Дисертації з теми "Oncogenic protein"
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Gundurao, Ramya Mavinkaihalli. "Systematic analysis of protein-protein interactions of oncogenic Human Papilloma Virus." Thesis, University of Edinburgh, 2013. http://hdl.handle.net/1842/8829.
Повний текст джерелаSumner, Evan T. "Characterizing the Oncogenic Properties of C-terminal Binding Protein." VCU Scholars Compass, 2016. http://scholarscompass.vcu.edu/etd/4153.
Повний текст джерелаDubé, Nadia Marie-Noël. "Protein tyrosine phosphatase 1B regulates metabolic, oncogenic, and hematopoietic function." Thesis, McGill University, 2004. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=85155.
Повний текст джерелаQuill, Lee. "Fragment-based screening of the oncogenic protein tyrosine phosphatase SHP2." Thesis, University of Birmingham, 2017. http://etheses.bham.ac.uk//id/eprint/7425/.
Повний текст джерелаTse, Wai Choi Eric. "Studies of oncogenic protein function and potential for cancer therapy." Thesis, University of Cambridge, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.620964.
Повний текст джерелаCen, Ling. "Phosphorylation profiling and targeting of oncogenic signaling proteins in cancer cells." Columbus, Ohio : Ohio State University, 2007. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1186666790.
Повний текст джерела徐智 and Zhi Xu. "Yes associated protein (YAP) in hepatocellular carcinoma: oncogenic functions and molecular targeting." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hub.hku.hk/bib/B43278589.
Повний текст джерелаXu, Zhi. "Yes associated protein (YAP) in hepatocellular carcinoma oncogenic functions and molecular targeting /." Click to view the E-thesis via HKUTO, 2009. http://sunzi.lib.hku.hk/hkuto/record/B43278589.
Повний текст джерелаMarchetti, Laura. "Dynamics and interactions of an oncogenic homeotic protein within human replicative complexes." Doctoral thesis, Scuola Normale Superiore, 2010. http://hdl.handle.net/11384/85944.
Повний текст джерелаGreen, Melanie M. L. "A study of carcinogenesis involving expression of the Epstein-Barr virus onco-protein LMPI." Thesis, King's College London (University of London), 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.368906.
Повний текст джерелаCurran, John Andrew. "The oncogenic activity of the latent membrane protein of EBV in transgenic mice." Thesis, University of Glasgow, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.388552.
Повний текст джерелаRosa, Jack. "Perturbation and Modulation of Microtubule Cytoskeletal Elements in Response to the Potentially Oncogenic Molecules, Survivin and P53, and Cytokinesis: A Dissertation." eScholarship@UMMS, 2006. https://escholarship.umassmed.edu/gsbs_diss/280.
Повний текст джерелаRatnayake, Wishrawana Sarathi Bandara. "Role of Oncogenic Protein Kinase C-iota in Melanoma Progression; A Study Based on Atypical Protein Kinase-C Inhibitors." Scholar Commons, 2019. https://scholarcommons.usf.edu/etd/7895.
Повний текст джерелаKauke, Monique Jacqueline. "Targeting immunosuppression in the tumor microenvironment and protein-based antagonism of oncogenic K-Ras." Thesis, Massachusetts Institute of Technology, 2017. http://hdl.handle.net/1721.1/114310.
Повний текст джерелаCataloged from PDF version of thesis.
Includes bibliographical references (pages 163-170).
Cancer is routinely treated with surgery, chemotherapy, and radiotherapy, but in recent decades, two new modes of treatment have emerged, targeted therapy and immunotherapy. Targeted therapies exploit differences between cancerous and healthy cells, targeting the proteins and pathways that exclusively drive cancer cell growth, while immunotherapies harness the body's immune system to destroy cancer cells. With these new treatment strategies, tumor regression and complete remission of disease have become attainable for a larger subset of patients. Nevertheless, the fight against cancer continues to be met with significant challenges, including development of resistance to targeted therapies and immunosuppressive factors that cripple anti-tumor immune responses. Broadly, the work presented in this thesis focuses on the development of novel therapeutic cancer agents using protein engineering. First, we explore combination immunotherapies designed to simultaneously activate an anti-tumor immune response, using a tumor-targeting antibody and a serum-persistent form of the immunostimulatory cytokine interleukin-2 (IL-2), and reduce immunosuppression in the tumor microenvironment, via blockade of either transforming growth factor-p (TGF-[beta]) or phosphatidylserine. We performed in vitro characterization and extensive preclinical evaluation of our constructs in syngeneic murine tumor models but failed to show therapeutic efficacy. Our studies nevertheless contribute to the field and demonstrate the complex and interdependent nature of the immune system, something that must be considered in future endeavors in combination immunotherapies. In the field of targeted therapy, mutant K-Ras continues to be the holy grail of oncogenic targets, but remains undruggable due to its high affinity for activating nucleotide GTP and a lack of welldefined drug-binding pockets. We engineered a protein binder RI 1.1.6 that binds mutant K-Ras with nanomolar affinity and exhibits specificity over the wildtype protein. The work in this thesis further characterizes RI 1.1.6 and shows inhibition of K-Ras-driven signaling in a model system. Translation to human cancer cell lines, however, failed to recapitulate this RI 1.1.6-mediated signaling disruption. Mathematical modeling of Raf-competitive Ras antagonism by R11.1.6 revealed that insufficient inhibition of Ras-Raf complexes is attained, offering an explanation of the lack of biological effects we observed.
