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Journal articles on the topic 'FBXO24'

Author: Grafiati

Published: 11 March 2023

Last updated: 31 July 2025

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1

Chen, Wei, Sheng Xiong, Jin Li, et al. "The Ubiquitin E3 Ligase SCF-FBXO24 Recognizes Deacetylated Nucleoside Diphosphate Kinase A To Enhance Its Degradation." Molecular and Cellular Biology 35, no. 6 (2015): 1001–13. http://dx.doi.org/10.1128/mcb.01185-14.

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The Skp-Cul-F box (SCF) ubiquitin E3 ligase machinery recognizes predominantly phosphodegrons or, less commonly, an (I/L)Q molecular signature within substrates to facilitate their recruitment in mediating protein ubiquitination and degradation. Here, we examined the molecular signals that determine the turnover of the multifunctional enzyme nucleoside diphosphate kinase A (NDPK-A) that controls cell proliferation. NDPK-A protein exhibits a half-life of ∼6 h in HeLa cells and is targeted for ubiquitylation through actions of the F-box protein FBXO24. SCF-FBXO24 polyubiquitinates NDPK-A at K85,

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2

Yuan, Lamei, Zhi Song, Xiong Deng, et al. "Genetic Analysis of FBXO2, FBXO6, FBXO12, and FBXO41 Variants in Han Chinese Patients with Sporadic Parkinson’s Disease." Neuroscience Bulletin 33, no. 5 (2017): 510–14. http://dx.doi.org/10.1007/s12264-017-0122-5.

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3

Yurtsever, I., A. Cornwell, D. Farkas, et al. "H. Influenzae Type B Infection Stabilizes an Immune Suppressor Protein, FBXO24." American Journal of Respiratory and Critical Care Medicine 211, Abstracts (2025): A3572. https://doi.org/10.1164/ajrccm.2025.211.abstracts.a3572.

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4

Chen, Wei, Denghui Gao, Long Xie, et al. "SCF-FBXO24 regulates cell proliferation by mediating ubiquitination and degradation of PRMT6." Biochemical and Biophysical Research Communications 530, no. 1 (2020): 75–81. http://dx.doi.org/10.1016/j.bbrc.2020.06.007.

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5

Zhang, Yuan-Meng, Ling-Bing Meng, Si-Jun Yu, and Dong-Xing Ma. "Identification of potential crucial genes in monocytes for atherosclerosis using bioinformatics analysis." Journal of International Medical Research 48, no. 4 (2020): 030006052090927. http://dx.doi.org/10.1177/0300060520909277.

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Objective To use bioinformatics tools to screen for gene biomarkers from monocytes, which play an important role in the pathogenesis of atherosclerosis. Methods Two expression profiling datasets (GSE27034 and GSE10195) were obtained from the Gene Expression Omnibus dataset and the differentially expressed genes (DEGs) between atherosclerotic human peripheral blood mononuclear cells (PBMC) samples and control subjects were screened using GEO2R. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses were conducted for the DEGs. STRING and MCODE plug-in of Cytoscape

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6

Angeli, Franca, Russell Wyborski, Bill Chen, Rama Mallampalli, and Michael Lark. "P157 FBXO3-FBXL2 AXIS MODULATORS AS A NOVEL CLASS OF ORAL SMALL MOLECULE COMPOUNDS FOR THE TREATMENT OF CROHN’S DISEASE." Inflammatory Bowel Diseases 26, Supplement_1 (2020): S6. http://dx.doi.org/10.1093/ibd/zaa010.014.

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Abstract Background Ubiquitination is a common post-translational modification, tagging proteins for degradation. The ubiquitin proteasome system is activated in Crohn’s Disease (CD), and modulation of its components might be a novel strategy for therapeutic intervention to control inflammation. The conjugation of ubiquitin to a target protein is orchestrated by a series of enzymatic reactions, the last step being catalyzed by a selective ubiquitin E3 ligase. Among ubiquitin E3 ligases, Fbxl2 serves as a sentinel gatekeeper to limit inflammation by targeting and enhancing the degradation of tu

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7

Masle-Farquhar, Etienne, Amanda Russell, Yangguang Li, et al. "Loss-of-function of Fbxo10, encoding a post-translational regulator of BCL2 in lymphomas, has no discernible effect on BCL2 or B lymphocyte accumulation in mice." PLOS ONE 16, no. 4 (2021): e0237830. http://dx.doi.org/10.1371/journal.pone.0237830.

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Regulation of the anti-apoptotic BCL2 protein determines cell survival and is frequently abnormal in B cell lymphomas. An evolutionarily conserved post-translational mechanism for over-expression of BCL2 in human B cell lymphomas and the BCL2 paralogue CED-9 in Caenorhabditis elegans results from loss-of-function mutations in human FBXO10 and its C.elegans paralogue DRE-1, a BCL2/CED-9-binding subunit of the SKP-CULLIN-FBOX (SCF) ubiquitin ligase. Here, we tested the role of FBXO10 in BCL2 regulation by producing mice with two different CRISPR/Cas9-engineered Fbxo10 mutations: an Asp54Lys (E54

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8

Manfiolli, Adriana O., Ana Leticia G. C. Maragno, Munira M. A. Baqui, et al. "FBXO25-associated Nuclear Domains: A Novel Subnuclear Structure." Molecular Biology of the Cell 19, no. 5 (2008): 1848–61. http://dx.doi.org/10.1091/mbc.e07-08-0815.

