Tesis sobre el tema "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/.
Texto completoThe FBXO25 is an E3 ligase RING type (Really Interesting New Gene), SCF oligomeric type, responsible for the specific recognition of the substrate to be degraded via the ubiquitin-proteasome system (SUP). SUP is the main intracellular proteolytic mechanism responsible for 80-90% degradation of cytosolic and nuclear proteins. The FBXO25 is capable of forming a complex SCF1 (formed by the interaction of proteins Skp1, Cul1, Roc1 protein and a type F-box), resulting in an active SCF complex which is able to ubiquitinate their substrates. This protein accumulates in the nucleus forming a subnuclear structure called FANDs (FBXO25 Associated Nuclear Domains) that are involved in nuclear ubiquitination. In this work, we purify complex SCF1 (WT or F- box, which is not able to interact with Skp1), treated or not with PMA, by immunoprecipitation technique. We identified by mass spectrometry, an essential phosphorylation site for FBXO25, when it is phosphorylated under the action of the mitogenic reagent PMA. We also search for differentially ubiquitinated substrates for these complexes, by testing in ProtoArrays® identifying substrates involved in the signaling pathway ERK1 / 2.
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/.
Texto completoThe FBXO25 protein is an SCF-type E3-ligase responsible for the selectivity of Ub binding to the protein and the targeting of the labeled protein to the 26s proteasome barrel. FBXO25 has been long known to be able to interact and ubiquitinate the Elk-1 protein in HEK293T cells, thereby inducing a decrease in the expression of important genes in the regulation of cell proliferation such as CFOS and EGR-1 after stimulation with the mitogen PMA. Here we show that FBXO25 acts at another point in the MAPK pathway by modulating the ERK1/2 phosphorylation levels. We observed that the treatment with PMA rised the phosphorylated levels of ERK1/2 in knockout cells for FBXO25 (FBXO25KO) when compared to its parental lineage. Stimulation with the mitogens PMA or ATP also led to an increase in cell proliferation unrelated to a direct modulation of the cell cycle in knockout cells, with a significant weight of apoptosis levels being observed. Taking these results together, we show that FBXO25 acts on MAPK signaling by reducing ERK1/2 activation and thus promotes a secondary response on the cell proliferation phenotype.
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.
Texto completoStavropoulou, Alexandra Vassiliki. "Histone deacetylase (HDAC) inhibitors and FBXL20 in breast cancer". Thesis, Imperial College London, 2008. http://hdl.handle.net/10044/1/7389.
Texto completoPatel, Shachi. "Fbxo7 in T cell development and oncogenesis". Thesis, University of Cambridge, 2015. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.709293.
Texto completoRowicka, 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.
Texto completoSammler, 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.
Texto completoLiu, Jia y 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.
Texto completopublished_or_final_version
Anatomy
Doctoral
Doctor of Philosophy
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.
Texto completoShang, 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.
Texto completoHorn, Moritz [Verfasser], Adam [Akademischer Betreuer] Antebi, Thorsten [Akademischer Betreuer] Hoppe y Günter [Akademischer Betreuer] Schwarz. "Coordination of Developmental Timing and Maturation by the F-box Protein DRE-1/FBXO11 / Moritz Horn. Gutachter: Adam Antebi ; Thorsten Hoppe ; Günter Schwarz". Köln : Universitäts- und Stadtbibliothek Köln, 2014. http://d-nb.info/1055038620/34.
Texto completoMukherjee, Chaitali [Verfasser], Judith [Akademischer Betreuer] Stegmüller y Mikael [Akademischer Betreuer] Simons. "Functional analysis of the CNS-specific F-box protein FBXO41 in cerebellar development / Chaitali Mukherjee. Betreuer: Judith Stegmüller. Gutachter: Judith Stegmüller ; Mikael Simons". Göttingen : Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2015. http://d-nb.info/1077913818/34.
Texto completoSimon-Kayser, Barbara. "Identification d'un gène humain localisé en 17q12, codant pour un membre de la famille F-box (Fbxo47) : étude des caractéristiques de la protéine". Nantes, 2006. http://archive.bu.univ-nantes.fr/pollux/show.action?id=9ed39bb9-3443-422a-a221-ce1ddba667f4.
