Relevant bibliographies by topics / FBXO24

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  2. Dissertations / Theses
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  5. Conference papers

Academic literature on the topic 'FBXO24'

Author: Grafiati
Published: 11 March 2023
Last updated: 31 July 2025

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Journal articles on the topic "FBXO24"

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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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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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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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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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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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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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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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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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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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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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Dissertations / Theses on the topic "FBXO24"

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Medeiros, Ana Carla. "Caracterização parcial do complexo SCF1 contendo a proteína FBXO25 fosforilada." Universidade de São Paulo, 2015. http://www.teses.usp.br/teses/disponiveis/17/17131/tde-09092015-110529/.

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A FBXO25 é parte de uma E3 ligase do tipo RING, (Really Interesting New Gene), oligomérica do tipo SCF, responsável pelo reconhecimento específico do substrato a ser degradado via Sistema Ubiquitina-Proteassoma (SUP). O SUP é o principal mecanismo proteolítico intracelular, responsável pela degradação de 80-90% das proteínas citosólicas e nucleares. A FBXO25 é capaz de formar um complexo SCF1 ativo (formado pela interação das proteínas Skp1, Cul1, Roc1 e uma proteína do tipo F-box), capaz de ubiquitinar seus substratos. Essa proteína se acumula no núcleo celular formando uma nova estrutura sub
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Vieira, Nichelle Antunes. "Caracterização de células humanas Hap1 nocaute para FBXO25: via de sinalização da ERK quinase e proliferação celular." Universidade de São Paulo, 2017. http://www.teses.usp.br/teses/disponiveis/17/17131/tde-25042018-143544/.

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A proteína FBXO25 é uma E3-ligase do tipo SCF, responsável pela seletividade da ligação da Ub à proteína substrato e pelo direcionamento da proteína marcada para o barril proteassomal 26s. Sabe-se que FBXO25 é capaz de interagir e ubiquitinar a proteína Elk-1 em células HEK293T e, assim, inibir a expressão de genes importantes na regulação da proliferação celular, como C-FOS e EGR-1, após estímulo com o mitógeno PMA. Aqui mostramos que FBXO25 atua em um outro ponto da via das MAPKs, modulando os níveis de fosforilação de ERK1/2. Por meio da utilização de células nocaute para FBXO25 (FBXO25KO)
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Tsui, Hoyee. "The role of p21-activated kinase 1 (Pak1) in the heart." Thesis, University of Manchester, 2015. https://www.research.manchester.ac.uk/portal/en/theses/the-role-of-p21activated-kinase-1-pak1-in-the-heart(8c34d7bc-a2aa-4ae0-a197-91ed905212f5).html.

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Heart failure is associated with a high mortality rate and is one of the most prevalent diseases worldwide whereby susceptibility increases with age. The development of heart failure occurs over an extensive period of time in which arrhythmias and hypertrophy are both very prevalent manifestations throughout this progression. Arrhythmias are defined as an irregular rhythm originating from intracellular calcium dysregulation, which can be fatal. Cardiac hypertrophy is a compensatory condition induced by increased workload involving augmented cardiomyocyte growth accompanied by myocardial remode
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Stavropoulou, Alexandra Vassiliki. "Histone deacetylase (HDAC) inhibitors and FBXL20 in breast cancer." Thesis, Imperial College London, 2008. http://hdl.handle.net/10044/1/7389.

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Research performed over the last decade has highlighted the role of HDAC inhibitors (HDACis) as modulators of transcriptional activity and as a potential new class of therapeutic agents against many types of malignacies including breast cancer. These drugs inhibit histone deacetylases, leading to derepression of transcription of various genes that are important for cell cycle arrest and cell death. Trichostatin A (TSA) is one of the best established HDAC inhibitors and has been shown to exhibit potent differentiating and anti-proliferative properties. My data demonstrated that treatment of the
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Patel, Shachi. "Fbxo7 in T cell development and oncogenesis." Thesis, University of Cambridge, 2015. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.709293.

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Rowicka, Paulina Aiko. "The role of FBXO7 in mitochondrial biology and Parkinson's disease." Thesis, University of Cambridge, 2018. https://www.repository.cam.ac.uk/handle/1810/282989.

