibody
- Tyrosine is known to influence melanin generation; however, its involvement in melanin production in chicken feathers is unknown. We evaluated the feather color of H-line chickens fed diets containing different concentrations of tyrosine (0, 0.4, 0.6, 0.8, and 1.0%). The results indicated that a diet containing 1.0% tyrosine fed for 40 days significantly increased melanin deposition in the feathers ( < 0.05). Following this observation, we collected feather follicle tissue from chickens fed either 0% or 1.0% tyrosine at the 40-day time point for transcriptome sequencing. RNA-seq analysis identified a total of 314 DEGs, comprising 116 upregulated and 198 downregulated genes. KEGG analysis of feather follicle tissue revealed that 7 DEGs (, and ) mapped to melanin-related pathways, including the melanogenesis, MAPK signaling and Wnt signaling pathways. We also identified specific protein interactions within the melanin pathway, including EDNRB2-MLPH and WNT3-FGF16 interactions. Notably, the expression level of the gene reached its peak at 10 weeks within the 0-12 week growth period in H-line chickens. In primary chicken melanocytes, expression was quantified following tyrosine supplementation and was found to be markedly elevated at a concentration of 10 mol/L, significantly higher than the control and other treatment groups ( < 0.05). Overall, our findings suggest the significant involvement of the tyrosine-induced regulatory network in melanin levels in sub-Columbian plumage. Taken together, these findings increase our understanding of the molecular mechanisms that regulate tyrosine-mediated melanin deposition in chicken plumage. - Source: PubMed
Publication date: 2025/11/28
Wang XinleiZhang LihengYang LiyuYang PengkunQiao YingyingHan ZhanbingFan JiayingLi QiangZhang DingdingLi ZhuanjianKang XiangtaoDu JuanLi Ruiting - This research aims to reveal the regulatory mechanism of miR-302a-3p in diabetic nephropathy (DN) and its role in inflammatory responses. - Source: PubMed
Publication date: 2025/10/16
Lv LingboZhang XinLuo Guoxia - Fibroblast growth factor (FGF) 16 is critically involved in embryonic heart development, adult cardiac homeostasis, and potentially in metabolic regulation. Initially recognized for its cardiac-specific role during embryogenesis, recent studies demonstrate that FGF16 significantly mitigates pathological cardiac remodelling, such as fibrosis and hypertrophy, through competitive inhibition of FGF2-induced transforming growth factor-β1 signalling via FGF receptor 1c. Molecular investigations further indicate that FGF16 exerts cardioprotective effects primarily through activation of key intracellular pathways, including phosphoinositide 3-kinase/protein kinase B and protein kinase C, as well as regulation by transcription factors GATA binding protein 4, nuclear Factor kappa-light-chain-enhancer of activated B cells, and cardiac-specific homeobox/NK2 homeobox 5, and RNA methyltransferase-mediated N6-methyladenosine modifications. However, detailed mechanisms underlying receptor-specific interactions remain unclear. This review systematically summarizes the genomic organization, receptor selectivity, cardiac signalling mechanisms, and emerging metabolic roles of FGF16, critically evaluates the current evidence, identifies key research gaps, and highlights therapeutic potentials for cardiovascular and metabolic disorders. - Source: PubMed
Publication date: 2025/07/13
Hui XiaodanLin QianLiu KaiqingGu ChunjieAbdelbaset-Ismail AhmedWintergerst Kupper ADeng ZhongbinCai LuTan Yi - Objective: The potential association between sepsis risk and circulating levels of fibroblast growth factors (FGFs) and their receptors (FGFRs) has been a focus of research; however, the causal relationship between them remains to be elucidated. We hypothesize a causal association between genetically predicted FGFs, FGFRs, and sepsis risk, and we conduct a Mendelian randomization (MR) study to validate this hypothesis. Methods: We utilized a two-sample MR design to assess the effect of genetic variants associated with various FGFs (FGF1, FGF2, FGF7, FGF16, FGF19, FGF21, FGF23, FGF5) and FGFRs (FGFR1, FGFR2, FGFR3, α-Klotho) on sepsis risk, using genome-wide association study summary statistics. Our MR analyses employed the inverse-variance weighted (IVW) method, along with weighted median, weighted mode, and MR-Egger regression, supplemented by sensitivity analyses to ensure robustness. Results: The MR analysis identified an unequal number of instrumental variables ranging from 2 to 17 for FGFs and FGFRs when sepsis was the outcome. No significant correlation was found between genetically determined FGF levels and sepsis risk by IVW analysis (all P > 0.05). Correspondingly, similar nonsignificant associations were observed for FGFRs (all P > 0.05). Other MR methods corroborated the IVW findings. Sensitivity analyses, including Cochran's Q test, MR-Egger, and MR pleiotropy residual sum and outlier, indicated no significant heterogeneity or pleiotropy in the relationships, with the exception of a nonsignificant correlation between FGFR1 and sepsis that persisted after the exclusion of an outlier (odds ratio, 0.84; P = 0.34). Conclusion: The analysis found no significant causal associations between FGFs, their receptors, and sepsis risk, indicating a need for further research on their complex interactions. - Source: PubMed
Publication date: 2025/03/03
Dai JunruXia BangboLiu NingShui Pengfei - Almost 90 % of head and neck malignancies are malignant squamous cell cancers, making it the sixth most common malignancy in the developing countries, with an overall five-year overall survival rate about 40 %-50 %. Early diagnosis and treatment can bring a better prognosis. Fibroblast growth factor (FGF) is an important polypeptide in vivo. Studies have found that FGF signal has carcinogenic potential and participates in a variety of carcinogenic behaviors. Some experiments have proved that FGF signal has the function of tumor inhibition in some cases, and the role of FGF signalling in tissue repair and homeostasis suggest a role for FGF in targeted therapy and prognosis. However, its manifestation and predictive role in HNSC have not been clearly defined. - Source: PubMed
Publication date: 2025/03/12
Zhang LiGao YingchunTian YumeiWei JianXu YingjiaoZhang XuanNie MinhaiLiu Xuqian