Ask about this productRelated genes to: FGFR4 antibody
- Gene:
- FGFR4 NIH gene
- Name:
- fibroblast growth factor receptor 4
- Previous symbol:
- -
- Synonyms:
- JTK2, CD334
- Chromosome:
- 5q35.2
- Locus Type:
- gene with protein product
- Date approved:
- 1991-07-25
- Date modifiied:
- 2015-08-25
Related products to: FGFR4 antibody
Related articles to: FGFR4 antibody
- While epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) are a cornerstone of therapy for advanced -mutant non-small cell lung cancer (NSCLC), resistance remains a major clinical challenge. The genomic landscape of early-stage (ES) -mutant NSCLC and its evolution to advanced-stage (AS) disease is not fully understood. This study aimed to characterize the molecular disparities between ES and AS -mutant NSCLC and to identify genomic alterations associated with EGFR-TKI treatment outcomes. - Source: PubMed
Publication date: 2026/02/26
Yoon DayoungLee Ji WonCho Byoung ChulKang Eun JooKim Jung SunLim TaekyuYi Seong YoonKim Yu JungAhn Mi SunKim Young SaingPark Ji HyunLim SeungtaekPark Hyung SoonCho Jang HoJang ByunghyunLee Ji YoonKim JiwonHong JisooKoo HarimChung SeokShin Sang WonKim Yeul HongSa Jason KChoi Yoon Ji - Heart failure (HF) is the leading cause of morbidity and mortality worldwide, while myocardial fibrosis acts as a pivotal hallmark, which exacerbates ventricular dysfunction and remodeling in HF. In this study, we found FGF23, a critical endocrine regulator, which regulates phosphate and vitamin D metabolism, was significantly upregulated in fibrotic mouse hearts after transverse aortic constriction (TAC). By using the FGF23 monoclonal antibody, we found that inhibition of FGF23 alleviated TAC-induced cardiac fibrosis, while injection of recombinant FGF23 (rFGF23) protein exacerbated tissue fibrosis in mouse hearts after TAC. RNA sequencing indicated that FGF23 may promote cardiac fibroblast proliferation and activation in stressed mouse hearts. In human primary cardiac fibroblasts, rFGF23 treatment further upregulated the expression of Ki67, Cyclin D1, Cyclin E1, PCNA, α-SMA, and collagen 1A1 after TGF-β stimulation. Further results indicated that FGF23 promoted cardiac fibroblast proliferation and activation through FGFR4 and activated the downstream MAPK/ERK signaling. This study suggests a role of FGF23 in the regulation of myocardial fibrosis, which shows the potential of targeting FGF23 in the treatment of HF and cardiac fibrosis. - Source: PubMed
Publication date: 2026/03/27
Shen LeyiHu MingqiXue MeiLi Santie - Fibroblast growth factor (FGF)-fibroblast growth factor receptor (FGFR) signaling constitutes a fundamental regulatory network governing epithelial turnover, metabolic homeostasis, and immune modulation across the gastrointestinal tract. Although discrete FGF pathways have been intensively investigated in inflammatory bowel disease, hepatobiliary disorders, and gastrointestinal malignancies, how these signaling programs are coordinated across pathological contexts remains insufficiently resolved. In this review, we integrate evidence from human cohorts, experimental systems, and clinical studies to conceptualize the FGF-FGFR axis as a context-dependent metabolic-barrier-immune rheostat. Paracrine activation of epithelial FGFR2b supports mucosal restitution and barrier re-establishment following injury, whereas endocrine FGFs-including FGF19, FGF21, and FGF23-couple bile acid signaling, systemic metabolic stress, and mineral balance to intestinal and hepatic inflammatory responses. Perturbation of these adaptive signaling circuits contributes to persistent inflammation and is frequently co-opted by oncogenic events, such as FGFR2b amplification, FGFR2 gene fusions, and aberrant FGF19-FGFR4 activation, during gastrointestinal tumorigenesis. Framing the FGF-FGFR network as an integrated rheostat offers a unifying mechanistic paradigm that links epithelial damage, metabolic dysregulation, and cancer development. It underscores the need for context-selective therapeutic interventions that reconcile tissue repair with long-term oncogenic risk. - Source: PubMed
