Ask about this productRelated genes to: FBXL5 antibody
- Gene:
- FBXL5 NIH gene
- Name:
- F-box and leucine rich repeat protein 5
- Previous symbol:
- -
- Synonyms:
- FBL4, FBL5, FLR1
- Chromosome:
- 4p15.32
- Locus Type:
- gene with protein product
- Date approved:
- 2000-09-27
- Date modifiied:
- 2016-10-05
Related products to: FBXL5 antibody
Related articles to: FBXL5 antibody
- - Source: PubMed
Publication date: 2026/04/22
Lan DonglianSun XiaojingYao LeiCao Bo - - Source: PubMed
- Ferroptosis, an iron-dependent form of regulated cell death characterized by lipid hydroperoxide accumulation, has attracted considerable attention because of its potential clinical applications. Ferroptosis is governed by redox reactions; however, the factors regulating this process, as well as their relationship with the central mediator of cellular redox homeostasis glutathione (GSH), warrant further investigation. Metallothioneins (MTs), cysteine-rich proteins that play central roles in zinc storage and homeostasis, comprise eleven isoforms in humans. This isoform multiplicity complicates functional analysis of human MTs, making it difficult to generate knockout cell lines and elucidate their precise roles in biological processes, including ferroptosis. Here, we established MT-knockout human cell lines and demonstrated that MTs protected against iron overload- or GSH depletion-induced ferroptosis in cooperation with GSH through their abundant thiol groups. Zinc enhanced this protective effect by inducing MT expression via metal-responsive transcription factor 1 (MTF1) activation. Importantly, this protective function was conserved across different human cell types, and MT expression levels may contribute to cell-type-specific susceptibility to ferroptosis. These findings highlight the zinc-MTF1-MT axis as a critical regulatory pathway that complements the GSH-glutathione peroxidase 4 system in controlling ferroptosis and may constitute a promising target for ferroptosis-directed therapeutic strategies. - Source: PubMed
Publication date: 2026/01/05
Wagatsuma TakumiYamamoto AkaneNishimura YuzunaKawami MasashiIto JunyaHirayama TasukuMasuda SeijiNakagawa KiyotakaUchida YasuoKambe Taiho - Neddylation modifications in immune and tumor cells are linked to poor tumor prognosis. This study identifies prognostic genes associated with neddylation-related genes (NRGs) in colorectal cancer (CRC) using single-cell and spatial transcriptome (ST) sequencing, aiming to advance CRC treatment strategies. - Source: PubMed
Publication date: 2025/12/24
Zhu ZimingZhang XinyueWang SongHuang YunsiHan XuedongLai DongpingYao XinLan WeixuanNong HuiZeng WenbinMo YanhuaXu Ri'anZhang Tao - Pediatric cholestatic liver diseases are rare but serious conditions that frequently progress to liver fibrosis and cirrhosis and often require transplantation. Despite the clinical importance of these diseases, the mechanisms driving disease progression remain poorly understood. Hepatic iron accumulation was identified as a pathologic feature associated with congenital cholestatic liver disease in mice with a liver-specific deletion of Yap, a gene critical for bile duct development. Further hepatic iron overload induced by liver-specific deletion of Fbxl5, a key regulator of cellular iron homeostasis, exacerbated cholestatic liver injury and fibrosis in Yap-deficient mice. Mechanistically, iron overload enhanced the susceptibility to bile acid-induced cytotoxicity via ferroptosis, a form of regulated cell death driven by iron-dependent lipid peroxidation. This ferroptotic process was confirmed by the suppression of bile acid-induced cell death through iron chelation and lipid peroxide scavenging in ex vivo liver slice cultures. Furthermore, both dietary iron restriction and antioxidant treatment mitigated liver injury in vivo. These findings identify iron accumulation as a key driver of disease progression and highlight iron metabolism and ferroptosis as potential therapeutic targets in congenital cholestatic liver disease. - Source: PubMed
Publication date: 2025/12/13
Ohta YudaiKanamori YoheiMaeda AyatoSaleh Mohamed FathiNita AkihiroMatsumoto TakashiNakayama Keiichi IMoroishi Toshiro