by Monique Jacqueline Kauke.
Ph. D.
Matthews, Benjamin Phillip. "The oncogenic protein E2a-Pbx1 alters cellular proliferation or apoptosis in haematopoietic and fibroblast tissues." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape4/PQDD_0003/MQ45287.pdf.
Повний текст джерелаPaluncic, Jasmina. "Identification of Melanotransferrin (MTf), as a Novel Pro-Oncogenic Signalling Protein Involved in Melanoma Pathogenesis." Thesis, The University of Sydney, 2019. http://hdl.handle.net/2123/21152.
Повний текст джерелаDarwish, Hanni. "Genomic and functional studies of SERTAD3, an oncogenic protein of the SERTAD family of transcription factors." Thesis, McGill University, 2006. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=100790.
Повний текст джерела曾可澄 and Ho-ching Felice Tsang. "Identification of ankyrin repeats and SOCS box protein 4 (ASB4) as oncogenic biomarker in liver cancer." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2008. http://hub.hku.hk/bib/B40738814.
Повний текст джерелаTamaki, Sakura. "SS18-SSX, the Oncogenic Fusion Protein in Synovial Sarcoma, Is a Cellular Context-Dependent Epigenetic Modifier." Kyoto University, 2016. http://hdl.handle.net/2433/215458.
Повний текст джерелаTsang, Ho-ching Felice. "Identification of ankyrin repeats and SOCS box protein 4 (ASB4) as oncogenic biomarker in liver cancer." Click to view the E-thesis via HKUTO, 2008. http://sunzi.lib.hku.hk/hkuto/record/B40738814.
Повний текст джерелаComelli, Laura. "Localization and dynamics of homeotic oncogenic protein HOXC13 in pre-initiation complex of human DNA replication origins." Doctoral thesis, Scuola Normale Superiore, 2010. http://hdl.handle.net/11384/85938.
Повний текст джерелаWaldman, Lynne K. "Effects of oncogenic Ras and p38 mitogen-activated protein kinase on the adhesion of normal human cells." Thesis, Massachusetts Institute of Technology, 2010. http://hdl.handle.net/1721.1/57995.
Повний текст джерелаVita. Cataloged from PDF version of thesis.
Includes bibliographical references.
Activating mutations in RAS oncogenes commonly arise in human cancers. However, in experimental settings, oncogenic RAS has most often been studied at supraphysiological levels of expression. Importantly, work by others showed that the response of murine cells to expression of oncogenic ras from the endogenous promoter is strikingly different from the response of both human and murine cells to high levels of ectopically expressed oncogenic RAS. Thus, to study the outcome of oncogenic Ras signaling in human cells at a more physiological level, I developed a system in which I could activate oncogenic Ras signaling to either low or high extents in normal human fibroblasts. A low level of oncogenic Ras signaling induced cellular hyperproliferation, whereas a high level of signaling induced cellular senescence. A growing body of literature links loss of p38 mitogen-activated protein kinase (MAPK) activity with the promotion of Ras-induced transformation in murine cells. Accordingly, I examined the effect of inhibiting p38 in normal human cells in which I also activated a low level of oncogenic Ras signaling. Interestingly, the inhibition of p38 cooperated with low activation of oncogenic Ras to alter the morphology and adhesive properties of cells. My results suggest that the inhibition of p38 could predispose human cells to partial transformation by oncogenic Ras through alterations in cellular adhesion.
by Lynne K. Waldman.
Ph.D.