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Skp1, Cul1, Rbx1, and the FBXO25 protein form a functional ubiquitin ligase complex. Here, we investigate the cellular distribution of FBXO25 and its colocalization with some nuclear proteins by using immunochemical and biochemical approaches. FBXO25 was monitored with affinity-purified antibodies raised against the recombinant fragment spanning residues 2-62 of the FBXO25 sequence. FBXO25 protein was expressed in all mouse tissues tested except striated muscle, as indicated by immunoblot analysis. Confocal analysis revealed that the endogenous FBXO25 was partially concentrated in a novel dot-

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9

Guo, Fengjie, Xiaoyu Jiang, Domenico Roberti, Lixin Rui, and Izidore S. Lossos. "FBXO10 Targets HGAL for Degradation." Blood 126, no. 23 (2015): 3904. http://dx.doi.org/10.1182/blood.v126.23.3904.3904.

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Abstract Expression of the Human Germinal center Associated Lymphoma (HGAL) gene is restricted to germinal center (GC) B-lymphocytes and GC-derived lymphomas. HGAL expression identifies lymphomas characterized by a better prognosis. We previously showed that HGAL is a unique adaptor protein that regulates both cell motility and B-cell receptor (BCR) signaling, processes that are central for successful completion of the GC reaction. In our previous studies we demonstrated that upon BCR activation HGAL binds to and increases Syk kinase activity, resulting in enhanced BCR signaling. Syk induces H

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10

Goda, Atsushi, Satoru Meguro, Yoshikazu Johmura, et al. "Abstract 5278: Fbxo22 regulates estrogen signaling and suppresses tamoxifen-induced endometrial cancer." Cancer Research 83, no. 7_Supplement (2023): 5278. http://dx.doi.org/10.1158/1538-7445.am2023-5278.

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Abstract Introduction: Selective estrogen receptor modulators (SERMs), such as tamoxifen, function as agonists or antagonists for estrogen receptors (ERs) in a tissue-specific manner. We have discovered that Fbxo22, a F-box subunit of SCF ubiquitin ligase complex is critical for the functional alteration of SERM (Johmura, et al., J Clin Invest, 2018). SCFFbxo22 ubiquitinates and degrades lysine demethylase 4B (KDM4B) complexed with SERM-bound ER, that triggers release of coactivator SRC from ER, thus mediating antagonistic function of SERM. Without Fbxo22, stabilized KDM4B mediates the interac

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11

Qie, Shuo. "The E3 Ubiquitin Ligase Fbxo4 Functions as a Tumor Suppressor: Its Biological Importance and Therapeutic Perspectives." Cancers 14, no. 9 (2022): 2133. http://dx.doi.org/10.3390/cancers14092133.

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Fbxo4, also known as Fbx4, belongs to the F-box protein family with a conserved F-box domain. Fbxo4 can form a complex with S-phase kinase-associated protein 1 and Cullin1 to perform its biological functions. Several proteins are identified as Fbxo4 substrates, including cyclin D1, Trf1/Pin2, p53, Fxr1, Mcl-1, ICAM-1, and PPARγ. Those factors can regulate cell cycle progression, cell proliferation, survival/apoptosis, and migration/invasion, highlighting their oncogenic or oncogene-like activities. Therefore, Fbxo4 is defined as a tumor suppressor. The biological functions of Fbxo4 make it a p

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Qie, Shuo. "The E3 Ubiquitin Ligase Fbxo4 Functions as a Tumor Suppressor: Its Biological Importance and Therapeutic Perspectives." Cancers 14, no. 9 (2022): 2133. http://dx.doi.org/10.3390/cancers14092133.

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Fbxo4, also known as Fbx4, belongs to the F-box protein family with a conserved F-box domain. Fbxo4 can form a complex with S-phase kinase-associated protein 1 and Cullin1 to perform its biological functions. Several proteins are identified as Fbxo4 substrates, including cyclin D1, Trf1/Pin2, p53, Fxr1, Mcl-1, ICAM-1, and PPARγ. Those factors can regulate cell cycle progression, cell proliferation, survival/apoptosis, and migration/invasion, highlighting their oncogenic or oncogene-like activities. Therefore, Fbxo4 is defined as a tumor suppressor. The biological functions of Fbxo4 make it a p

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13

Wong, Siau Yen, Peiran Lu, Lei Wu, et al. "Hepatic F-box Only Protein 2 (FBXO2) Might Not Mediate Glucose Homeostasis in Obese Diabetic Mice." Current Developments in Nutrition 4, Supplement_2 (2020): 1281. http://dx.doi.org/10.1093/cdn/nzaa058_039.

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Abstract Objectives F-box only protein 2 (FBXO2) is an E3 ubiquitin protein ligase highly expressed in the brain and cochlea, hepatic FBXO2 protein levels are very low in healthy mice. It was reported that hepatic FBXO2 elevation causes hyperglycemia in obese mice. Here, we investigated whether hepatic FBXO2 expression was enhanced in diabetic human samples; and if so, whether deficiency of FBXO2 could improve blood glucose control in diet-induced obese diabetic mice. Methods Human liver specimen samples from healthy and type 2 diabetic human subjects were subject to transcriptomics and proteo

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14

Chang, Shu-Chun, Chin-Sheng Hung, Bo-Xiang Zhang, Tsung-Han Hsieh, Wayne Hsu, and Jeak Ling Ding. "A Novel Signature of CCNF-Associated E3 Ligases Collaborate and Counter Each Other in Breast Cancer." Cancers 13, no. 12 (2021): 2873. http://dx.doi.org/10.3390/cancers13122873.

