FGF19 siRNA_Lentivectors
- Known as:
- FGF19 siRNA_Lentivectors
- Catalog number:
- i007902d
- Product Quantity:
- 500ng
- Category:
- -
- Supplier:
- ABM
- Gene target:
- FGF19 siRNA_Lentivectors
Related genes to: FGF19 siRNA_Lentivectors
- Gene:
- FGF19 NIH gene
- Name:
- fibroblast growth factor 19
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 11q13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1999-05-06
- Date modifiied:
- 2016-10-05
Related products to: FGF19 siRNA_Lentivectors
Related articles to: FGF19 siRNA_Lentivectors
- The pregnane X receptor (Pxr; Nr1i2) plays a role in metabolic regulation. However, its contribution to systemic energy homeostasis under physiological conditions remains unclear. Here, we investigated the metabolic consequences of Nr1i2 deficiency in chow-fed mice. - Source: PubMed
Publication date: 2026/09/19
Benoit BérengèreJalabert AudreyMeugnier EmmanuelleChanon StéphanieVieille-Marchiset AurélieBeau AlicePesenti SandraLoizon EmmanuelleVitalis OrianeBendridi NadiaNawrot MargauxMakki KassemLe Magueresse-Battistoni BrigitteRieusset JenniferMichalski Marie-CarolineRainteau DominiqueChikh KarimVidal HubertRuzzin Jérôme - Oral cavity squamous cell carcinoma (OCSCC) is a common epithelial malignancy for which site-specific biomarkers with proven prognostic utility remain limited. In this study, we present one of the largest single-center, site-specific molecular analyses of OCSCC to date. Using two separate versions of multigene next-generation sequencing (NGS), we sought to identify a focused set of clinically actionable and widely accessible biomarkers that could support diagnosis, prognostication, and therapeutic decision-making. Our findings highlight the potential of a limited molecular panel to capture key prognostic information, supporting a more accessible and scalable approach to precision oncology in OCSCC. - Source: PubMed
Publication date: 2026/09/18
Afkhami MichelleHaghighi NMa HReyes AFei FDyer TTelatar MArias-Romero JHaghighi YMehrazma AMassarelli EBakkar RTizro PBell DVillaflor V M - Hepatocellular carcinoma (HCC) is the predominant histological subtype of primary liver cancer and remains a leading cause of cancer-related mortality because of its molecular heterogeneity, high recurrence rate, and incomplete responses to systemic therapy. Among dysregulated oncogenic networks, fibroblast growth factor/fibroblast growth factor receptor (FGF/FGFR) signaling contributes to hepatocarcinogenesis, angiogenesis, stromal remodeling, immune escape, and therapeutic resistance. This review critically examines the biological organization and translational implications of FGF/FGFR signaling in HCC, with particular emphasis on the FGF19-KLB-FGFR4 axis and a cautious appraisal of its current translational maturity. FGF2, the FGF8 subfamily, FGF9, and FGF19 drive context-dependent tumor programs shaped by etiology, cirrhosis, stromal interactions, intratumoral heterogeneity, and crosstalk with major oncogenic pathways. Although FGF19-KLB-FGFR4 is the most mature and clinically testable FGF-related therapeutic framework in HCC, selective FGFR4 inhibition is still limited by early-phase clinical evidence, bile-acid-related toxicity, FGFR3/KLB-mediated redundancy, bypass signaling, and acquired resistance. Early clinical data with irpagratinib support the rationale for combining FGFR4 inhibition with immune checkpoint blockade, but definitive validation and reproducible biomarker assays are still needed. Future translation should prioritize prospectively validated biomarker panels, mechanism-based combinations, longitudinal resistance monitoring, and models that recapitulate the cirrhotic, immune-active liver microenvironment. - Source: PubMed
Publication date: 2026/09/17
Jin QiangliLiu YangJin Penghui - This study investigated the effects of graded dietary barley replacement for corn on growth performance, rumen fermentation, carcass traits, meat quality, fatty acid profiles, and the rumen microbiome in Arbas White Cashmere goats, and further applied untargeted muscle metabolomics to elucidate the metabolic mechanisms underlying meat quality alterations. Growth performance was monitored for all goats (n = 10 per group); rumen fermentation, carcass traits, serum biochemistry and meat quality were determined in six randomly selected goats per group (n = 6); and rumen microbiota profiling and muscle metabolomics were performed on three selected goats per group (n = 3). Partial barley substitution (33% and 67% of starch