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Parkinson's disease is a progressive neurodegenerative disorder of the central nervous system, manifesting with both motor and non-motor symptoms. Autosomal recessive mutations in the FBXO7 gene have been identified to cause a rapidly progressing early-onset form of PD. Canonically, FBXO7 functions as a substrate-recruiting subunit of the SCF-type E3 ubiquitin ligase. However, it also has a variety of other atypical functions, such as cell cycle regulation, proteasome regulation, and mitophagy. The overall aim of this research was to characterise the functional role of FBXO7 in various in vitr
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Sammler, Esther. "Signalling pathway of FBXO7 and its role in hereditary Parkinsonism." Thesis, University of Dundee, 2014. https://discovery.dundee.ac.uk/en/studentTheses/2a2889b3-20b5-4353-af11-72782c07ef3a.

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Parkinson’s Disease (PD) is the second most common neurodegenerative disorder after Alzheimer’s and old age is the strongest risk factor for developing PD. PD has traditionally been seen as a motor disorder, but its non-motor symptoms such as dysautonomia, sensory dysfunction, sleeping problems and neuropsychiatric features equally add to the disease burden. There is no cure for PD and this is probably a reflection of our poor understanding of the disease pathogenesis. One way of tackling this is to focus on the small, but significant number of PD patients with a family history compatible with
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Liu, Jia, and 劉佳. "Role of FBXO31 in regulating MAPK-mediated genotoxic stress response and cancer cell survival." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2013. http://hdl.handle.net/10722/205657.

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Esophageal cancer is the third most common digestive tract malignancy. Along with surgery, genotoxic drugs (e.g. cisplatin) and radiotherapy are the mainstays of treatment for this disease. Environmental factors and environmental stress-induced responses contribute to esophageal tumorigenesis and chemoresistance. Studying key molecules in stress-induced signal pathway can help unravel the underlying mechanisms and discover rational therapeutic targets. Cyclin D1 is DNA damage response protein. Genotoxic stress induces rapid cyclin D1 degradation and the molecules mediating this response are
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Kleppa, Marc-Jens [Verfasser]. "Charakterisierung des Gens Fbxl22 und seiner Funktion während der Muskelentwicklung der Maus / Marc-Jens Kleppa." Hannover : Technische Informationsbibliothek und Universitätsbibliothek Hannover (TIB), 2011. http://d-nb.info/1019235071/34.

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Shang, Jinsai. "STRUCTURAL AND FUNCTIONAL STUDIES OF F-BOX-ONLY PROTEIN FBXO7 AND ITS INTERACTIONS WITH PROTEASOME INHIBITOR PI31." OpenSIUC, 2015. https://opensiuc.lib.siu.edu/dissertations/1053.

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F-box only protein 7 (Fbxo7), a member of the F-box-only subfamily of FBPs, is a biologically and pathophysiologically important human protein that assumes many critical functions. The different functions of Fbxo7 depend on the formation of various multi-protein complexes. Possible interplay between different Fbxo7 functions further complicate the protein-protein interaction networks involved in Fbxo7 biology. Although significant progresses have been made to understand the functions, regulation, specificity, and protein interaction network of Fbxo7, a myriad of questions remain to be answere
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Books on the topic "FBXO24"

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Haydu, Julie Erika M. The Roles of F-box and Leucine-Rich Repeat Protein 4 (FBXL4) in Mitochondrial Encephalopathy and T-cell Acute Lymphoblastic Leukemia. [publisher not identified], 2015.

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Book chapters on the topic "FBXO24"

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Morton, Sarah U., Edward G. Neilan, Roy W. A. Peake, et al. "Hyperammonemia as a Presenting Feature in Two Siblings with FBXL4 Variants." In JIMD Reports. Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/8904_2016_17.

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Antoun, Ghadi, Skye McBride, Jason R. Vanstone, et al. "Detailed Biochemical and Bioenergetic Characterization of FBXL4-Related Encephalomyopathic Mitochondrial DNA Depletion." In JIMD Reports. Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/8904_2015_491.