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Breast cancer (BRCA) malignancy causes major fatalities amongst women worldwide. SCF (Skp1-cullin-F-box proteins) E3 ubiquitin ligases are the most well-known members of the ubiquitination–proteasome system (UPS), which promotes cancer initiation and progression. Recently, we demonstrated that FBXL8, a novel F-box protein (SCFF-boxes) of SCF E3 ligase, accelerates BRCA advancement and metastasis. Since SCFF-boxes is a key component of E3 ligases, we hypothesized that other SCFF-boxes besides FBXL8 probably collaborate in regulating breast carcinogenesis. In this study, we retrospectively profi

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15

Lee, Eric K., Zhaorui Lian, Kurt D'Andrea, et al. "The FBXO4 Tumor Suppressor Functions as a Barrier to BrafV600E-Dependent Metastatic Melanoma." Molecular and Cellular Biology 33, no. 22 (2013): 4422–33. http://dx.doi.org/10.1128/mcb.00706-13.

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Cyclin D1–cyclin-dependent kinase 4/6 (CDK4/6) dysregulation is a major contributor to melanomagenesis. Clinical evidence has revealed that p16INK4A, an allosteric inhibitor of CDK4/6, is inactivated in over half of human melanomas, and numerous animal models have demonstrated that p16INK4Adeletion promotes melanoma. FBXO4, a specificity factor for the E3 ligase that directs timely cyclin D1 proteolysis, has not been studied in melanoma. We demonstrate that Fbxo4 deficiency induces Braf-driven melanoma and that this phenotype depends on cyclin D1 accumulation in mice, underscoring the importan

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Lin, T. B., M. C. Hsieh, C. Y. Lai, et al. "Fbxo3-Dependent Fbxl2 Ubiquitination Mediates Neuropathic Allodynia through the TRAF2/TNIK/GluR1 Cascade." Journal of Neuroscience 35, no. 50 (2015): 16545–60. http://dx.doi.org/10.1523/jneurosci.2301-15.2015.

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17

Dhar, Ruby, Goura Kishor Rath, and Subhradip Karmakar. "FBXO4 as a novel ubiquitin ligase that targets Cyclin D in the pathogenesis of breast cancer." Journal of Clinical Oncology 37, no. 15_suppl (2019): e14722-e14722. http://dx.doi.org/10.1200/jco.2019.37.15_suppl.e14722.

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e14722 Background: Members of ubiquitin ligase family are reported to be associated with cancer. Genome wide RNAi screen using Dharmacon on target Plus RNAi library identified FBXO4 as one of the potential hit . We therefore aimed to study its detailed role on proliferation of MCF7 breast cancer cells with special focus on cell cycle genes. We want to expand it further and study its involvement in context to E2 signaling in breast cancer. We hypothesized that increase in CCND1 expression, could mimic some of the E2 transcriptional regulation and that CCND1 overexpression could lead to E2 indep

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Selander, Erik, Jan Heuschele, and Ann I. Larsson. "Hydrodynamic properties and distribution of bait downstream of a zooplankton trap." Journal of Plankton Research 39, no. 6 (2017): 1020–27. http://dx.doi.org/10.1093/plankt/fbx024.

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19

Zhang, Jihui, and Xiaobing Wu. "The Whole Genome DNA Methylation Signatures of Hindlimb Muscles in Chinese Alligators during Hibernation and Active Periods." Animals 14, no. 13 (2024): 1972. http://dx.doi.org/10.3390/ani14131972.

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Many ectotherms hibernate to increase their chances of survival during harsh winter conditions. The role of DNA methylation in regulating gene expression related to hibernation in ectotherms remains unclear. Here, we employed whole-genome bisulfite sequencing (WGBS) technology to construct a comprehensive genome-wide DNA methylation landscape of the hindlimb muscles in the Chinese alligator during hibernation and active periods. The results indicated that methylation modifications were most abundant at CG sites, identifying 9447 differentially methylated regions (DMRs) and 2329 differentially

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20

Chen, Ningyuan, Ruican Cao, Zhao Zhang, Sai Zhou, and Sanyuan Hu. "Sleeve Gastrectomy Improves Hepatic Glucose Metabolism by Downregulating FBXO2 and Activating the PI3K-AKT Pathway." International Journal of Molecular Sciences 24, no. 6 (2023): 5544. http://dx.doi.org/10.3390/ijms24065544.

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Type 2 diabetes mellitus (T2DM), a chronic metabolic disease, is a public health concern that seriously endangers human health. Sleeve gastrectomy (SG) can relieve T2DM by improving glucose homeostasis and enhancing insulin sensitivity. However, its specific underlying mechanism remains elusive. SG and sham surgery were performed on mice fed a high-fat diet (HFD) for 16 weeks. Lipid metabolism was evaluated via histology and serum lipid analysis. Glucose metabolism was evaluated using the oral glucose tolerance test (OGTT) and insulin tolerance test (ITT). Compared with the sham group, the SG

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Mazumdar, Varadendra Balaji, Kirnami Joshi, Binita Roy Nandi, and Girish K. Radhakrishnan. "Elucidating the role of the host protein, FBXO22, in the infection of macrophages with the zoonotic bacterial pathogen, Brucella." Journal of Immunology 210, no. 1_Supplement (2023): 242.03. http://dx.doi.org/10.4049/jimmunol.210.supp.242.03.

