Ask about this productRelated genes to: FGFR1 antibody
- Gene:
- FGFR1 NIH gene
- Name:
- fibroblast growth factor receptor 1
- Previous symbol:
- FLT2, KAL2
- Synonyms:
- H2, H3, H4, H5, CEK, FLG, BFGFR, N-SAM, CD331
- Chromosome:
- 8p11.23
- Locus Type:
- gene with protein product
- Date approved:
- 1992-02-25
- Date modifiied:
- 2019-04-23
Related products to: FGFR1 antibody
Related articles to: FGFR1 antibody
- Mitochondrial dysfunction and defective repair are central drivers of secondary injury following spinal cord injury (SCI), yet effective strategies to restore mitochondrial quality control remain limited. Here, we develop an engineered long-acting fibroblast growth factor 21 fusion protein (SFGF21) by incorporating a linker peptide to enhance molecular targeting and oxidative stability. In a mouse model of SCI, sustained delivery of SFGF21 specifically potentiated dynamic crosstalk between mitochondria and lysosomes, thereby activating the BNIP3/BNIP3L pathway-mediated mitophagic flux and clearing dysfunctional mitochondria in injured neurons. This process restored mitochondrial homeostasis, suppressed lipid peroxidation, and alleviated oxidative stress in injured neurons. Loss-of-function experiments confirmed that both FGFR1 and BNIP3 are required for SFGF21-induced mitophagy and neuroprotection. Together, our findings establish engineered modulation of organelle crosstalk as a therapeutic strategy to activate mitophagy and support neural repair after SCI, highlighting mitochondria-targeted protein engineering as a potential therapeutic path for spinal cord repair. - Source: PubMed
Publication date: 2026/09/11
Chen XuehaiYing YiboZhang YuchaoLv JialiJiang MinghaoMo YujunWu ZhiyiLin HuixinHuang ZhiyangJiang DaweiZuo YanmingLi XiaokunWang Zhouguang - Fibroblast growth factor receptors 1 and 4 (FGFR1/4) regulate diverse cellular processes, including proliferation, differentiation, and metabolic homeostasis. Although ligand-dependent FGFR signaling has been extensively characterized, the signaling properties of these receptors in their ligand-independent state remain poorly understood. Here, we investigated the intrinsic signaling outputs of FGFR1 and FGFR4 in the absence of ligands using quantitative immunoblotting and electrophysiological analyses. Overexpression of FGFR1 or FGFR4 alone robustly increased the phosphorylation of phospholipase Cγ (PLCγ) and extracellular signal-regulated kinase 1/2 (ERK1/2), whereas activation of the PI3K-Akt pathway was minimal. Strikingly, co-expression of the co-receptor βKlotho acted as a molecular switch, selectively suppressing FGFR-driven PLCγ phosphorylation while preserving ERK1/2 signaling. Functionally, this βKlotho-dependent attenuation of PLCγ signaling markedly reduced the sustained TRPC6-mediated currents observed in βKlotho-deficient cells, linking constitutive FGFR-PLCγ coupling to aberrant Ca influx. Together, our findings identify βKlotho as a specialized signaling filter that safeguards FGFR signaling fidelity by uncoupling deleterious PLCγ-TRPC6 signaling while maintaining canonical MAPK output. These results reveal a previously unrecognized ligand-independent role of βKlotho in reconfiguring the FGFR signaling architecture. - Source: PubMed
Publication date: 2026/10/02
Dang Bao T NNguyen Phan AnhLee SuboJeong HyungminCha Seung-Kuy - Titanium (Ti) is widely used in oral implants but is limited by insufficient osteogenic activity, angiogenic capacity, and antibacterial performance. To address this, pure Ti was modified by micro-arc oxidation (MAO) to form a porous layer, followed by magnetron sputtering of a TaCu nanocoating under different conditions to prepare three composite samples (MAO-Ti/TaCu1, MAO-Ti/TaCu4, and MAO-Ti/TaCu7). The samples were characterized for surface properties and Cu release, and their biological performance was evaluated experiments. Results showed that MAO-Ti/TaCu coatings maintained the MAO porous structure and achieved cytocompatible, sustained Cu release. MAO-Ti/TaCu4 exhibited optimal osteogenic activity, with the highest cell viability, ALP activity, matrix mineralization, and expression of osteogenic-related genes (ALP, Runx2, Col-I, and OPN). MAO-Ti/TaCu7 showed the strongest angiogenic capacity, reflected by superior HUVEC morphology, migration, and angiogenic-related gene (eNOS, VEGF, and FGFR1) expression. All TaCu-modified groups had significant antibacterial activity. The enhanced performance was attributed to the synergistic effect of the porous MAO layer and TaCu nanocoating, with moderate Cu release favoring osteogenesis and higher release promoting angiogenesis. This study provides a new strategy for titanium implant surface modification to improve osseointegration. - Source: PubMed
Publication date: 2026/10/01
Yao LitaoTong YuanhaoLin XiaohongHuang MengmengLi LiJiang JingJiang XinweiWang Haiyan - Broad-panel next-generation sequencing (NGS) improves detection of clinically relevant genomic alterations beyond those detected by conventional targeted panels in advanced non-small cell lung cancer (NSCLC). However, the influence of these additional findings on shared decision-making (SDM) in routine clinical practice remains poorly described. This study evaluated the incremental value of an institutional 50-gene NGS panel in documenting SDM and characterized the genomic landscape in advanced NSCLC. - Source: PubMed
Publication date: 2026/08/31
Krishnan M P ArunThovarayi VyshakhShenoy Praveen KDevi R NandiniRoshan Deepak - The renowned traditional Chinese medicine (TCM) classical prescription Gualou-Xiebai-Banxia decoction (GXBD) exhibits remarkable therapeutic effects on coronary artery disease (CAD). However, its material basis and molecular targets remain unclear. Our previous studies found that its ethyl acetate fraction (GXB-E) exhibited the most pronounced cardioprotective effect among its series extracts and could potentially activate the Fibroblast Growth Factor Receptor Substrate 2α (FRS2α), the crucial gatekeeper within FGF21/FGFR1/β-Klotho-FRS2α pathway. This study aimed to rapidly screen for FRS2α-targeted components from GXB-E and to verify their cardioprotective effects. An integrated strategy combining affinity ultrafiltration with UHPLC-Orbitrap-Exploris MS (AUF-LC-MS) was established to screen for affinity components, binding sites of which to FRS2α were inferred via molecular docking. Forty-nine compounds were identified in GXB-E, among which 10 showed specific binding affinity to FRS2α. These compounds interacted with the active site of FRS2α mainly through hydrogen bonds and other intermolecular forces. Among them, vanillic acid (VA) and cynaroside (Cyn) exhibited stronger binding energies. Both components significantly improved the growth state of myocardial cells (MCs) injured by ischemia-hypoxia, inhibited apoptosis and necrosis, and markedly increased cell viability. In zebrafish hearts injured by doxorubicin (DOX), they notably alleviated myocardial hypertrophy and pathological damage, reduced the SV-BA distance, pericardial edema area, and myocardial enzyme activity. Meanwhile, the decreased p-FRS2α level was dramatically upregulated by these two components in both the MCs and zebrafish models. This work validated the feasibility of using AUF-LC-MS for lead compound screening. Our findings help clarify the multi-component synergistic mechanism underlying the therapeutic effect of GXBD on CAD, lay a foundation for exploring novel CAD therapeutics derived from this TCM classic prescription. - Source: PubMed
Publication date: 2026/09/24
Gao HongdaLiu LuWang HaiyuZhao PanZhao Qitao