Texto completoGenetic alterations of chromosome arm 17q occur in numerous tumor types, including papillary renal cell carcinoma (pRCC). It suggests the presence of a tumor suppressor gene on the long arm of chromosome 17, which is critical for carcinogenesis. In this study, we analyzed 15 cases of pRCC for LOH. We identified a minimal deleted region in which the D17S250 marker (17q12). We isolated the cDNA of a novel gene named FBXO47. FBXO47 cDNA is preferentially expressed in normal tissue, particularly in the testis. The search of characteristic protein domains showed the presence of: a F-box domain, that we showed the functionality in vitro and in vivo; a Leucine-zipper; and a sequence of addressing mitochondrial. Most proteins of the family defined by the F-box motif belong to the ubiquitine-proteasome pathway. In order to determine the cellular function of Fbxo47, we sought to identify its protein partners. A screening in two- hybrid system enabled us to identify the protein Gfm1, the principal elongation factor of the mitochondrial translation. This thesis work represents indeed the first description of the presence of F-box system in mitochondrial matrix in human
Simon-Kayser, Barbara Bezieau Stéphane. "Identification d'un gène humain localisé en 17q12, codant pour un membre de la famille F-box (Fbxo47) étude des caractéristiques de la protéine /". [S.l.] : [s.n.], 2006. http://theses.univ-nantes.fr/thesemed/DOCsimon.pdf.
Texto completoVadhvani, Mayur [Verfasser], Judith [Akademischer Betreuer] Stegmüller, Klaus-Armin [Akademischer Betreuer] Nave y Till [Akademischer Betreuer] Marquardt. "The role of E3 ubiquitin ligase FBXO31-SCF in neuronal morphogenesis / Mayur Vadhvani. Gutachter: Judith Stegmüller ; Klaus-Armin Nave ; Till Marquardt. Betreuer: Judith Stegmüller". Göttingen : Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2013. http://d-nb.info/1044047453/34.
Texto completoSlimani, Samira. "Rôle de la protéine FBXW4 dans le complexe SCF et dans le développement du split hand/split foot malformation de type 3 (SHFM3)". Master's thesis, Université Laval, 2020. http://hdl.handle.net/20.500.11794/66675.
Texto completoProtein degradation, also known as proteolysis, is essential for cell function and survival. It is most often achieved through the ubiquitination of proteins, a process that allows the proteasome to recognize and cleave such proteins. In this project, I studied two clinical cases in which the protein F-box/WD repeat-containing protein 4 (FBXW4) was believed to play a role. Both patients suffered from a polymalformative syndrome characterized by an ectrodactyly called type 3 split hand/split foot malformation (SHFM3) and chronic renal failure. Both patients also bore a P376Q mutation in FBXW4. As previous studies was consistent with the possibility that FBXW4 was part of an ubiquitination complex, we hypothesized that the mutation affected the assembly of this complex and resulted in the observed clinical disorders. I therefore reproduced the mutation in vitro among others at this location and characterized the effects of such mutations in Xenopus laevis oocyte expression system. I found that FBXW4 was organized in homooligomers and that the nature of the residue of position 376 played a role in assembly of the FBXW4 containing complex. I also found that the nature of residue 376 affected the binding of FBXW4 to another protein in the complex, that is, to Skp1. These results allow us to draw the following conclusions: 1) the mutation identified affects the oligomeric assembly of FBXW4, 2) it is thus very likely to be causative, and 3) it could cause an ubiquitination disorder in which certain proteins are not properly degraded during development
Schwarz, Tobias. "Charakterisierung von humanem PI31 und neuen alternativen Spleißvarianten des PI31 Gens PSMF1". Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2009. http://dx.doi.org/10.18452/15919.
Texto completoThe ubiquitin–proteasome pathway is the major intracellular system for protein degradation. It plays an important role in the regulation of cellular processes like cell cycle control, signal transduction and gene transcription. The protein proteasome inhibitor 31 (PI31) was initially characterized as a potent inhibitor of proteasomal activity in vitro. Furthermore it was shown that PI31 modulates the assembly of the murine immunoproteasome (i20S). The function and regulation of PI31 in the human system is so far unexplored and therefore the topic of this study. It was shown that at least nine alternatively spliced variants of the PI31 gene PSMF1 exist additionally to the PI31 transcript. The PI31 isoforms V2 to V10 differ from PI31 (V1) in parts of the N-terminus and in a modified C-terminus. Only the isoform V5 is tissue specific expressed in testis and localized in the nucleus. After overexpression only the isoform V3 has the ability to inhibit the proteasomal activity in vivo. In contrast to the murine system neither PI31 nor the isoforms showed a modulatory effect on the assembly of the i20S. The overexpression of PI31 and V3 in human cells results instead in the accumulation and delayed degradation of proteasomal substrates. Furthermore the expression of human PI31 can be induced by virus associated stimuli like dsRNA and type I interferones. In addition, for the 3kb long 3’UTR of the PI31-mRNA an inhibitory effect on the expression and therefore a regulatory role was shown. Together with data from Kirk et al. (2008), who show the heterodimerization of PI31 with the F-box protein Fbxo7, the presented results suggest a function of PI31 and its isoforms in the process of ubiquitination of proteasomal substrates.