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Abstract Brucella spp. are facultative intracellular bacterial pathogens that have the ability to survive and multiply in professional and nonprofessional phagocytes. Successful invasion and chronic intracellular persistence indicate that Brucella manipulates various host cellular processes to create a replication permissive niche. The essential mechanisms and host factors that support the invasion and intracellular replication of Brucella remain poorly understood. RNA interference (RNAi) is a potent molecular tool for understanding gene function by downregulating the target gene expression th

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22

Yoshida, Yukiko, Sayaka Yasuda, Toshiharu Fujita, et al. "Ubiquitination of exposed glycoproteins by SCFFBXO27 directs damaged lysosomes for autophagy." Proceedings of the National Academy of Sciences 114, no. 32 (2017): 8574–79. http://dx.doi.org/10.1073/pnas.1702615114.

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Ubiquitination functions as a signal to recruit autophagic machinery to damaged organelles and induce their clearance. Here, we report the characterization of FBXO27, a glycoprotein-specific F-box protein that is part of the SCF (SKP1/CUL1/F-box protein) ubiquitin ligase complex, and demonstrate that SCFFBXO27 ubiquitinates glycoproteins in damaged lysosomes to regulate autophagic machinery recruitment. Unlike F-box proteins in other SCF complexes, FBXO27 is subject to N-myristoylation, which localizes it to membranes, allowing it to accumulate rapidly around damaged lysosomes. We also screene

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Niederkorn, Madeline, Lavanya Bezavada, Anitria Cotton, et al. "Ubiquitin Ligase SCF-FBXO11 Controls a Network of RNA-Binding Proteins and Splicing in MDS." Blood 142, Supplement 1 (2023): 712. http://dx.doi.org/10.1182/blood-2023-187094.

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The F-Box protein FBXO11 is a substrate receptor of Skp-Cullin-F-Box (SCF) ubiquitin ligase complexes. Loss-of-function mutations in FBXO11 are associated with diffuse large B-cell lymphoma, and FBXO11 has been shown to regulate epigenetic drivers of erythroid cell maturation. In our prior study, we found that deletion of FBXO11 improved cell survival under cytokine deprivation in an MDS cell line. Furthermore, we had observed a striking decrease in FBXO11 protein levels in AML patient samples. However, how FBXO11 contributes to myeloid malignancies is unclear. Here, using RNA-sequencing, prot

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Zhou, Huijun, Chong Zeng, Jie Liu, Haijun Luo, and Wei Huang. "F-Box Protein 43, Stabilized by N6-Methyladenosine Methylation, Enhances Hepatocellular Carcinoma Cell Growth and Invasion via Promoting p53 Degradation in a Ubiquitin Conjugating Enzyme E2 C -Dependent Manner." Cancers 15, no. 3 (2023): 957. http://dx.doi.org/10.3390/cancers15030957.

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The roles of F-box protein 43 (FBXO43) in carcinogenesis have been rarely revealed. The present study investigates the expression, function, and underlying mechanism of FBXO43 in hepatocellular carcinoma (HCC). Firstly, the expression and clinical significance of FBXO43 in HCC were investigated bioinformatically and experimentally using online omics data and local tissue samples. The role of N6-methyladenosine modification (m6A) of mRNA in regulating FBXO43 expression and the effects of m6A/FBXO43 axis alteration on cell proliferation and invasion were investigated further. Moreover, the under

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Deng, Chao, Hongzhi Li, and Qingmin Li. "F-box protein 17 promotes glioma progression by regulating glycolysis pathway." Bioscience, Biotechnology, and Biochemistry 86, no. 4 (2022): 455–63. http://dx.doi.org/10.1093/bbb/zbac008.

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ABSTRACT F-box protein 17 (FBXO17) is associated with high-grade glioma and acted as a promotor of glioma development. This study investigated the effect and underlying pathway of FBXO17 on glioma. The Cancer Genome Atlas database was applied to analyze FBXO17 expression information in glioma. First, high FBXO17 expressions are associated with glioma and poor prognosis. Then, FBXO17 was upregulated in glioma cells. Meanwhile, knock-down of FBXO17 inhibited cell proliferation, migration, and invasion, but increased the cell apoptosis. Besides, knock-down of FBXO17 inhibited mitochondrial membra

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Ma, Rulan, Wenbo Liu, Tuanhe Sun, Chengxue Dang, and Kang Li. "Clinical significance of FBXO43 in hepatocellular carcinoma and its impact on tumor cell proliferation, migration and invasion." PeerJ 11 (May 22, 2023): e15373. http://dx.doi.org/10.7717/peerj.15373.