from barley) significantly improved final body weight and average daily gain ( < 0.05), whereas total replacement (100% barley starch) did not confer additional growth advantages. Moderate barley inclusion increased ruminal propionate concentration ( = 0.001) and enriched the fiber-degrading bacterium Prevotella, while total barley replacement markedly reduced rumen microbial diversity (Sobs, Chao1, ACE, and Shannon indices; < 0.01) and depleted multiple fibrolytic and hydrogenotrophic genera, including , , and . The 33% barley group exhibited elevated serum total bile acids, FGF-19, and CYP27A1 levels ( < 0.05), suggestive of modulated bile acid metabolism, along with decreased glucose-6-phosphatase ( < 0.05), pointing to suppressed hepatic gluconeogenesis. Muscle metabolomics revealed that moderate barley substitution predominantly affected glycerophospholipid metabolism, with upregulation of PE(P-18:1/20:4) and PC(16:0/16:0), whereas total replacement induced extensive metabolic reprogramming characterized by downregulation of glycine and glutathione-related metabolites, indicative of compromised antioxidant defense. The 33% barley group also exhibited the highest muscular C18:3n-3 content ( < 0.01), while the 67% and total replacement groups showed increased C22:6n-3 deposition ( < 0.05). Correlation analysis confirmed that PE(P-18:1/20:4) and PC(16:0/16:0) were significantly positively correlated with ruminal propionate and ADG (r = 0.841-0.986; < 0.05), and Prevotella abundance showed a strong negative trend with G-6-Pase (r = -0.771). Collectively, these findings demonstrate that replacing one-third of dietary corn starch with barley starch optimally balances productivity, rumen health, and meat quality through enrichment of Prevotella, enhanced propionate production, and modulation of bile acid metabolism, while excessive barley inclusion destabilizes the rumen ecosystem and triggers muscle oxidative stress, providing a theoretical basis for precision grain formulation in intensive cashmere goat production. - Source: PubMed
Publication date: 2026/09/06
Jin LuZhang ChunhuaLi ShengliSa ChulaNuo MinYang DingLi WentingFu LeChen PanliangZhao YaxingWang BoSun Haizhou - Pancreatic ductal adenocarcinoma (PDAC) is characterized by extensive adaptive signaling plasticity and metabolic reprogramming that contribute to therapeutic resistance. While the PI3K-mTOR pathway is a central regulator of these processes, the role of the FGF19-FGFR4 axis and its interaction with PI3K-mTOR signaling remains incompletely defined in PDAC. This study investigated whether co-targeting FGFR4 and PI3K-mTOR signaling could overcome adaptive pathway reactivation and suppress tumor-promoting phenotypes. PDAC cell lines representing a spectrum of FGFR4 dependence were treated with the selective FGFR4 inhibitor fisogatinib in combination with the clinically relevant PI3K-mTOR inhibitor gedatolisib. Transcriptomic analyses of TCGA data, along with molecular and functional responses, were evaluated. Transcriptomic analysis demonstrated a positive association between FGFR4 and PI3K-mTOR signaling and linked combined pathway components with poorer overall survival. Across heterogeneous PDAC models, combined inhibition reduced viability, clonogenic survival, migration, and cell-cycle progression more consistently than monotherapy. Apoptosis induction was driven principally by fisogatinib and combination treatment, resulting in comparable apoptotic responses across cell lines. Mechanistically, combined inhibition converged on increased 4E-BP1 inhibitory activity, despite compensatory ERK-RSK pathway activation, indicating that adaptive MAPK was insufficient to restore downstream translational output. In FGFR4-dependent cells, the combined inhibition also reduced secretion of the FGFR4 ligand FGF19. The FGFR4 and PI3K-mTOR signaling comprises a partially interconnected network in PDAC that converges on 4E-BP1-dependent translational control. Dual pathway inhibition consistently and additively suppressed tumor-associated phenotypes despite compensatory MAPK activation, with the clearest added benefit over fisogatinib alone in migration, cell-cycle control, and 4E-BP1 modulation, supporting translational regulation as a shared therapeutic vulnerability. These findings provide a preliminary rationale for biomarker-guided strategies targeting FGFR4 and PI3K-mTOR signaling in pancreatic cancer. - Source: PubMed
Publication date: 2026/08/28
Goode Joseph AHarris Savannah AAltomare Deborah A