Dontcheva, Guergana Ivanova [Verfasser], Judith [Akademischer Betreuer] Stegmüller, Nils [Gutachter] Brose, Anastassia [Gutachter] Stoykova y Tiago Fleming [Gutachter] Outeiro. "Functional analysis of the parkinsonism-associated protein FBXO7 (PARK15) in neurons / Guergana Ivanova Dontcheva ; Gutachter: Nils Brose, Anastassia Stoykova, Tiago Fleming Outeiro ; Betreuer: Judith Stegmüller". Göttingen : Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2017. http://d-nb.info/1139491571/34.
Texto completoJoseph, Sabitha Lis [Verfasser], Judith [Akademischer Betreuer] Stegmüller, Judith [Gutachter] Stegmüller y Klaus-Armin [Gutachter] Nave. "A novel role for the E3 ubiquitin ligase FBXO7 in axonb-myelin interaction / Sabitha Lis Joseph ; Gutachter: Judith Stegmüller, Klaus-Armin Nave ; Betreuer: Judith Stegmüller". Göttingen : Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2018. http://d-nb.info/1160753474/34.
Texto completoBrockelt, David [Verfasser], Judith [Akademischer Betreuer] [Gutachter] Stegmüller y Tiago Fleming [Gutachter] Outeiro. "The role of the E3 ubiquitin ligase FBXO7-SCF in early-onset Parkinson's disease / David Brockelt. Betreuer: Judith Stegmüller. Gutachter: Judith Stegmüller ; Tiago Fleming Outeiro". Göttingen : Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2016. http://d-nb.info/1112736522/34.
Texto completoHolubowska, Anna [Verfasser], Judith [Akademischer Betreuer] Stegmüller, Hannelore [Akademischer Betreuer] Ehrenreich, André [Akademischer Betreuer] Fischer, Anastassia [Akademischer Betreuer] Stoykova, Andreas [Akademischer Betreuer] Wodarz y Ralf [Akademischer Betreuer] Heinrich. "Characterization of the CNS-specific F-box protein FBXO41 in cerebellar development / Anna Holubowska. Gutachter: Judith Stegmüller ; Hannelore Ehrenreich ; André Fischer ; Anastassia Stoykova ; Andreas Wodarz ; Ralf Heinrich. Betreuer: Judith Stegmüller". Göttingen : Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2014. http://d-nb.info/1051740568/34.
Texto completoBaumann, Ursula [Verfasser], Florian [Akademischer Betreuer] [Gutachter] Bassermann, Bernhard [Gutachter] Küster y Claus [Gutachter] Belka. "The role of the ubiquitin-proteasome system in the pathology and treatment of B-cell lymphoma : Characterization of the PRKCD-FBXO25-HAX1 axis in lymphomagenesis and treatment resistance of B-cell lymphoma / Ursula Baumann ; Gutachter: Bernhard Küster, Claus Belka, Florian Bassermann ; Betreuer: Florian Bassermann". München : Universitätsbibliothek der TU München, 2017. http://d-nb.info/1137010452/34.
Texto completoKirk, Rebecca Jane. "Structural and functional analysis of the proteasome inhibitor PI31 and its interaction with the F-box protein Fbxo 7". Thesis, University College London (University of London), 2005. http://discovery.ucl.ac.uk/1445730/.
Texto completoVingill, Siv [Verfasser], Judith [Akademischer Betreuer] Stegmüller, Thomas A. [Gutachter] Bayer, Tiago Fleming [Gutachter] Outeiro, Nils [Gutachter] Brose, Ralf [Gutachter] Heinrich y Thomas [Gutachter] Dresbach. "Characterization of FBXO7 (PARK15) knockout mice modeling Parkinsonian-Pyramidal Syndrome / Siv Vingill ; Gutachter: Thomas A. Bayer, Tiago Fleming Outeiro, Nils Brose, Ralf Heinrich, Thomas Dresbach ; Betreuer: Judith Stegmüller". Göttingen : Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2017. http://d-nb.info/1130400816/34.