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Background The effects of FBXO43 on hepatocellular carcinoma (HCC) and its clinical significance have not yet been determined. This study aims to determine the clinical significance of FBXO43 in HCC and its impact on the biological functions of HCC cells. Methods Data from TCGA database were downloaded to investigate the expression of FBXO43 in HCC and its correlation with prognosis and immune infiltration. Immunohistochemical staining images of FBXO43 in HCC were acquired from the HPA website. HCC cells (BEL-7404 and SMMC-7721) were transfected with the lentivirus targeting FBXO43 to decrease

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Lai, C. Y., Y. C. Ho, M. C. Hsieh, et al. "Spinal Fbxo3-Dependent Fbxl2 Ubiquitination of Active Zone Protein RIM1 Mediates Neuropathic Allodynia through CaV2.2 Activation." Journal of Neuroscience 36, no. 37 (2016): 9722–38. http://dx.doi.org/10.1523/jneurosci.1732-16.2016.

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Mo, Angela, Linda Ya-Ting Chang, Gerben Duns, et al. "Elucidating the Mechanisms of Leukemogenesis Driven By FBXO11 Depletion." Blood 138, Supplement 1 (2021): 3328. http://dx.doi.org/10.1182/blood-2021-145384.

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Abstract Mutations in SKP1 and CUL1 (Zhang et. al. Oncol Lett 2018), which encode components of the SKP1-CUL1-F-BOX (SCF) ubiquitin E3-ligase complex, have previously been reported or characterized in AML. FBXO11, which encodes the substrate recognizing component, however, has not been studied in AML. We performed whole exome sequencing and RNA-seq on140 clinical AML samples and identified recurrent inactivating mutations in FBXO11. Of the components of the SCF FBXO11 complex, FBXO11 transcript expression is most significantly reduced in AML samples compared to normal. We show that loss of FBX

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Zhao, Xinyue, Zhihui Han, Ruiying Liu, Zehao Li, Ling Mei, and Yue Jin. "FBXO11 Mediates Ubiquitination of ZEB1 and Modulates Epithelial-to-Mesenchymal Transition in Lung Cancer Cells." Cancers 16, no. 19 (2024): 3269. http://dx.doi.org/10.3390/cancers16193269.

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Epithelial-to-mesenchymal transition (EMT) affects the invasion and migration of cancer cells. Here, we show that FBXO11 recognizes and promotes ubiquitin-mediated degradation of ZEB1. There is a strong association between FBXO11 and ZEB1 in non-small cell lung cancer (NSLC) in a clinical database. FBXO11 interacts with ZEB1, a core inducer of EMT. FBXO11 leads to increased ubiquitination and proteasomal degradation of ZEB1. Depletion of endogenous FBXO11 causes ZEB1 protein accumulation and EMT in A549 and H1299 cells, while overexpression of FBXO11 reduces ZEB1 protein abundance and cellular

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Liu, Wuguang, Bin Xu, Kashif Kifayat, et al. "FBXO10 Drives Hepatocellular Carcinoma Proliferation via K63-Linked Ubiquitination and Stabilization of FRMPD1." Current Issues in Molecular Biology 47, no. 6 (2025): 391. https://doi.org/10.3390/cimb47060391.

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Aberrant ubiquitination drives hepatocellular carcinoma (HCC) progression, yet the role of FBXO10—a key F-box E3 ubiquitin ligase component—remains uncharacterized. Through bioinformatics analyses and functional validation, we establish FBXO10 as a critical oncogenic driver in HCC. Transcriptomic data from public databases (TIMER, UALCAN, GEO) revealed significant FBXO10 upregulation in HCC tissues, with elevated expression predicting advanced tumor stage, metastasis, and reduced survival. Functionally, FBXO10 silencing suppressed HCC cell proliferation while its overexpression promoted tumor

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Habel, Nadia, Najla El-Hachem, Frédéric Soysouvanh, et al. "FBXO32 links ubiquitination to epigenetic reprograming of melanoma cells." Cell Death & Differentiation 28, no. 6 (2021): 1837–48. http://dx.doi.org/10.1038/s41418-020-00710-x.

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AbstractUbiquitination by serving as a major degradation signal of proteins, but also by controlling protein functioning and localization, plays critical roles in most key cellular processes. Here, we show that MITF, the master transcription factor in melanocytes, controls ubiquitination in melanoma cells. We identified FBXO32, a component of the SCF E3 ligase complex as a new MITF target gene. FBXO32 favors melanoma cell migration, proliferation, and tumor development in vivo. Transcriptomic analysis shows that FBXO32 knockdown induces a global change in melanoma gene expression profile. Thes

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Saiga, Toru, Takaichi Fukuda, Masaki Matsumoto, et al. "Fbxo45 Forms a Novel Ubiquitin Ligase Complex and Is Required for Neuronal Development." Molecular and Cellular Biology 29, no. 13 (2009): 3529–43. http://dx.doi.org/10.1128/mcb.00364-09.

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ABSTRACT Fbxo45 is an F-box protein that is restricted to the nervous system. Unlike other F-box proteins, Fbxo45 was found not to form an SCF complex as a result of an amino acid substitution in the consensus sequence for Cul1 binding. Proteomics analysis revealed that Fbxo45 specifically associates with PAM (protein associated with Myc), a RING finger-type ubiquitin ligase. Mice deficient in Fbxo45 were generated and found to die soon after birth as a result of respiratory distress. Fbxo45 − / − embryos show abnormal innervation of the diaphragm, impaired synapse formation at neuromuscular j

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Wang, Ning, Qian Song, Hai Yu та Gang Bao. "Overexpression of FBXO17 Promotes the Proliferation, Migration and Invasion of Glioma Cells Through the Akt/GSK-3β/Snail Pathway". Cell Transplantation 30 (1 січня 2021): 096368972110073. http://dx.doi.org/10.1177/09636897211007395.