Ercolani, Luisa. "Protein S-glutathionylation: new insights on pre-oncogenic cellular model and formulation of a new molecular mechanism." Doctoral thesis, Università Politecnica delle Marche, 2013. http://hdl.handle.net/11566/242733.
Повний текст джерелаProtein S-glutathionylation is an important post-translational modification which allows to protect cysteine residues against irreversible oxidation during redox imbalance and to affect proteins changes in structure, activity or sub-cellular localization. Modifications in S-glutathionylation are been associated with a number of human pathologies, such as diabetes, cardiovascular, lung and neurodegenerative diseases and cancer. Aims of this work were 1) to investigate possible links between this post-translational modification and oncogene-induced senescence in oncogenic H-Ras expressing cells, and 2) to discover a new possible catalyst of glutathionylation. H-Ras oncogene requires deregulation of additional oncogenes or inactivation of tumor suppressor proteins to increase cell proliferation rate and completely transform cells. Indeed, the expression of the constitutively activated H-RasV12 induces cell growth arrest and premature senescence, which act like barriers in pre-neoplastic lesions. H-RasV12 transfected cells showed a dramatic modification of morphology and premature senescence followed by cell death induced by autophagy and apoptosis. This phenotype is induced mainly by the PI3K and MAPK pathways. Moreover, it was provided evidence that the premature senescence is associated with cellular redox imbalance (due to a strong reduction of total antioxidant capacity and significant decrease of glutathione levels) as well as with altered S-glutathionylation. Different proteins S-glutathionylation patterns were observed in control and H-RasV12 expressing cells. Particularly, three proteins were identified by mass spectrometry: vimentin, ATP synthase β-subunit and α-enolase. So, antioxidant defense reduction, glutathione depletion and subsequent modification of S-glutathionylation of target proteins contribute to arrest cell growth, leading to death of fibroblasts expressing constitutively active H-Ras oncogene, thus acting as oncogenic barriers that obstacle the progression of cell transformation. Mechanisms of protein S-glutathionylation are far to be completely understood and several reactions can promote it, either spontaneously or catalyzed. To date, three potential catalysts of protein glutathionylation are been proposed, however, other enzymes may be implicated in this type of catalysis. In this work, it was studied glyoxalase II as a new potential candidate to promote S-glutathionylation. To demonstrate its active involvement in protein glutathionylation were used purified proteins known to be glutathionylated for in vitro experiments. For the first time this work shows active involvement of cytosolyc glyoxalase II for in vitro protein Sglutathionylation, suggesting a new mechanism of protein-SSG formation. Glyoxalase II, indeed, allows a rapid and specific protein-SSG formation, allowing enzymatic regulation of S-glutathionylation in proteins of different origin and cellular compartmentalization.
Arcipowski, Kelly Marie. "Molecular mechanisms of TRAF6 function in signaling pathways of the oncogenic viral mimic of CD40, LMP1." Diss., University of Iowa, 2012. https://ir.uiowa.edu/etd/3560.
Повний текст джерелаTong, Michael. "Evaluation of protein kinases for solution NMR spectroscopy and the structural mechanism of inhibition and activation of an oncogenic calcium calmodulin dependent protein kinase." Thesis, University of Birmingham, 2012. http://etheses.bham.ac.uk//id/eprint/3877/.
Повний текст джерелаTichauer, Ruth Elena. "In silico screening of NRas protein oncogenic mutations : new structural and physico-chemical insights into the catalytic activity." Electronic Thesis or Diss., Toulouse 3, 2019. http://www.theses.fr/2019TOU30028.