Texto completoTargosz, Bianca-Sabrina [Verfasser], Florian C. [Akademischer Betreuer] Bassermann y Claus [Akademischer Betreuer] Schwechheimer. "The role of the SCF-Fbxo9 in the pathogenesis and therapy of Multiple Myeloma / Bianca-Sabrina Yvonne Targosz. Gutachter: Claus Schwechheimer ; Florian C. Bassermann. Betreuer: Florian C. Bassermann". München : Universitätsbibliothek der TU München, 2013. http://d-nb.info/1036495167/34.
Texto completoViñas, Castells Rosa. "Ubiquitin ligases involved in the regulation of Snail1". Doctoral thesis, Universitat Pompeu Fabra, 2013. http://hdl.handle.net/10803/145483.
Texto completoLa transició epiteli-mesènquima (per l’acrònim en anglès de: “epithelial to mesenchymal transition”, EMT) és un procés durant el qual cèl•lules epitelials adquireixen un fenotip mesenquimal. Està caracteritzat per la baixada de l’E-caderina, una proteïna de les unions adherents, i és important en el desenvolupament embrionari. L’expressió de Snail1 és suficient per desencadenar la EMT en cèl•lules en cultiu i s’ha trobat sobre-expressada en alguns càncers. Snail1 s’estabilitza tant a nivell de mRNA com de proteïna i en aquest projecte hem analitzat l’acció de les lligases d’ubiquitina que afecten els nivells de la proteïna. Apart de la ja descrita β-Trcp1, que degrada Snail1 de manera depenent a la fosforilació de Snail1 per GSK-3β, hem trobat les proteïnes F-box FBXL14 i FBXL5 con a noves lligases d’ubiquitina E3 que degraden Snail1. La FBXL14 és citoplasmàtica i els seus nivells disminueixen en hipòxia a través d’un mecanisme transcripcional. La FBXL5 és nuclear i modula tant la unió de Snail1 al DNA com la seva ubiquitinació nuclear. La proteïna FBXL5 es desestabilitza degut a la radiació gamma (γ) induint els nivells de Snail1.
陳映如. "A Study on the Institution of Working Time in Taiwan: Focusing on Working besides Regular Working Hours". Thesis, 2019. http://ndltd.ncl.edu.tw/handle/fbxe2q.
Texto completo國立政治大學
勞工研究所
107
As we view the revisal of the Labor Standard Act for the past few years, surely the issue of cutting down working time has become something that draws quite a few attentions. Even so, as confronting the actual need when it comes to operating a company, some exceptions are made besides the principles of regular working hours.However, while the Act has been revised, it seems like nothing has changed, people still work besides regular working hours, people still dispute about how to have their regular leave, and people still work overtime. In this article, the concept of working besides regular working hours has divided into two parts, which is a part that includes working besides regular hours and working on a rest day, and a part that includes working on a regular leave and working on a holiday. Due to the affection of the Act, these two parts will have different situation. The purpose of the article is to study the requirements base on the Act, and the affection and issue they cause. By using document analysis, with the assistance of comparative law, after the analysis, it is found that even though it shouldn’t be normal to work besides regular working hours, it is quite common for three reasons. First of all, the Act set the employer’s necessity as a reason, but the definition of necessity is questionable. Secondary, the Act makes a consent made by the labor union or a lobor-management conference as the approval of extending working hours, however, it may not occur restriction for individual labor, which may be favorable for employers. The third reason, which should be review and make improvement as soon as possible, is that there is no cleary specification for the requirement of working on a rest day. In addition, since it is possible to adjust regular leave or holiday, it opens up many disturbing situaions. Finally, it is found that when dealing with issues that contain extending working time by voluntary, the judicial authourities doesn’t have indentical views for the determination standard. Moreover, due to the calculation stardard which doesn’t indentical views for that as well, it causes issues of working exceed more than two calendar days.
Chen, Wan-Rou y 陳婉柔. "Genetic Study of Two Candidate Genes, FBXO25 and ARHGEF10, in Autism Spectrum Disorders". Thesis, 2012. http://ndltd.ncl.edu.tw/handle/26818068096871531634.