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FBXO17 is a newly studied F-box protein associated with high-grade glioma. However, its exact role in glioma remains unclear. In the present study, we aimed to investigate the role of FBXO17 in glioma both in vitro and in vivo and explore the underlying mechanism. Our results showed that FBXO17 mRNA and protein levels were upregulated in glioma cells including U87, U251, SHG44, and U-118-MG cells as compared to the HA1800 cells. Downregulation of FBXO17 significantly suppressed the cellular behaviors of glioma cells including cell proliferation, migration, and invasion. In addition, FBXO17 kno

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Choppara, Srinadh, Sunil K. Malonia, Ganga Sankaran, Michael R. Green, and Manas Kumar Santra. "Degradation of FBXO31 by APC/C is regulated by AKT- and ATM-mediated phosphorylation." Proceedings of the National Academy of Sciences 115, no. 5 (2018): 998–1003. http://dx.doi.org/10.1073/pnas.1705954115.

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The F-box protein FBXO31 is a tumor suppressor that is encoded in 16q24.3, for which there is loss of heterozygosity in various solid tumors. FBXO31 serves as the substrate-recognition component of the SKP/Cullin/F-box protein class of E3 ubiquitin ligases and has been shown to direct degradation of pivotal cell-cycle regulatory proteins including cyclin D1 and the p53 antagonist MDM2. FBXO31 levels are normally low but increase substantially following genotoxic stress through a mechanism that remains to be determined. Here we show that the low levels of FBXO31 are maintained through proteasom

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Sahasrabuddhe, Anagh Anant, Xiaofei Chen, Kaiyu Ma, et al. "A Novel FBXO45-Gef-H1 Axis Controls Oncogenic Signaling in B-Cell Lymphoma." Blood 138, Supplement 1 (2021): 711. http://dx.doi.org/10.1182/blood-2021-151245.

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Abstract Introduction: Diffuse large B cell lymphoma (DLBCL) is the most common form of malignant lymphoma and may arise de novo, or through transformation from a pre-existing low-grade B cell lymphoma such as follicular lymphoma (FL). However, the post-translational mechanisms and deregulated pathways underlying the pathogenesis of disease evolution are not fully understood. Methods: We employed integrated functional and structural genomics and mass spectrometry (MS)-driven proteomics which implicated a possible novel tumor suppressor role for a conserved E3 ubiquitin ligase FBXO45 in DLBCL p

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Xin, Ye, Xiaowen Chen, Mengli Zhang, et al. "Ubiquitin-Mediated Degradation of MORF4L1 By FBXO11 Suppresses Cholesterol Biosynthesis in T Cell Acute Lymphoblastic Leukemia." Blood 142, Supplement 1 (2023): 4148. http://dx.doi.org/10.1182/blood-2023-184388.

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The substrate receptor of SKP1-Cullin1-FBOX complex, FBXO11, is frequently mutated in both diffuse large B cell lymphoma and acute myeloid leukemia, and typically functions as a tumor suppressor by targeting substrates for ubiquitin-mediated degradation. Although FBXO11 is also mutated in human T-cell acute lymphoblastic leukemia (T-ALL) cell lines, the underlying mechanism in T-ALL development remains to be established. Here, we identified that both endogenous activation and exogenous overexpression of FBXO11 could suppress the growth of T-ALL cell in vitro and in vivo. While conversely, loss

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Hatayama, Yasuyoshi, Kei Miyakawa, Yayoi Kimura, et al. "Identification of Putative Serum Autoantibodies Associated with Post-Acute Sequelae of COVID-19 via Comprehensive Protein Array Analysis." International Journal of Molecular Sciences 26, no. 4 (2025): 1751. https://doi.org/10.3390/ijms26041751.

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Post-acute sequelae of SARS-CoV-2 infection (PASC), commonly known as “Long COVID”, represents a significant clinical challenge characterized by persistent symptoms following acute COVID-19 infection. We conducted a comprehensive retrospective cohort study to identify serum autoantibody biomarkers associated with PASC. Initial screening using a protein bead array comprising approximately 20,000 human proteins identified several candidate PASC-associated autoantibodies. Subsequent validation by enzyme-linked immunosorbent assay (ELISA) in an expanded cohort—consisting of PASC patients, non-PASC

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Brewer, Kelly, Isabel Nip, Justin Bellizzi, Jessica Costa-Guda, and Andrew Arnold. "Molecular analysis of cyclin D1 modulators PRKN and FBX4 as candidate tumor suppressors in sporadic parathyroid adenomas." Endocrine Connections 10, no. 3 (2021): 302–8. http://dx.doi.org/10.1530/ec-21-0055.

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Objective Primary hyperparathyroidism is most often caused by a sporadic single-gland parathyroid adenoma (PTA), a tumor type for which cyclin D1 is the only known and experimentally validated oncoprotein. However, the molecular origins of its frequent overexpression have remained mostly elusive. In this study, we explored a potential tumorigenic mechanism that could increase cyclin D1 stability through a defect in molecules responsible for its degradation. Methods We examined two tumor suppressor genes known to modulate cyclin D1 ubiquitination, PRKN and FBXO4 (FBX4), for evidence of classic

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Pighi, Chiara, Mara Compagno, Qi Wang, et al. "FBXO11, a Regulator of BCL6 Stability, Is Recurrently Mutated in Burkitt Lymphoma." Blood 126, no. 23 (2015): 3673. http://dx.doi.org/10.1182/blood.v126.23.3673.3673.

