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
- 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 - Biallelic loss-of-function variants in FBXO31 cause autosomal-recessive intellectual disability. A recurrent de novo variant, c.1000G>A(p.Asp334Asn), has been described in association with an autosomal-dominant phenotype. To refine this phenotype and its clinical implications, we re-evaluated three published cases and ascertained four additional probands via advocacy networks, GeneMatcher, and clinician referral. Phenotyping included neurologic, behavioral, and dysmorphology assessment. All seven individuals carried the recurrent de novo FBXO31 p.Asp334Asn variant. A core neurodevelopmental profile was observed and included cerebral palsy (mixed hypotonia, spasticity, and dystonia), global developmental delay/intellectual disability, and speech impairment. Neuropsychiatric features were sometimes prominent and included attention-deficit/hyperactivity disorder, anxiety, stereotypies, autistic features, and behavioral dysregulation. Neuroimaging often showed a hypoplastic corpus callosum and posterior-predominant white-matter changes. In one individual, gray matter heterotopias were also observed. A subtle but consistent facial gestalt was noted. Recurrent FBXO31 p.Asp334Asn variants lead to a recognizable neurodevelopmental syndrome. Based on our findings, we recommend including FBXO31 in diagnostic algorithms for cerebral palsy and neurodevelopmental disorders. We propose the descriptive term "autosomal dominant FBXO31-associated neurodevelopmental disorder," and-consistent with the validating laboratory and with support from the FBXO31 Foundation-propose the eponym "Kruer syndrome." - Source: PubMed
Publication date: 2026/03/20
Galaz-Montoya Carolina ILewis Sara AGalindo Maureen KCornejo PatriciaSkidmore Peter TBisarad PrithaMagee HelenBontempo KellyKeren BorisAfenjar AlexandraSkorvanek MatejZech MichaelWentzensen Ingrid MGurnett Christina AChung Wendy KBakhtiari SomayehKruer Michael C - 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 rapid and potent target degradation. Mechanistic studies confirm FBXO31-mediated ternary complex formation and identify key residues in FBXO31 required for recruiter engagement and target degradation. We further show that an FBXO31-based multi-kinase degrader exhibits a distinct and broader degradation profile than a CRBN-based degrader, highlighting a potentially expanded degradable target space beyond CRBN. - Source: PubMed
Publication date: 2026/01/29
Zhang ChenluJin XiaokangZhou ChenJenkins M JamalRiha Isabella AZhang Xiaoyu