Ask about this productRelated genes to: FBXO31 Blocking Peptide
- Gene:
- FBXO31 NIH gene
- Name:
- F-box protein 31
- Previous symbol:
- -
- Synonyms:
- FBX14, FBXO14, Fbx31, MGC15419
- Chromosome:
- 16q24.2
- Locus Type:
- gene with protein product
- Date approved:
- 2001-09-12
- Date modifiied:
- 2016-10-05
Related products to: FBXO31 Blocking Peptide
Related articles to: FBXO31 Blocking Peptide
- Proteostasis hinges on the precise recognition and elimination of damaged proteins through the ubiquitin-proteasome system (UPS), where E3 ubiquitin ligases recognize degradation signals, or degrons. While degrons have traditionally been viewed as genetically encoded or enzymatically generated motifs, emerging evidence suggests that nonenzymatic chemical damage can also create functional degradation signals. Oxidative stress-induced peptide backbone fragmentation, including hydroxyl radical-mediated cleavage, generates proteins bearing C-terminal amide groups (CTAPs), a chemically derived degron class recognized by the SCF-FBXO31 E3 ligase complex. Genome-wide CRISPR screening identified FBXO31 as a selective CTAP reader required for ubiquitination and proteasomal clearance of amidated substrates. Disruption of this pathway impairs proteostasis and, in disease-associated FBXO31 mutants, promotes aberrant degradation of non-amidated proteins such as SUGT1, contributing to cytotoxicity and neurodevelopmental dysfunction. Collectively, these findings redefine degron biology via establishing chemically induced modified amino acid degrons (MAADs) as mechanistic links between oxidative damage and selective protein degradation. - Source: PubMed
McLauchlan IanWhite JackEldeeb Mohamed - F-box only protein 31 (FBXO31) has been implicated in tumorigenesis and development across various human cancers. However, the role of FBXO31 in breast cancer progression remains poorly understood. In this study, we identified FBXO31 as a tumor suppressor in triple-negative breast cancer (TNBC), where it inhibited cell proliferation, migration, and invasion. Furthermore, FBXO31 promoted cystine-glutamate antiporter (xCT)-mediated ferroptosis in TNBC cells. Notably, overexpression of FBXO31 suppressed tumor growth in mice. Mechanistically, ABL-related gene (ABL2) was identified as a novel ubiquitin substrate of FBXO31. FBXO31 specifically interacted with ABL2 and promoted ABL2 ubiquitination and subsequent degradation through its F-box motif. Functionally, ABL2 acted as an oncogenic factor in TNBC cells by promoting cell proliferation, migration, and invasion, while inhibiting xCT-mediated ferroptosis. Rescue experiments showed that FBXO31 inhibited TNBC progression at least partly through down-regulating ABL2 expression. Collectively, our findings reveal a novel molecular mechanism for TNBC progression and provide a potential therapeutic strategy for its treatment. - Source: PubMed
Publication date: 2026/04/15
Zhang YuhaoLuo JingjingXu QingZeng XianzhenWang XinyuXu HuiPan XueshanCao TongHuang HuaMa Jia - Ankylosing spondylitis (AS) is a chronic inflammatory disorder with poorly defined pathogenic mechanisms. The integrated stress response (ISR), an evolutionarily conserved signaling network, is implicated in AS development. This research endeavored to identify biomarkers for AS, thereby offering novel targets and approaches for therapeutic intervention. - Source: PubMed
Publication date: 2026/03/26
Wang ShuaiZhu JingliangZhang HonghuiHu ShengxuanMei JiaxinZhou ChusongShi Benchao - Understanding how host gene regulation responds to viral infection is essential for developing effective antiviral strategies. Emerging evidence suggests that host transcripts undergo dynamic chemical modifications to counteract viral invasion. Conversely, viruses that rely on nuclear transcription exploit host RNA methyltransferases to enhance mRNA export and translation. Orthopoxviruses, however, complete their entire replication cycle within compartmentalized cytoplasmic "factories" utilizing enzymes encoded by their large double-stranded viral DNA genomes. The dynamic interplay between host and poxviral epitranscriptome remains poorly characterized. - Source: PubMed
Publication date: 2026/04/11
Kwon TaehyungMorales Demosthenes PMikolitis Abigale SMach Phillip MGleasner Cheryl DMicheva-Viteva Sofiya N - Targeted protein degradation (TPD) is a powerful strategy for controlling protein abundance. Here, we establish FBXO31 as a TPD-competent E3 ligase by exploiting its recognition of C-terminal amide-bearing degrons. Using an amidated Ala-Phe motif as a chemical recruiter, multiple small-molecule binders can be transformed into FBXO31-dependent degraders that induce the rapid and potent degradation of FKBP12, multiple kinases, and BET proteins BRD2, BRD3, and BRD4. Mechanistic studies confirm FBXO31-mediated ternary complex formation and identify key residues in FBXO31 required for recruiter engagement and target degradation. - Source: PubMed
Publication date: 2026/04/10
Zhang ChenluJin XiaokangZhou ChenJenkins M JamalRiha Isabella AZhang Xiaoyu