Human FGFR4 _CD334 Protein Vector: HEK293
- Known as:
- Human FGFR4 _CD334 Protein Vector: HEK293
- Catalog number:
- 10109-H01H
- Product Quantity:
- 200μg
- Category:
- -
- Supplier:
- Provo
- Gene target:
- Human FGFR4 _CD334 Protein Vector: HEK293
Related genes to: Human FGFR4 _CD334 Protein Vector: HEK293
- 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: Human FGFR4 _CD334 Protein Vector: HEK293
Related articles to: Human FGFR4 _CD334 Protein Vector: HEK293
- To integrate global clinical trial data and multi-omics evidence in metabolic dysfunction-associated steatotic liver disease (MASLD) and evaluate therapeutic strategies, target distribution, tissue-specific safety profiles, and expression patterns across disease stages. - Source: PubMed
Publication date: 2026/08/26
Mu YanxiZhu WeixiongWei ZhihaoGuo ZhaoChen HaofeiCheng YushengZhou Wence - Fibroblast growth factor 19 (FGF19) signaling is a promising therapeutic target for metabolic diseases and cancers, and several agents targeting the FGF19 signaling are currently undergoing clinical trials. However, as an endocrine FGF, FGF19's organism-wide functions remain vague, which hinders the advancing of FGF19 signaling-based therapies. To systematically explore its systemic effects, we performed a multi-tissue transcriptomic profiling in a FGF19 knock-in mouse model. Sustained FGF19 exposure induced extensive, tissue‑specific transcriptional reprogramming. For instance, lipid metabolic pathways were broadly altered not only in canonical metabolic organs but also in immune‑related tissues including the spleen and thymus. Furthermore, integrated analysis and functional validation demonstrated that FGF19 promoted monocyte/macrophage (Mo/MΦ) migration in an FGFR4‑involved manner, associated with an M2-like polarization state. Moreover, we developed a macrophage‑targeted sustained‑release FGF19 delivery system, which significantly accelerated wound healing and enhanced M2 macrophage infiltration in a murine full‑thickness skin injury model. Overall, our study establishes a multi‑tissue transcriptional atlas of FGF19 action, reveals broad metabolic and immune regulatory responses to sustained human FGF19 exposure in mice, and provides a targeted therapeutic strategy for modulating macrophage. - Source: PubMed
Publication date: 2026/08/22
Xiao YangKuang LiwenHe JuanLiu XudongYi YiSong MiaoyuXia JieZhou YuLei JuanChen YuLiu XiChen JiongmingChen YijiaoZeng XianghuaLi YongshengZhao Huakan - The fibroblast growth factor receptor (FGFR) pathway is frequently dysregulated in cancer and contributes to tumor progression and immune evasion; however, the underlying immunosuppressive mechanisms remain incompletely understood. Here, we identify FGFR4 as a key FGFR family member that suppresses antitumor immunity. Mechanistically, FGFR4 promotes GRB2-dependent phosphorylation and inactivation of the deubiquitinase CYLD, leading to ubiquitin-proteasome-mediated degradation of STING and FDX1. Loss of STING attenuates type I interferon signaling and impairs cytotoxic immune responses, while destabilization of FDX1 diminishes sensitivity to cuproptosis. Inhibition of FGFR4 restores CYLD activity, stabilizes STING and FDX1, and enhances responsiveness to the STING agonist diABZI. Notably, CYLD-dependent stabilization of FDX1 potentiates elesclomol-induced cuproptosis, triggering mitochondrial stress and cytosolic mtDNA release, thereby activating the cGAS-STING pathway and amplifying STING-dependent immune signaling. Combination therapy with lenvatinib and elesclomol synergistically suppressed tumor growth in immunocompetent mouse models. Across patient cohorts, FGFR4-high/STING-low tumors were associated with inferior responses to anti-PD-1-based therapy. Together, these findings establish FGFR4 as a central regulator of antitumor immunity and cuproptosis and highlight combined FGFR4 inhibition and cuproptosis induction as a promising therapeutic strategy. - Source: PubMed
Publication date: 2026/08/19
Zhong HongguangHuang RuixuanDeng WenyuanRuan RuiwenDai XiaofengHuang ChunyeZeng QinruWu ZhipengWen QinLiao QuanLi LiXiong JianpingLei WanYao YangyangDeng Jun - Aberrant activation of fibroblast growth factor receptors (FGFRs) due to gene rearrangements or fusions, single-nucleotide variants, and copy number amplifications has been linked to several human cancers. Therefore, FGFRs increasingly recognized as a significant cancer therapy target. We herein designed and synthesized a series of quinoline derivatives as new type II covalent pan-FGFRs inhibitors based on our previous pan-FGFRs I-5. Of which, 18 exhibited a significant improvement in prominent pan-tumor inhibitory activities when substantially inhibited the kinase activities of FGFRs (FGFR1: IC = 5.70 nM, FGFR2: IC = 2.37 nM, FGFR3: IC = 3.78 nM, FGFR4: IC = 7.67 nM). Additionally, 18 blocked cellular FGFR phosphorylation and exhibited highly potent anti-tumor efficacy in vitro. Moreover, in vivo pharmacokinetic profiles and the safety property of 18 were found to be excellent (F % = 41.70%). Nevertheless, Oral administration of 18 significantly suppressed the tumor growth of the HuH-7 (TGI = 92.71%; 60 mg/kg, QD), SNU-16 (TGI = 49.80%; 30 mg/kg, QD) and RT112 (TGI = 67.61%; 30 mg/kg, QD) xenograft mouse models without obvious changes in body weight. - Source: PubMed
Publication date: 2026/08/16
Hu ShiheJiang CuihuaZhang XiaoyangChen KeLi XinJin Qiaomei - Aggressive thyroid cancer remains difficult to treat, partly because molecular programs linking malignant behavior to cancer-associated fibroblast (CAF)-related support are incompletely defined. This study investigated whether ATF4 and FGFR4 cooperate in thyroid cancer cells and whether this relationship persists in a CAF-associated context. - Source: PubMed
Publication date: 2026/08/15
Zhang JinsongCai JiehaoRuan Weihong