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Abstract INTRODUCTION: We recently described inactivating mutations of the FBXO11 gene in Diffuse Large B Cell Lymphoma (DLBCL). One major function of FBXO11 is to regulate BCL6 stability as well as other targets such as SNAIL. BCL6 acts as an oncogene in several human B-cell lymphomas and its expression levels can be increased by several mechanisms including chromosomal translocations, point mutations in the promoter region and reduced degradation by inactivation of FBXO11. Thus, FBXO11 acts as an oncosuppressor in DLBCL by promoting the accumulation of BCL6. However, a clear and complete pic

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Li, Yunfeng, Kai Jin, Eric Bunker, et al. "Structural basis of the phosphorylation-independent recognition of cyclin D1 by the SCFFBXO31 ubiquitin ligase." Proceedings of the National Academy of Sciences 115, no. 2 (2017): 319–24. http://dx.doi.org/10.1073/pnas.1708677115.

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Ubiquitin-dependent proteolysis of cyclin D1 is associated with normal and tumor cell proliferation and survival. The SCFFBXO31 (Skp1–Cul1–Rbx1–FBXO31) ubiquitin ligase complex mediates genotoxic stress-induced cyclin D1 degradation. Previous studies have suggested that cyclin D1 levels are maintained at steady state by phosphorylation-dependent nuclear export and subsequent proteolysis in the cytoplasm. Here we present the crystal structures of the Skp1–FBXO31 complex alone and bound to a phosphorylated cyclin D1 C-terminal peptide. FBXO31 possesses a unique substrate-binding domain consistin

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von Danwitz, Marthe, Niklas Klümper, Marit Bernhardt, et al. "Identification of F-Box/SPRY Domain-Containing Protein 1 (FBXO45) as a Prognostic Biomarker for TMPRSS2–ERG-Positive Primary Prostate Cancers." Cancers 15, no. 6 (2023): 1890. http://dx.doi.org/10.3390/cancers15061890.

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Background: F-box/SPRY domain-containing protein 1 (FBXO45) plays a crucial role in the regulation of apoptosis via the ubiquitylation and degradation of specific targets. Recent studies indicate the prognostic potential of FBXO45 in several cancers. However, its specific role in prostate carcinoma remains unclear. Methods: A systematic analysis of FBXO45 mRNA expression in PCA was performed using The Cancer Genome Atlas database and a publicly available Gene Expression Omnibus progression PCA cohort. Subsequently, FBXO45 protein expression was assessed via immunohistochemical analysis of a co

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Xu, Ke, Qin Liu, Wushuang Huang, et al. "Promotive Effect of FBXO32 on the Odontoblastic Differentiation of Human Dental Pulp Stem Cells." International Journal of Molecular Sciences 24, no. 9 (2023): 7708. http://dx.doi.org/10.3390/ijms24097708.

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Odontoblastic differentiation of human dental pulp stem cells (hDPSCs) is crucial for the intricate formation and repair processes in dental pulp. Until now, the literature is not able to demonstrate the role of ubiquitination in the odontoblastic differentiation of hDPSCs. This study investigated the role of F-box-only protein 32 (FBXO32), an E3 ligase, in the odontoblastic differentiation of hDPSCs. The mRNA expression profile was obtained from ribonucleic acid sequencing (RNA-Seq) data and analyzed. Immunofluorescence and immunohistochemical staining identify the FBXO32 expression in human

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Liu, Yaqian, Bo Pan, Weikun Qu, Yilong Cao, Jun Li, and Haidong Zhao. "Systematic analysis of the expression and prognosis relevance of FBXO family reveals the significance of FBXO1 in human breast cancer." Cancer Cell International 21, no. 1 (2021). http://dx.doi.org/10.1186/s12935-021-01833-y.

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Abstract Background Breast cancer (BC) remains a prevalent and common form of cancer with high heterogeneity. Making efforts to explore novel molecular biomarkers and serve as potential disease indicators, which is essential to effectively enhance the prognosis and individualized treatment of BC. FBXO proteins act as the core component of E3 ubiquitin ligase, which play essential regulators roles in multiple cellular processes. Recently, research has indicated that FBXOs also play significant roles in cancer development. However, the molecular functions of these family members in BC have not b

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Fischer, Maximillian, Moritz Jakab, Marc N. Hirt, Tessa R. Werner, Stefan Engelhardt, and Antonio Sarikas. "Identification of hypertrophy-modulating Cullin-RING ubiquitin ligases in primary cardiomyocytes." Frontiers in Physiology 14 (March 8, 2023). http://dx.doi.org/10.3389/fphys.2023.1134339.

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Cullin-RING ubiquitin ligases (CRL) regulate numerous biological processes in the heart and have been implicated in regulating cardiac hypertrophy. This study aimed to identify novel hypertrophy-modulating CRLs in cardiomyocytes (CM). A functional genomic approach using siRNA-mediated depletion and automated microscopy was employed to screen for cell size-modulating CRLs in neonatal rat CM. Screening hits were confirmed by 3H-isoleucine incorporation. Of 43 targets screened, siRNA-mediated depletion of Fbxo6, Fbxo45, and Fbxl14 resulted in decreased cell size, whereas depletion of Fbxo9, Fbxo2

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Zheng, Yunlong, Bingbing Wu, Fucheng Dong, et al. "FBXO24 targets SLC25A26 for K6-linked polyubiquitination to maintain mitochondrial function during spermiogenesis." Development, July 14, 2025. https://doi.org/10.1242/dev.204761.

