Ask about this productRelated genes to: FBXO16 Blocking Peptide
- Gene:
- FBXO16 NIH gene
- Name:
- F-box protein 16
- Previous symbol:
- -
- Synonyms:
- FBX16
- Chromosome:
- 8p21.1
- Locus Type:
- gene with protein product
- Date approved:
- 2003-06-09
- Date modifiied:
- 2014-11-19
Related products to: FBXO16 Blocking Peptide
Related articles to: FBXO16 Blocking Peptide
- 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 - Cognitive and behavioral impairment affects up to half of individuals with amyotrophic lateral sclerosis (ALS), but their molecular origin remains unresolved. Here, we identify mislocalization of the RNA-binding protein FUS in cortical neurons as a defining feature in ALS patients with cognitive impairment (ALS-ci). Selective mislocalization of FUS in adult cortical projection neurons in mice is sufficient to trigger ALS-ci- and ALS with behavioral impairment (ALS-bi)-like phenotypes, including deficits in sociability, and neurodegeneration. Single-nucleus transcriptomics reveal a conserved FUS-dependent gene network downregulated in these mice and ALS-ci patients. This regulon is enriched for ALS genetic risk factors and newly implicates in ALS-bi. Carriers of protein-truncating variants display behavioral abnormalities, frontotemporal atrophy, and increased levels of dementia-linked biomarkers. These findings define a neuron-intrinsic mechanism for cognitive and behavioral dysfunction in ALS and nominate FUS mislocalization and its downstream gene network as therapeutic targets. - Source: PubMed
Publication date: 2025/06/17
Cassel RaphaelleLorenc FélicieBombardier AurélieDE Tapia ClaudiaDieterle StéphaneGouveia Roque CláudioJackson Christopher AStuart-Lopez GeoffreyRouaux CarolineGuillot Simon JBirling Marie-ChristineKessler PascalGrassano MaurizioTraynor BryanChio AdrianoRoy RajuShorter JamesWaldron Fergal MGregory Jenna MPhatnani HemaliDupuis LucMegat Salim - Activation of transcription factor NF-κB is tightly regulated by negative regulatory systems that prevent excessive inflammation leading to autoimmune diseases. We previously demonstrated that PDLIM2, a PDZ-LIM domain-containing nuclear protein, functions as a ubiquitin E3 ligase that targets the p65 subunit of NF-κB and STAT3/STAT4 transcription factors for proteasomal degradation, thus terminating immune responses in dendritic cells and CD4T cells, respectively. In this study, we have demonstrated that PDLIM2 forms a ubiquitin ligase complex with Cullin 1, a scaffold protein, providing a platform consisting of complex and Skp1, an adaptor protein. Moreover, by screening using siRNA for F-box-containing proteins, we have identified Fbxo16 as a substrate-recognition receptor for p65 in this complex. Fbxo16 bound to p65 and promoted its polyubiquitination and degradation, thereby suppressing NF-κB transactivation. Consistently, Fbxo16 deficiency in dendritic cells resulted in a larger amount of nuclear p65 and thus enhanced production of proinflammatory cytokines. On the other hand, Fbxo16 could not promote the degradation of STAT3 or STAT4, and Fbxo16 deficiency did not affect STAT3- and STAT4-mediated immune responses of CD4T cells. These results delineate a role of Fbxo16, as a substrate receptor for p65 in a PDLIM2-containing ubiquitin ligase complex, in negatively regulating NF-κB-mediated inflammatory responses in dendritic cells. - Source: PubMed
Publication date: 2025/06/03
Sugimoto-Ishige AkikoJodo AyaTanaka Takashi - Glioblastoma is a highly aggressive brain tumor, and the transition from the proneural to mesenchymal subtype is associated with more aggressive and therapy-resistant features. However, the signaling pathways and genes involved in this transition remain largely undefined. - Source: PubMed
Publication date: 2025/04/05
Guo ShanchunSidhu RajveerRamar VanajothiGuo Alyssa AWang GuangdiLiu Mingli - High-grade serous ovarian carcinoma (HGSOC) is one of the most lethal gynecological cancer. Genetic studies have revealed gene copy number alterations (CNAs) frequently occurred in HGSOC pathogenesis, however the function and mechanism of CNAs for microRNAs are still not fully understood. Here, we show the dependence on gene copy number amplification of MIR937 that enhances cell autophagy and dictates HGSOC proliferative activity. Data mining of TCGA database revealed MIR937 amplification is correlated with increased MIR937 expression and cell proliferation of HGSOC. Deletion of MIR937 in HGSOC cells led to impaired autophagy and retarded cell proliferation, and the extent for its inhibitory effects scaled with the degree of MIR937 copy loss. Rescue assay confirmed miR-937-5p, a mature product of MIR937, was sufficient to restore its oncogenic function. Mechanistically, MIR937 amplification raised the expression of miR-937-5p, enhanced its binding to 3' UTR of FBXO16 transcript, and thereby restricting FBXO16 degradative effects on ULK1. Our results demonstrate that MIR937 amplification augments cell autophagy and proliferation, and suggest an alternative strategy of MIR937/FBXO16/ULK1 targeting for HGSOC treatment. - Source: PubMed
Publication date: 2024/10/09
Zhang ZhenLiu XinkuiChu ChuZhang YingjieLi WeiYu XiaoyanHan QiaoqiaoSun HaoyuZhang YunhongZhu XiaoxiaoChen LiangWei RanFan NannanZhou MiaomiaoLi Xia