Texto completo慈濟大學
分子生物暨人類遺傳學系碩士班
100
Autism spectrum disorder (ASD) is a heterogeneous group of neurodevelopment disorders, it can be diagnosed before three years of age, the syndromes of ASD are defined by the damage of social interaction, abnormal development of speech and language, and highly restricted interests and stereotyped behavior. Previous studies showed that ASD are highly heritable, however, the disease causing genes are poorly known. We recently reported that using Array Comparative Genomic Hybridization analysis (array CGH), a boy with ASD who had a terminal deletion at the short arm of chromosome 8, was detected.The deletion region contains 23 genes. To further elucidate which genes might be associated with ASD, we investigated two genes in this study, i.e. F-box protein 25 (FBXO25) and the Rho guanine nucleotide exchange factor 10 (ARHGEF10). To investigate whether the FBXO25 and the ARHGEF10 are associated with ASD, we set out to screen mutations of these two genes in ASD. We used PCR-based direct sequencing to screen mutations at all the exonic regions of these two genes in 360 ASD patients and 400 controls. We identified a missense mutation R38H in the FBXO25 in one patient. In ARHGEF10 gene, we identified several missense mutations, including D96N, G118C, G187S, E189V, R275H, V700I, T970M, T1173S, I1241F, Y1282C, and R1320S. Five mutations, G118C, G187S, E189V, T970M and Y1282C, were only found in patients, but not in controls. Computer programs of PolyPhen and SIFT predict that G118C, R275H and T1173S mutations of ARHGEF10 gene are probably damaging. And only in SIFT, E189V was probably damaging. In ARHGEF10, E189V mutation had significant difference of genotype frequency and allele frequency of case-control analysis (genotype frequency, p=0.03, allele frequency, p=0.04). These mutations might be result in increased risk to ASD.
Vadhvani, Mayur. "The role of E3 ubiquitin ligase FBXO31-SCF in neuronal morphogenesis". Doctoral thesis, 2012. http://hdl.handle.net/11858/00-1735-0000-000D-F0CA-7.
Texto completoHolubowska, Anna. "Characterization of the CNS-specific F-box protein FBXO41 in cerebellar development". Doctoral thesis, 2013. http://hdl.handle.net/11858/00-1735-0000-0022-5ECB-7.
Texto completoHuang, Ting-Wei y 黃廷瑋. "Interaction of FBXL14 and a Schizophrenia Associated Gene DISC1 in Mouse Embryonic Brain". Thesis, 2014. http://ndltd.ncl.edu.tw/handle/95791312336805945594.
Texto completo國立臺灣大學
腦與心智科學研究所
103
Disrupted in Schizophrenia 1 (DISC1), first identified in human (Homo sapiens), is a disease-related gene that is associated with schizophrenia and other psychiatric disorders including bipolar disorder and autism spectrum disorders (Soares et al, 2011). DISC1 protein is known to be involved in neurodevelopment processes such as neuronal migration (Ishizuka et al, 2011) and neuronal progenitor proliferation (Singh et al, 2010). F-box and leucine-rich repeat protein 14 (FBXL14) is a subunit of E3 ubiquitin ligase complex involved in proteasome-mediated protein degradation (Cardozo et al, 2004). Preliminary data from our lab showed that mouse DISC1 (mDISC1) co-immunoprecipitates (co-IP) with mouse FBXL14 (mFBXL14), suggesting that these two proteins together may play a role in regulating neurodevelopment. To characterize the interaction of mDISC1 and mFBXL14, the deletion constructs of these two genes were prepared to define their respective interaction domains by co-IP assays. GST pull-down assay was also performed to address whether the interactions are via direct binding. Using in utero electroporation (IUEP), we found knock-down of mFbxl14 caused mouse embryonic cortical neurons gathering in the intermediate zone while knock-down of mDisc1 were reported to cause cortical neuron migration defects (Kamiya et al, 2005). How the interaction of mDISC1 and mFBXL14 may affect embryonic cortical neuronal migration and proliferation in vivo was also explored. Through these studies, the molecular basis of the interaction of mDISC1 and mFBXL14 was characterized, which provides insight into the developmental role of mDISC1 and mFBXL14 in the embryonic corticogenesis.
