FGF16 siRNA_Lentivectors
- Known as:
- FGF16 siRNA_Lentivectors
- Catalog number:
- i007899b
- Product Quantity:
- 500ng
- Category:
- -
- Supplier:
- ABM
- Gene target:
- FGF16 siRNA_Lentivectors
Related genes to: FGF16 siRNA_Lentivectors
- 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 siRNA_Lentivectors
Related articles to: FGF16 siRNA_Lentivectors
- The fat mass and obesity-associated gene () has been shown to play a critical role in fat deposition in both humans and livestock. However, its involvement in subcutaneous and intramuscular fat deposition in chickens remains underexplored. In this study, we investigated the regulatory effects and pathways of on subcutaneous and intramuscular fat deposition in chickens through functional gene verification and bioinformatics analysis. Our results demonstrated that, compared to the control group, exogenous transfection of an lentiviral overexpression vector significantly inhibited cell proliferation and increased lipid accumulation in both subcutaneous and intramuscular adipocytes ( < 0.05). Furthermore, transfection of siRNA markedly increased cell proliferation and reduced lipid accumulation in both subcutaneous and intramuscular adipocytes. A total of 413 and 164 differentially expressed genes were regulated by in subcutaneous and intramuscular adipocytes, respectively. Pathway analysis revealed that the regulation of the actin cytoskeleton was a key process involved in -mediated fat deposition in both subcutaneous and intramuscular adipocytes. Additionally, and (subcutaneous fat), as well as , , , and (intramuscular fat), were identified as key genes enriched in this pathway. In conclusion, differentially regulates fat deposition in chicken subcutaneous and intramuscular adipocytes by targeting distinct functional genes within the actin cytoskeleton pathway. - Source: PubMed
Publication date: 2026/05/14
Huang Hua-YunKong YiLi Chun-MiaoSui Yu-LeWang Qian-BaoZhao Zhen-HuaKong Ling-LinWu Zhao-LinHan Wei - 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