Publication date: 2026/03/26
Saad Khamis Salem SaeedZhou ChunfangLu GuangxinWei GangCha HuolongAlwabri EzzaddinZhang ZhifangSun ZequnLiao Yingying - This study characterizes the expression of fibroblast growth factors (FGFs) and their receptors in the porcine corpus luteum (CL) across distinct stages of the oestrous cycle, and evaluates the regulatory role of FGF2 on angiogenesis, steroidogenesis, and cell survival in vitro. The CL was classified morphologically into four phases: Phase I (days 1-8; corpus haemorrhagicum; ELP), Phase II (days 9-14; highly vascularized CL; MLP), Phase III (day 15 onward; ischemic regression; LLP), and Phase IV (corpus albicans; avascular and regressed; RR). Each phase included 10 biological replicates (n = 10). Quantitative RT-PCR revealed significant upregulation (p < 0.001) of FGF1, FGF2, FGF7, FGFR1, FGFR2, and FGFR4 during early and mid-luteal stages. FGFR3 and FGFR2IIIC showed no significant variation, while FGFR2IIIB was downregulated (p < 0.001) during early/mid-luteal stages and upregulated during luteal regression. FGF10 expression declined significantly (p < 0.001) during regression. Western blotting Densitometry confirmed trends mRNA expression. In-vitro supplementation of FGF2 (1, 10, and 100 ng/ml) during the mid-luteal stage enhanced mRNA expression of angiogenic (vWF), steroidogenic (StAR, CYP11A1, 3β-HSD), and cell survival (PCNA, BAX) markers. StAR, CYP11A1, and 3β-HSD were significantly upregulated (p < 0.001) from 24 to 72 h in a dose-dependent manner. vWF and PCNA showed significant increases at 48 and 72 h, while BAX expression progressively declined (p > 0.001). The 100 ng/ml dose elicited the most pronounced effects. These findings suggest that FGF family members exert autocrine/paracrine effects that support luteal cell proliferation, differentiation, angiogenesis, steroidogenesis, and survival, underscoring their critical role in porcine ovarian physiology. - Source: PubMed
Publication date: 2026/04/09
Nanda RishiChouhan V SYadav PoonamSamad H ABorah SanjibSoren SimsonDutta DevojyotiMaurya V PSingh Gyanendra - Genetic alterations in FGFR2 drive multiple malignancies, most notably intrahepatic cholangiocarcinoma, where they occur in ∼10-15% of patients. While approved pan-FGFR inhibitors provide clinical benefit, their durability is limited by acquired, often polyclonal, on-target resistance mutations affecting key regions of the FGFR2 kinase domain, including the gatekeeper residue (V565), molecular brake residues (N550, E566, K642), and other key variants. These liabilities motivate the development of next-generation inhibitors. Given FGFR2-associated toxicities and the need for subtype selectivity, FGFR4 inhibition was prioritized as a selectivity determinant, while sparing FGFR1 was considered less critical. Guided by structure-based drug design, a reversible aminopyrimidine screening hit was optimized into a novel covalent inhibitor series active against FGFR2 wild-type and clinically relevant resistance mutations. An advanced lead showed favorable potency, ADME properties, and demonstrated proof-of-concept efficacy in an FGFR2-amplified xenograft model comparable with the standard of care. - Source: PubMed
Publication date: 2026/03/30
Hudkins Robert LAllen EricIyer SamhitaBalcer AlexandraNeal MelissaYe QingRideout MarcFrye Caleb BNelson Kirk JHoffman Isaac DStarrett Jacqueline HHarris ToddSwanson Ronald VBensen Daniel C