Mukherjee, Chaitali. "Functional analysis of the CNS-specific F-box protein FBXO41 in cerebellar development". Doctoral thesis, 2015. http://hdl.handle.net/11858/00-1735-0000-0023-9648-1.
Texto completoVingill, Siv. "Characterization of FBXO7 (PARK15) knockout mice modeling Parkinsonian-Pyramidal Syndrome". Doctoral thesis, 2016. http://hdl.handle.net/11858/00-1735-0000-0023-3E1B-6.
Texto completoDontcheva, Guergana Ivanova. "Functional analysis of the parkinsonism-associated protein FBXO7 (PARK15) in neurons". Doctoral thesis, 2017. http://hdl.handle.net/11858/00-1735-0000-0023-3EF5-7.
Texto completoChen, Ying-Lin y 陳映伶. "Investigating up-regulating FBXO7 expression as a preventive strategy for Parkinson's disease". Thesis, 2014. http://ndltd.ncl.edu.tw/handle/92758321094666163111.
Texto completo國立臺灣師範大學
生命科學研究所
102
Parkinson’s disease (PD), the second most common neurodegenerative disorder, is pathologically characterized by loss of dopaminergic neurons in the substantia nigra of the midbrain. Mutations in the F-box only protein 7 gene (FBXO7), the substrate-specifying subunit of Skp1-Cullin-F-Box (SCF) E3 ubiquitin ligase complex, cause PD-15 (PARK15). Previously we identified an amino acid changed variant Y52C in association with decreased risk of developing PD. Upon expression in cells, Y52C variant displayed significantly reduced rate of decay in cycloheximide chase experiment. The human FBXO7 gene promoter has not been analyzed. To investigate cis elements controlling FBXO7 expression, we cloned FBXO7 promoter fragments from -1240, -694, -538, -438, -202 and -56 to +261 by PCR amplification and placed in front of GFP reporter for transfection assay in HEK-293T cells. The expression of GFP was monitored by both high content analysis and flow cytometry. When the expressed GFP level of the -56~+261 promoter fragment was set as 100%, significantly increased FBXO7 promoter activity was observed with the -202~+261 and -694~+261 fragments by both methods. As the protective role of increased FBXO7 level in PD was implicated, Flp-In 293 cell line expressing GFP reporter driven by FBXO7 -694~+261 promoter fragment was constructed and used as a platform to screen herbal extracts provided by Industrial Technology Research Institute for enhancing FBXO7 expression. Herbal extracts NTNU-319, 379, 395 and 439 were found to increase endogenous FBXO7 protein expression in both Flp-In 293 and SH-SY5Y cells. Treatment of the above herbal extracts protected SH-SY5Y cells against MPP+-induced cell death. In addition, herbal extracts NTNU-319, 395 and 439 significantly alleviated MPP+-induced loss of mitochondrial membrane potential. As lack of treatment to prevent or slow PD progression, the proposed study may provide new insights into the therapeutic approach to PD.
Joseph, Sabitha Lis. "A novel role for the E3 ubiquitin ligase FBXO7 in axon-myelin interaction". Doctoral thesis, 2017. http://hdl.handle.net/11858/00-1735-0000-002E-E414-8.
Texto completoChou, Jian-Liang y 周建良. "The Role of Aberrant Epigenetic Alteration of the TGF-β Targets FBXO32 and ABCA1 In Ovarian Cancer". Thesis, 2013. http://ndltd.ncl.edu.tw/handle/19886517080024773013.
