Ask about this productRelated genes to: FBXO25 Blocking Peptide
- Gene:
- FBXO25 NIH gene
- Name:
- F-box protein 25
- Previous symbol:
- -
- Synonyms:
- FBX25
- Chromosome:
- 8p23.3
- Locus Type:
- gene with protein product
- Date approved:
- 2000-09-27
- Date modifiied:
- 2014-11-18
Related products to: FBXO25 Blocking Peptide
Related articles to: FBXO25 Blocking Peptide
- Autism spectrum disorder (ASD) is a neurodevelopmental disorder characterized by deficits in social communication and restricted repetitive behaviors. Genetic studies have implicated chromosomal microdeletions in the 8p23.2-pter region in ASD and related disorders, highlighting FBXO25 as a candidate gene. FBXO25 encodes an F-box protein component of the SCF E3 ubiquitin ligase complex, which is involved in protein degradation through the ubiquitin-proteasome system. To investigate the impact of FBXO25 deletion, we generated Fbxo25-deficient mice and conducted behavioral, structural, molecular, transcriptomic, and proteomic analyses. Homozygous Fbxo25 mutant mice exhibited excessive self-grooming, a core ASD-related repetitive behavior. In contrast, both heterozygous and homozygous mice displayed impaired recognition memory in the novel object recognition test. However, social behaviors, anxiety-like responses, and spatial memory were preserved. Golgi staining revealed reduced dendritic complexity in hippocampal dentate gyrus granule cells of both heterozygous and homozygous mice. Western blotting revealed altered protein expression, including decreased PSD95 and CaMKII alpha, and elevated Arc in homozygous mice. Transcriptomic and proteomic analyses identified 17 differentially expressed proteins (DEPs) shared between heterozygous and homozygous mutants, supporting a model of FBXO25 haploinsufficiency. Many DEPs are involved in focal adhesion, cytoskeletal organization, synaptic transmission and signaling, oxidative stress, and protein degradation. These findings suggest that FBXO25 deletion impairs ubiquitin-mediated degradation, leading to synaptic dysfunction and ASD-relevant phenotypes. Our study establishes a novel mouse model of FBXO25 deficiency. It provides mechanistic insight into how disrupted protein degradation may contribute to ASD pathogenesis, highlighting protein degradation as a potential therapeutic target. - Source: PubMed
Publication date: 2026/06/30
Lin Szu-YuChang Ho-ChingChang Ya-HanBayansan OdvogmedNg Chi-HouLung KaitlynChen Chia-HsiangGau Susan Shur-FenLee Li-Jen - F-box proteins serve as substrate adapters in SCF ubiquitin ligase complexes, regulating proteolysis to modulate eukaryotic signaling, such as cell cycle progression and stress responses. Here, we characterize the F-box gene family in water buffalo (Bubalus bubalis), identifying 70 genes across 24 autosomes and the X chromosome using HMMER and BLASTP searches against Pfam domains. Phylogenetic analysis with orthologs from human, sheep, goat, horse, and cattle grouped them into four subfamilies (FBX, FBXL, FBXW, FBXO), with 58 core buffalo genes aligning closely to mammalian clades (bootstrap >95%). MEME analysis identified nine conserved motifs, including the F-box domain (motifs 1-2, e.g., LPDELLLYIFSYLDA), LRRs for specificity (motif 3), and WD40 repeats for scaffolding (motifs 5-7,9), confirmed by Pfam. Gene structures ranged from 2 to 23 exons, indicating regulatory diversity. Synteny with cattle conserved ∼85% of orthologs, reflecting artiodactyl ancestry. Physicochemical properties spanned MW 18.10-93.71 kDa (mean 49.2 kDa, excluding outliers), pI 4.27-10.41, and GRAVY -0.75 to 0.143 (mean - 0.32), consistent with hydrophilic profiles. Five segmental duplications (e.g., FBXO25/FBXO32) showed Ka/Ks ratios of 0.144-1.194 (four <1), suggesting purifying selection and divergence 48-220 MYA (Ks Poisson correction, refined ruminant rate). nsSNP analysis in 70 genes via nine tools predicted >95% benign/synonymous effects, with deleterious exceptions like FBXO16 V160T (consensus score 0.82, disrupting binding) and FBXO48 R7G (0.91, affecting stability). WoLF PSORT localized 17 nuclear, 10 cytoplasmic, 12 plasma membrane, 7 mitochondrial, 5 extracellular, and 7 dual sites, implying roles in transcription, degradation, and trafficking. These genes may represent potential candidates for future functional studies and genome-editing approaches; however, experimental validation will be required before their application in breeding programs. - Source: PubMed
Publication date: 2026/04/04
Nasir TanveerSafdar MuhammadImran SafdarTariq MuhammadJunejo YasmeenOzaslan MehmetYounus Muhammad - Given the high morbidity and mortality of colorectal cancer (CRC), as well as its challenging treatment, the present study was conducted to identify reliable prognostic signatures for predicting clinical outcomes. - Source: PubMed
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Wang QiangChen ZhongshengLi LiangheZhang JiandongLi QingZhan Wei - is a bacterium that causes chlamydia, the most diagnosed bacterial sexually transmitted infection (STI) in the world. In the U.S., chlamydia is most prevalent among non-Hispanic African American (AA) individuals, implying substantial racial disparity. Despite prevention and control efforts, reinfection is common, suggesting that some individuals have insufficient protective immunity to . To better understand the genetically mediated risks of chlamydia reinfection, we sought to identify genetic loci associated with reinfection using a Genome-Wide Association Study (GWAS) approach. - Source: PubMed
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Tiwari Hemant KPatki AmitSrinivasasainagendra VinodhVejandla Sandeep CSadeesh ArchishGupta KanupriyaAppah MaryGeisler William M - Ubiquitination, a pivotal posttranslational modification, plays a central role in regulating many biological processes. Nevertheless, its prognostic significance in cervical cancer remain largely unexplored. - Source: PubMed
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