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Guo, Jianping, Brian J. North, Adriana E. Tron, Hiroyuki Inuzuka, and Wenyi Wei. "The Role of FBXO Subfamily of F-box Proteins in Tumorigenesis." In SCF and APC E3 Ubiquitin Ligases in Tumorigenesis. Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-05026-3_4.

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Madduri, Lepakshe S. V., Alison L. Camero, Keith R. Johnson, Michel M. Ouellette, and Ying Yan. "p53 Negatively Regulates the PR55α Subunit of PP2A Ser/Thr Phosphatase Via FBXL20-mediated Proteasomal Degradation." In Achievements and Challenges of Medicine and Medical Science Vol. 3. BP International, 2024. http://dx.doi.org/10.9734/bpi/acmms/v3/2910.

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Conference papers on the topic "FBXO24"

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Johnson, B., D. Farkas, R. Elmergawy, et al. "Degradation of Mitochondrial Aspartyl-TRNA Synthetase (DARS2) by the Ubiquitin E3 Ligase Subunit FBXO24 Impacts Innate Immunity in Experimental Pneumonia." In American Thoracic Society 2024 International Conference, May 17-22, 2024 - San Diego, CA. American Thoracic Society, 2024. http://dx.doi.org/10.1164/ajrccm-conference.2024.209.1_meetingabstracts.a6642.

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Johnson, B., D. Farkas, R. El-Mergawy, J. D. Londino, and R. K. Mallampalli. "The Novel E3-ligase F-box Only Protein 24 (fbxo24) Is Induced By Bacterial Infection And Suppresses Mitochondrial Function In Epithelial Cells." In American Thoracic Society 2023 International Conference, May 19-24, 2023 - Washington, DC. American Thoracic Society, 2023. http://dx.doi.org/10.1164/ajrccm-conference.2023.207.1_meetingabstracts.a1263.

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Elmergawy, R., L. Chafin, J. D. Londino, J. Adair, and R. K. Mallampalli. "Regulation of Forkhead Box K2 (foxk2) By the E3-ligase F-box Only Protein 24 (fbxo24) Leads to Its Ubiquitination and Degradation in Lung Epithelia." In American Thoracic Society 2023 International Conference, May 19-24, 2023 - Washington, DC. American Thoracic Society, 2023. http://dx.doi.org/10.1164/ajrccm-conference.2023.207.1_meetingabstracts.a5693.

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Aryal, Sadikshya, Harrison J. McNabb, and Benita Sjogren. "Discovery and Validation of RGS2-FBXO44 Protein-Protein Interaction Inhibitors." In ASPET 2023 Annual Meeting Abstracts. American Society for Pharmacology and Experimental Therapeutics, 2023. http://dx.doi.org/10.1124/jpet.122.164970.

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McNabb, Harrison, Eugene Cho, Phillip Rushton, Mary Pitman, David Mobley, and Benita Sjogren. "Determining molecular characteristics of the RGS2-FBXO44 interaction – A multipronged approach." In ASPET 2024 Annual Meeting Abstract. American Society for Pharmacology and Experimental Therapeutics, 2024. http://dx.doi.org/10.1124/jpet.163.128664.

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Ravindranath, Abhilash K., Swayamjot Kaur, and Lorna Rodriguez. "Abstract 4226: CD44 increases drug resistance by protecting FBXO21 mediated ubiquitination of P-glycoprotein." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-4226.

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Tsai, M. J., W. Osman, A. Elhance, et al. "FBXO45 Targets IFNLR1 to Impair IFN-lambda Signaling During Influenza Infection." In American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a3622.

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Nelson, David E., and Heike Laman. "Abstract 2961: Spatiotemporal regulation of the SCF ubiquitin ligase component, Fbxo7." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-2961.

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Katayama, Kazuhiro, Kohji Noguchi, Junko Mitsuhashi, and Yoshikazu Sugimoto. "Abstract 810: FBXO15 is an F-box protein in E3 ligase complex for P-glycoprotein." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-810.

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Lu, Jianrong, Yue Jin, Anitha K. Shenoy, et al. "Abstract 1425: FBXO11 suppresses epithelial plasticity and proliferation by ubiquitinating the Snail family of transcription factors." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-1425.

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