Ask about this productRelated genes to: FGF13 Blocking Peptide
- Gene:
- FGF13 NIH gene
- Name:
- fibroblast growth factor 13
- Previous symbol:
- -
- Synonyms:
- FHF2, FGF2
- Chromosome:
- Xq26.3-q27.1
- Locus Type:
- gene with protein product
- Date approved:
- 1996-12-16
- Date modifiied:
- 2018-02-13
Related products to: FGF13 Blocking Peptide
Related articles to: FGF13 Blocking Peptide
- Mitochondrial damage in dorsal root ganglion (DRG) neurons contributes to the pathogenesis of paclitaxel (PTX)-induced peripheral neuropathic pain (PIPNP). Fibroblast growth factor 13 (FGF13), abundantly expressed in DRG neurons, is crucial for the regulation of somatosensation; however, its role in PIPNP remains unclear. Here, we demonstrated that FGF13 expression is upregulated in DRG neurons of PIPNP model mice. Conditional knockout of Fgf13 in DRG neurons effectively alleviates PTX-induced mitochondrial damage and neuropathic pain. RNA sequencing analysis revealed that mitophagy mediates the regulatory effects of FGF13 in PIPNP. Mechanistically, FGF13 physically interacts with vasohibin 1 (VASH1), regulating the binding of VASH1 to microtubules and promoting microtubule detyrosination. FGF13 ablation disrupts assembly of the FGF13-VASH1-α-tubulin ternary complex, impairing VASH1-mediated microtubule detyrosination and increasing microtubule tyrosination. The resulting accumulation of tyrosinated microtubules facilitates kinesin-3 (KIF1A)-driven lysosomal trafficking, which in turn promotes mitophagy activation and ultimately ameliorates PTX-induced mitochondrial damage and PIPNP. Furthermore, VASH1 overexpression in DRG neurons reversed the alleviating effects of FGF13 deficiency on PTX-induced mitochondrial damage and PIPNP. In summary, our findings demonstrate that FGF13 deficiency alleviates mitochondrial dysfunction and PIPNP by suppressing VASH1-dependent microtubule detyrosination and subsequently activating mitophagy. Targeting FGF13 may be a promising therapeutic strategy for PIPNP. - Source: PubMed
Publication date: 2026/06/18
Dong YimingWang YidanLv SimengDong ZishanZhi KaixiGuo XiuhuaLi XuyanYu RuoxiZhang YiyiCheng SiyuanWang Chuan - Despite understanding the pathophysiology of Alzheimer's disease (AD), the mechanisms of neuronal regeneration mediated by oleanolic acid (OA) through m6A RNA methylation remain unexplored, forming the crux of this study. In a streptozotocin (STZ)-induced AD rat model, we administered OA and conducted behavioral tests to evaluate cognitive functions. We employed BrdU incorporation assays and immunofluorescence to investigate NSC proliferation, and Western blotting, chromatin immunoprecipitation (ChIP), RNA immunoprecipitation (RIP), and MeRIP-qPCR assays to analyze protein expression and RNA stability. Bioinformatic predictions focused on the interaction between KLF5, YTHDF2, and FGF13. OA significantly reversed cognitive impairment and enhanced NSC differentiation in the AD model. The modulation of OA on KLF5 expression led to the repression of YTHDF2, which was pivotal in the m6A-dependent RNA decay of FGF13, promoting axonal regeneration. Furthermore, FGF13 harbors multiple m6A modification sites, which contribute to its mRNA stability and translation, thereby influencing neuronal polarization and migration. In addition, the neuroprotective mechanism of OA also involved the upregulation of NSCs, while impaired neurogenesis and reduced NSC function are known to be associated with AD pathology. This research reveals that OA's therapeutic potential in AD is mediated through a previously unidentified mechanism involving modulation of m6A-dependent RNA regulation, highlighting the significance of m6A RNA methylation in neuronal regeneration. The findings pave the way for new therapeutic strategies targeting RNA modifications in neurodegenerative diseases. - Source: PubMed
Publication date: 2026/06/15
Ren DanXu JiangxiXiao LanZhang TingLi BiyanLi RuomengZhu Hong - Osteoporotic fracture (OPF) disrupts bone homeostasis via resorption-formation imbalance. This study investigates the expression and role of the long non-coding RNA FGF13 antisense RNA 1 (FGF13-AS1) in OPF bone healing. - Source: PubMed
Publication date: 2026/04/22
Yao ShanchuanMeng JiandeQin ZhouZhang Yuanyuan - - Source: PubMed
Liao XianghuiLi TuhuaYang LiLi HaiwenLi WeiruLiu YutingXie Zhong - Pathogenic variants within the unique N-terminal inactivation particle of FGF13 isoform A (FGF13A) have so far been associated only with an X-linked dominant epileptic encephalopathy (DEE). - Source: PubMed
Publication date: 2026/03/11
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