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Asthenozoospermia is one of the major causes for male infertility, typically resulting from malformed flagella and dysfunctional mitochondria. However, the pathogenic mechanisms underlying asthenozoospermia remain unclear. Here, we show an F-box protein within the SCF E3 ubiquitin ligase complex, FBXO24, is required for maintaining mitochondrial function and ATP production during spermiogenesis. Using Fbxo24 knockout mice, we demonstrated that the depletion of FBXO24 leads to male infertility due to malformed sperm head and severe motility defects. The decreased motility comes from dysfunction

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Li, Zhiming, Xingping Liu, Yan Zhang, Yuanyuan Li, Liquan Zhou, and Shuiqiao Yuan. "FBXO24 modulates mRNA alternative splicing and MIWI degradation and is required for normal sperm formation and male fertility." eLife 12 (March 12, 2024). http://dx.doi.org/10.7554/elife.91666.3.

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Spermiogenesis is a critical, post-meiotic phase of male gametogenesis, in which the proper gene expression is essential for sperm maturation. However, the underFlying molecular mechanism that controls mRNA expression in the round spermatids remains elusive. Here, we identify that FBXO24, an orphan F-box protein, is highly expressed in the testis of humans and mice and interacts with the splicing factors (SRSF2, SRSF3, and SRSF9) to modulate the gene alternative splicing in the round spermatids. Genetic mutation of FBXO24 in mice causes many abnormal splicing events in round spermatids, thus a

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Zhang, Yalu, Qiaofei Liu, Ming Cui, et al. "Comprehensive Analysis of Expression, Prognostic Value, and Immune Infiltration for Ubiquitination-Related FBXOs in Pancreatic Ductal Adenocarcinoma." Frontiers in Immunology 12 (January 3, 2022). http://dx.doi.org/10.3389/fimmu.2021.774435.

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Pancreatic ductal adenocarcinoma (PDAC) is one of the most refractory human malignancies. F-box only proteins (FBXO) are the core components of SKP1-cullin 1-F-box E3 ubiquitin ligase, which have been reported to play crucial roles in tumor initiation and progression via ubiquitination-mediated proteasomal degradation. However, the clinical implications and biological functions of FBXOs in PDAC have not been fully clarified. Herein we perform a comprehensive analysis for the clinical values and functional roles of FBXOs in PDAC using different public databases. We found that FBXO1 (CCNF), FBXO

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Dong, Bo, Xiang Song, Xinzhao Wang, et al. "FBXO24 suppresses breast cancer tumorigenesis by targeting LSD1 for Ubiquitination." Molecular Cancer Research, August 4, 2023. http://dx.doi.org/10.1158/1541-7786.mcr-23-0169.

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Abstract LSD1, a critical chromatin modulator, functions as an oncogene by demethylation of H3K4me1/2. The stability of LSD1 is governed by a complex and intricate process involving ubiquitination and deubiquitination. Several deubiquitinases preserve LSD1 protein levels. However, the precise mechanism underlying the degradation of LSD1, which could mitigate its oncogenic function remains unknown. To gain a better understanding of LSD1 degradation, we conducted an unbiased siRNA screening targeting all the human SCF family E3 ligases. Our screening identified FBXO24 as a genuine E3 ligase that

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Johnson, Benjamin S., Daniela Farkas, Rabab El-Mergawy, et al. "Targeted degradation of extracellular mitochondrial aspartyl-tRNA synthetase modulates immune responses." Nature Communications 15, no. 1 (2024). http://dx.doi.org/10.1038/s41467-024-50031-7.

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AbstractThe severity of bacterial pneumonia can be worsened by impaired innate immunity resulting in ineffective pathogen clearance. We describe a mitochondrial protein, aspartyl-tRNA synthetase (DARS2), which is released in circulation during bacterial pneumonia in humans and displays intrinsic innate immune properties and cellular repair properties. DARS2 interacts with a bacterial-induced ubiquitin E3 ligase subunit, FBXO24, which targets the synthetase for ubiquitylation and degradation, a process that is inhibited by DARS2 acetylation. During experimental pneumonia, Fbxo24 knockout mice e

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Korec, Evžen, Lenka Ungrová, Jiří Hejnar, and Adéla Grieblová. "Four novel genes associated with longevity found in Cane corso purebred dogs." BMC Veterinary Research 18, no. 1 (2022). http://dx.doi.org/10.1186/s12917-022-03290-9.

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Abstract Background Longevity-related genes have been found in several animal species as well as in humans. The goal of this study was to perform genetic analysis of long-lived Cane corso dogs with the aim to find genes that are associated with longevity. Results SNPs with particular nucleotides were significantly overrepresented in long-lived dogs in four genes, TDRP, MC2R, FBXO25 and FBXL21. In FBXL21, the longevity-associated SNP localises to the exon. In the FBXL21 protein, tryptophan in long-lived dogs replaced arginine present in reference dogs. Conclusions Four SNPs associated with long

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