Ask about this productRelated genes to: FBXO24 antibody
- Gene:
- FBXO24 NIH gene
- Name:
- F-box protein 24
- Previous symbol:
- -
- Synonyms:
- FBX24
- Chromosome:
- 7q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 2000-09-27
- Date modifiied:
- 2016-10-05
Related products to: FBXO24 antibody
Related articles to: FBXO24 antibody
- The ubiquitin E3 ligase SCF targets key proteins for degradation that regulate important biological processes, but the mechanisms controlling cellular concentrations of its receptor subunit, F-box only protein 24 (FBXO24), remain unknown. Here, Haemophilus influenzae type B (HiB), an important cause of pneumonia, protects FBXO24 from lysosomal degradation in THP-1 macrophage cells by reducing its ubiquitylation levels. We identified that the ubiquitin-specific peptidase 4 (USP4) mediates FBXO24 deubiquitylation and stabilization in response to HiB infection in a TLR4 receptor-dependent manner. In experimental HiB pneumonia, either nanoparticle delivery of encapsulated USP4 siRNA or targeted genetic disruption of Fbxo24 in mice led to increased alveolar mononuclear cells coupled with reduced bacterial loads, attenuated pulmonary edema and decreased lung injury severity compared to control mice. Collectively, these findings demonstrate the ability of a bacterial pathogen to exploit a deubiquitylation mechanism to preserve cellular levels of an E3 ligase component, thereby impairing innate host defense responses. - Source: PubMed
Publication date: 2026/07/22
Yurtsever IlknurFarkas DanielaCornwell AlexJoseph Jessica AXu SiyingEnglert Joshua ABednash Joseph SLondino James DJohnson Benjamin SMallampalli Rama K - Gastric cancer is the fifth most commonly diagnosed cancer. Although 10% of cases show familial clustering, a monogenic hereditary cause is rarely observed. Little is known about the molecular profile of familial gastric cancer cases in Brazil. Thus, we aimed to characterize the germline genomic profile of patients with potentially hereditary gastric cancer in the Brazilian population. - Source: PubMed
Publication date: 2026/07/14
de Souza Deivid CalebeBuranello ThalianeNeto Dario Tenorio TavaresPisani Janina PontesRibeiro Giovanna Napolitano PereiraOlandoski MarciaSchlesinger DavidKitajima João PauloViana Danilo VilelaAchatz Maria Isabel - The etiology of non-obstructive azoospermia (NOA) remains largely idiopathic, emphasizing the urgent need for molecular biomarkers to predict sperm retrieval outcomes. Here, we integrate bioinformatic analyses of public transcriptomic data with experimental expression profiles to investigate a potential regulatory network involving hsa-circ_0081481, miR-3960 and FBXO24 in NOA. Seven GEO datasets were analyzed to identify differentially expressed genes, and FBXO24 was found to be a consistently downregulated gene in NOA. Upstream regulators and interacting non-coding RNAs were predicted, leading to the selection of miR-3960 (a microRNA targeting FBXO24) and hsa-circ_0081481 (a circular RNA predicted to sponge miR-3960). Subsequently, FBXO24, miR-3960 and hsa-circ_0081481 expression levels were measured in the plasma of 60 men with NOA (categorized by histopathology and sperm retrieval outcome) and 40 fertile controls. FBXO24 and hsa-circ_0081481 were significantly downregulated in NOA (especially in hypospermatogenesis and maturation arrest), whereas miR-3960 was significantly upregulated in these subgroups. Of note, hsa-circ_0081481 achieved excellent diagnostic performance (AUC 0.920) in distinguishing NOA cases with successful and failed sperm retrieval, respectively. miR-3960 also showed high accuracy (AUC 0.861) after its inverse expression pattern was taken into account, and FBXO24 showed moderate predictive value. Our findings suggest that the hsa-circ_0081481/miR-3960/FBXO24 axis is dysregulated in NOA and may serve as a novel trio of non-invasive biomarkers. This study provides new insights into the molecular mechanisms of spermatogenic failure in NOA and provides a basis for improved diagnosis and personalized fertility treatment. - Source: PubMed
Publication date: 2026/05/21
Babakhanzadeh EmadKhodadadian AliEsmaeili Dahaj ForouzanSolatzadeh HormozNazari MajidMozhdeh MahyaVahidi Mehrgardi SerajoddinJafari Mohammad HassanDehghani MohammadrezaGhafouri-Fard SoudehGhasemi Nasrin - Dysregulation of MYC proto-oncogene, bHLH transcription factor (MYC) represents a common yet mechanistically unresolved driver of hepatocellular carcinoma (HCC). While MYC remains an elusive therapeutic target, developing strategies to promote its degradation emerges as a promising alternative approach. Here we show that vaccinia-related kinase 2 (VRK2) functions as a direct MYC-interacting kinase that stabilizes the oncoprotein through phosphorylation at Serine (Ser)281/293. This phosphorylation enables VRK2 to compete with the Skp1-Cullin-F-box protein complex containing FBXO24 (SCF-FBXO24) E3 ligase, thereby blocking MYC polyubiquitination and proteasomal degradation. The stabilized MYC-VRK2 complex amplifies transcriptional activation of protumorigenic programs, including the immune checkpoint programmed cell death ligand 1 (PD-L1) and VRK2 itself, establishing a self-reinforcing oncogenic circuit. Therapeutic inhibition of VRK2 in HCC models reduces MYC protein levels, suppresses tumor progression, and synergizes with anti- programmed cell death-1 (PD-1) immunotherapy. Our results reveal VRK2-mediated stabilization of MYC as a critical nexus linking hepatocarcinogenesis to immune evasion, proposing VRK2 kinase inhibition as a mechanism-based therapeutic strategy for MYC-driven HCC. - Source: PubMed
Publication date: 2025/10/10
Su ChenLiao ZhibinMo JieLiu FurongWang WeijianZhang HaoquanZhang HongweiLiu YachongPan YonglongZhu HeChen XiaopingZhang ZhanguoZhu PengZhang Bixiang - Triple-negative breast cancer (TNBC) is an aggressive subtype lacking targetable proteins for treatment. PARP inhibitors (PARPi) are effective in BRCA-mutated cancers but have limited utility in non-germline BRCA-mutated (non-gBRCAm) TNBC. We hypothesized that inducing BRCAness by targeting RAD51, a key homologous recombination protein, could sensitize non-gBRCAm TNBC to PARPi. - Source: PubMed
Publication date: 2025/08/05
Tsoi HoLeung George Man HongMan Ellen Pui SumYou Chan PingCheung Koei Ho LamChan Kelvin Yuen KwongGong ChunHuen Michael Shing YanKhoo Ui Soon