Повний текст джерелаRas subfamily of small GTPase proteins holds a key position in cell proliferation pathways. Indeed, the transmission of cell growth signals is controlled by proteins belonging to it. In their GTP-bound conformation, these proteins interact and activate downstream effectors of cell replication and differentiation. The hydrolysis reaction that takes place in their center, terminates these interactions, thereby leading to the GDP-bound inactive state. Point mutations of key residues lead to a hydrolysis rate drop that keeps Ras in a GTP-bound active state. Now, high concentrations of active Ras have been associated to abnormal cell proliferation, emblematic of cancerous tissues dissemination. With this into consideration, the elucidation of Ras mechanisms for accelerating GTP cleavage appears as a major step in the development of cancer targeted therapies that would consist in restoring the hydrolysing capabilities within oncogenic Ras to a wild-type rate. In an attempt to gain insight into Ras catalysing properties at the atomic level, unconstrained Molecular Dynamics (MD) simulations describing the G domain at different levels of theory (Molecular Mechanics (MM), Semi-empirical and Density Functional Theory (DFT)) were carried out for NRas member in its wild-type and Gln 61 mutated forms. These simulations were coupled to biomechanic characterisations of the complexes under inspection employing the static modes approach. The latter method, allows the identification of hot spots {\it i.e.} responsive residues of the biomolecule, that have a mechanical influence on the GTPase function of the protein. Hence, they could serve as suitable sites to host drug-like molecules containing specific chemical groups that would facilitate GTP hydrolysis. The obtained results show that water molecules positioning is crucial for efficiently catalysing the reaction that takes place in NRas center. Indeed, the precise positioning observed within the wild-type is lost within the mutants studied here. Furthermore, the active site structural modifications undergone upon Gln 61 substitutions, together with solvent distribution in it, impact directly GTP electronic density. The latter is accommodated to a GDP-like state within the wild-type protein only, as experimentally determined in previous investigations. Thus, oncogenic Gln 61 mutations impair this major catalysing effect. Among three engineered NRas proteins of the Q61R mutated form, proposed during this thesis, one is presented during the defence while the three are described in the manuscript. The chemical groups inserted at the identified site enable the recovery of water distribution as within the wild-type. To end, during the defence only, an alternative reaction pathway of the enzymatic reaction is proposed
Edelbrock, Michael Aaron. "Cell Cycle Regulation of DNA Mismatch Repair Protein Expression and Activity at the H-ras Oncogenic Hot Spot." University of Toledo Health Science Campus / OhioLINK, 2007. http://rave.ohiolink.edu/etdc/view?acc_num=mco1192129938.
Повний текст джерелаBaxter, Daniel. "Combining library screening approaches, and modifying peptides with helix constraints, to generate novel antagonists of oncogenic Activator Protein-1." Thesis, University of Bath, 2017. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.715244.
Повний текст джерелаChan, Steven Man Cheong. "Protein microarray technology for profiling signaling patwhays [sic] : insights into pro-oncogenic notch signaling in T cell acute lymphoblastic leukemia /." May be available electronically:, 2006. http://proquest.umi.com/login?COPT=REJTPTU1MTUmSU5UPTAmVkVSPTI=&clientId=12498.
Повний текст джерелаFreudenberger, Nora [Verfasser], and Thomas [Akademischer Betreuer] Dobner. "Role of minor core protein V during productive infection with human adenovirus type 5 and the proteins relevance to oncogenic transformation processes / Nora Freudenberger ; Betreuer: Thomas Dobner." Hamburg : Staats- und Universitätsbibliothek Hamburg, 2017. http://d-nb.info/1139492837/34.
Повний текст джерелаGonterman, Ryan M. "Parathyroid hormone-related protein gene expression and function relationship with oncogenic pathways in the skin and squamous cell carcinomas of the lung /." [Bloomington, Ind.] : Indiana University, 2008. http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&res_dat=xri:pqdiss&rft_dat=xri:pqdiss:3324517.
Повний текст джерелаTitle from PDF t.p. (viewed on May 13, 2009). Source: Dissertation Abstracts International, Volume: 69-08, Section: B, page: 4693. Adviser: John G. Foley.
Genera, Mariano. "Structural and functional study of the human phosphatase PTPN3 and its interaction with oncogenic viruses." Electronic Thesis or Diss., Sorbonne université, 2019. http://www.theses.fr/2019SORUS112.
Повний текст джерелаThe human protein tyrosine phosphatase non-receptor type 3 (PTPN3) is a PDZ (PSD-95/Dlg/ZO-1) domain-containing phosphatase with a tumor-suppressive or a tumor-promoting role in many cancers, although its role in cell signalling is still unclear. Interestingly, the high-risk genital human papillomavirus (HPV) types 16 and 18 and the hepatitis B virus (HBV) target the PDZ domain of PTPN3 through PDZ-binding motifs (PBMs) in their E6 and HBc proteins. Here, I report a detailed study of the interactions between the PDZ domain of PTPN3 and its cellular and viral ligands. First, we combined biophysical, NMR and X-ray experiments to investigate the structural and functional properties of the PDZ domain of PTPN3 and its interaction with the E6 PBM. We then extended our structural study of PTPN3-PDZ to other cellular and viral partners, and gained insights into the main structural determinants of recognition of PBMs. We then focused on the HBV HBc protein. We screened a library of human PDZ-containing proteins for HBc binders and identified 28 cellular HBc-interacting partners, most of which are involved in cell polarity. We confirmed that PTPN3 can bind the HBc PBM in the context of the viral capsid, and we showed that viral PBMs interact with PTPN3-PDZ with similar affinities to endogenous PTPN3 ligands. Using HBV-infected hepatocytes we observed that overexpression of PTPN3 has multiple effects on HBV infection. Finally, we investigated the interactome of PTPN3-PDZ to gain insights into the role of this protein in cell signalling and the disruptive effects of HBV
Xu, Shenyuan. "Nuclear Magnetic Resonance Spectroscopy Studies of At2g44920, a Pentapeptide Repeat Protein from Arabidopsis thaliana and X-ray Crystallography, Isothermal Titration Calorimetry Studies of K-Ras, a Human Oncogenic GTP-ase Signaling Protein." Miami University / OhioLINK, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=miami1500896385881469.
