FGF16 antibody - N - terminal region (OAAB08105)
- Known as:
- FGF16 (anti-) - N - terminal region (OAAB08105)
- Catalog number:
- oaab08105
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- FGF16 antibody - terminal region (OAAB08105)
Related genes to: FGF16 antibody - N - terminal region (OAAB08105)
- 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 - N - terminal region (OAAB08105)
Related articles to: FGF16 antibody - N - terminal region (OAAB08105)
- Environmental toxicants (ENVOTOX) have emerged as critical risk factors for congenital malformations (CMFs) in the modern industrial era. Although epidemiological evidence underscores their adverse impact on pregnancy outcomes, the underlying molecular mechanisms remain insufficiently defined. This review consolidates current insights into exposome toxicity profiling, developmental pathway disruptions, and molecular mapping to identify potential biomarkers and mechanistic links between ENVOTOX and CMFs. Protein-protein interaction (PPI) network analysis identified 35 CMF-associated proteins, with ten fibroblast growth factors (FGFs: FGF4, FGF5, FGF8, FGF9, FGF10, FGF16, FGF17, FGF18, FGF20, and FGF22) prioritized as hub nodes. Molecular docking analysis showed high binding affinity of FGF9 and FGF4 toward dioxin-associated toxicants, with dibenzo-p-dioxin (DBPDO) exhibiting the strongest interaction (binding energy: -7.2 kcal/mol), followed by polychlorinated dibenzofurans (PCDBFs) (-6.7 kcal/mol) with FGF9. Notably, FGF9 exhibited mutagenic binding potential at ASN146, mediated through π-donor hydrogen bonding with DBPDO. Comparative toxicity data further highlighted the acute risks, as DBPDO demonstrated a lower LD (2.26 mol/kg) relative to PCDBFs (4.134 mol/kg). Collectively, this review emphasizes the central role of FGFs in mediating ENVOTOX-induced teratogenicity and offers molecular-level perspectives to guide biomarker discovery and intervention strategies for mitigating CMF risk. - Source: PubMed
Shukla Adarsh KumarMahajan RashmiTyagi Anuj KumarSwaroop Kamendra - N-methyladenosine (mA) RNA modification plays critical roles in physiological and pathological processes. Our prior study demonstrated that IGFBP5 expression is upregulated in the ischemic limb, whereas endothelial-specific IGFBP5 knockout (Igfbp5) protects against hind limb ischemia by enhancing angiogenesis. Here, we show that IGFBP5 deficiency elevates global mA levels and upregulates the expression of mA methyltransferase complex components METTL3, METTL14 and WTAP in endothelial cells. We further identified a direct interaction between IGFBP5 and the MT-A70 domain of METTL14. Knockdown of METTL14, METTL3 or WTAP attenuated the pro-angiogenic effects of IGFBP5 deficiency in vitro. In vivo, endothelial knockdown of METTL14 abolished the improved hind-limb ischemia recovery in Igfbp5 mice. Methylated RNA immunoprecipitation sequencing revealed that IGFBP5 depletion in endothelial cells increases both mA modification and mRNA abundance of FGF16. Notably, METTL14 or METTL3 silencing suppressed IGFBP5-dependent FGF16 upregulation. Enhanced translational efficiency of FGF16 in IGFBP5-deficient cells was reversed by METTL14 knockdown, indicating that IGFBP5 regulates FGF16 translation via mA modification. Mechanistically, IGFBP5 modulates FGF16 mA modification via interaction with the mA reader protein IGF2BP2, targeting the mA site at position 255 of FGF16 mRNA. In summary, our study establishes METTL14-mediated mA modification of FGF16 as a key mechanism underlying IGFBP5-driven angiogenesis. Targeting the IGFBP5-METTL14-mA-FGF16 axis may offer novel therapeutic strategies for ischemic disease. - Source: PubMed
Publication date: 2026/08/04
Song FeiHu YuHong Yi-XiangZhao Shan-ShanHuang Hui-ZhuWang YutianZhang LeWu Wei-YinWang YanLi Gang - 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
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