Texto completo國立中正大學
分子生物研究所
101
The Dysregulation of TGF-β signaling plays a key role in ovarian carcinogenesis and maintaining cancer stem cell properties. In this study, we utilized previous ChIP-chip, mDIP-chip, and expression array data to identify TGF-β/SMAD4 relative genes: FBXO32 and ABCA1. In the first part of study, we found that expression of FBXO32 was observed in normal ovarian surface epithelium but not in ovarian cancer cell lines. FBXO32 methylation was seen in ovarian cancer cell lines, and epigenetic drug treatment restored FBXO32 expression in ovarian cancer cell lines, suggesting that epigenetic modifications regulate the expression of this gene in ovarian cancer. In advanced stage ovarian tumors, significant (29.3%; p<0.05) methylation frequency of FBXO32 was observed and the association between FBXO32 methylation and shorter progression free survival was significant (Kaplan-Meier, p<0.05). Re-expression of FBXO32 markedly reduced proliferation of ovarian cancer line both in vitro and in vivo, due to increased apoptosis of the cells, and resensitized ovarian cancer cells to cisplatin. In the second part of the study, we identified ABCA1 by mDIP-Chip which was methylated in ovarian cancer cell line, A2780 and CP70. ABCA1 was expressed not only in IOSE, but in HeyC2, SKOV3, MCP3, and MCP2 ovarian cancer cell lines. In A2780 and CP70 ovarian cancer cell line, ABCA1 was down-regulated and was associated with promoter hypermethylation as demonstrated by bisulfite pyro-sequencing. Analysis of ABCA1 methylation in 8 normal OSE and 76 ovarian cancer patient samples demonstrated that patients with higher ABCA1 methylation is associated with high stage and high grade (p=0.0169 vs. p=0.0024). Importantly, patients with higher methylation of ABCA1 have shorter progression free survival (p=0.09) and overall survival (p=0.016). In conclusion, both of FBXO32 and ABCA1 were repressed by DNA methylation in ovarian cancer, and hypermethylation of them was associated with poor prognosis in cancer patients.
Brockelt, David. "The role of the E3 ubiquitin ligase FBXO7-SCF in early-onset Parkinson's disease". Doctoral thesis, 2015. http://hdl.handle.net/11858/00-1735-0000-0028-881A-3.
Texto completoHagens, Olivier [Verfasser]. "Search for genes involved in human cognition : molecular characterisation of two novel genes, FBXO25 and KIAA1202, disrupted by a translocation in a mentally retarded patient / vorgelegt Olivier Hagens". 2007. http://d-nb.info/985002883/34.
Texto completoNeilsen, Paul Matthew. "Functional analysis of ANKRD11 and FBXO31: two candidate tumour suppressor genes from the 16q24.3 breast cancer loss of heterozygosity region". 2008. http://hdl.handle.net/2440/59014.
Texto completohttp://proxy.library.adelaide.edu.au/login?url= http://library.adelaide.edu.au/cgi-bin/Pwebrecon.cgi?BBID=1325445
Thesis (Ph.D.) -- University of Adelaide, School of Medicine, Discipline of Medicine, 2008
Neilsen, Paul Matthew. "Functional analysis of ANKRD11 and FBXO31: two candidate tumour suppressor genes from the 16q24.3 breast cancer loss of heterozygosity region". Thesis, 2008. http://hdl.handle.net/2440/59014.
Texto completoThesis (Ph.D.) -- University of Adelaide, School of Medicine, Discipline of Medicine, 2008
Rizk, Rana. "Analyzing KDM4A protein interaction network using proximity-dependent biotin identification assay". Thesis, 2020. http://hdl.handle.net/1866/24711.
Texto completoThis study was designed to identify potential interacting proteins of Lysine-specific demethylase 4A (KDM4A) in the context of cancer using proximity-dependent biotin identification 2 (BioID2) assay. KDM4A is a lysine demethylase and an epigenetic regulator that plays a role in carcinogenesis by promoting proliferation. Herein, we sought out to identify the protein interactome of KDM4A in cervical cancer cell line HeLa. These protein interactions were characterized by their dependency on KDM4A’s catalytic activity and/or Tandem Tudor domain. It succeeded at detecting novel interactors of KDM4A as well as previously studied interactions, such as FBXO22. KDM4A seems to be interacting with some members of the pBAF chromatin remodeling complex, specifically, ARID2, BRD7, and SMARCA2. The pBAF complex facilitates or prevents accessibility to DNA by restructuring the nucleosome. Further analysis is required to validate whether the KDM4A-pBAF complex interaction is direct or indirect. This study also implied the importance of the Tandem Tudor domain in KDM4A’s role in the double stranded break repair. Finally, we also propose the potential involvement of KDM4A in mRNA splicing and organic anion transport. This study provides new insights into KDM4A’s role in cancer development.
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". Thesis, 2015. https://doi.org/10.7916/D8028Q64.
Texto completoMagalhães, Ana Luísa Dos Santos. "Identificação de Novos Genes de Susceptibilidade para o Cancro do Cólon e Recto do Tipo X". Master's thesis, 2017. http://hdl.handle.net/10362/63366.
Texto completoRostosky, Christine Melina. "Onset and Progression of Neurodegeneration in Mouse Models for Defective Endocytosis". Doctoral thesis, 2018. http://hdl.handle.net/21.11130/00-1735-0000-0005-1286-F.
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