Повний текст джерелаLowe, Julie. "Identification of NF-kappa B and DNA-dependent protein kinase (DNA-PK) as new players in the regulation and signaling of the oncogenic phosphatase Wip1." Connect to Electronic Thesis (CONTENTdm), 2010. http://worldcat.org/oclc/642326246/viewonline.
Повний текст джерелаMaurizio, Elisa. "Post-translational modifications and conformational transitions of the intrinsically disordered oncoproteins High-Mobility Group A." Doctoral thesis, Università degli studi di Trieste, 2011. http://hdl.handle.net/10077/4591.
Повний текст джерелаIntrinsically disordered proteins (IDPs) are flexible molecules, able to adapt to the surfaces of different molecular partners by means of specific, but easily reversible interactions. IDPs carry out pivotal biological functions participating in almost all cell signaling and regulatory pathways. Importantly, IDPs activities are finely modulated by the addition/removal of numerous post-translational modifications (PTMs) which are important conformational modulators. Prototypes of IDPs are High Mobility Group A (HMGA) proteins, which are expressed at high levels and play essential functions both in embryonic and cancer cells. HMGA protein family (HMGA1a, HMGA1b, and HMGA2) belong to the non-histone HMG chromatin protein super-family and are multifunctional architectural transcription factors. HMGA conformational adaptability and intricate pattern of dynamic and constitutive PTMs are thought to be responsible for this multifunctionality. We performed a liquid chromatography-mass spectrometry (LC-MS) screening in twenty different cell lines in order to evaluate HMGA proteins PTM pattern and we evidenced relevant intra-family differences. Moreover, we focused on the poorly characterized HMGA2 and we mapped HMGA2 phosphorylation sites by mass sequencing demonstrating that, similarly to HMGA1, it is phosphorylated on the acidic C-terminal tail by CK2. Importantly, this modification turned out to affect HMGA2 DNA binding. Since truncated HMGA proteins are more oncogenic than full-length ones and since HMGA are in vivo heavily modified on their C-terminal domain, we dissected the role of this domain and its phosphorylations from a structural point of view. We probed HMGA IDPs compactness and accessibility taking advantage of an innovative approach combining limited proteolysis and MS-based techniques. By limited proteolysis, ESI (electrospray ionization)-MS, and IMS (ion mobility separation)-MS we demonstrated that HMGA can assume a compact conformation and that their compactness degree is dependent upon the presence of the acidic C-terminal domain and its constitutive phosphorylations. Moreover, LC-MS analyses after enzymatic assays showed that HMGA forms with a deletion of acidic C-terminal tail are more susceptible to PTMs, thus supporting the idea that the acidic tail is involved in masking the accessibility of modifying enzymes to their own consensus sites. We evidenced macroscopic differences regarding PTMs affecting the three HMGA family members and provided the first data about in vivo HMGA2 PTMs and their effect on DNA binding. Our structural investigations revealed a structure/PTMs relationship dictated by the presence of the C-terminal domain. This evidence, together with the already known in vivo functional outcome of HMGA C-terminal truncation, suggests a structure/function link between HMGA tails, their PTMs, and their oncogenic properties, paving the way for the development of interfering therapeutic strategies based on targeting HMGA proteins.
Le proteine intrinsecamente disordinate (PID) sono molecole flessibili in grado di adattarsi alle superfici di differenti partner molecolari tramite interazioni specifiche, ma facilmente reversibili. Queste proteine compiono funzioni biologiche essenziali partecipando in quasi tutte le vie di segnalazione e regolazione cellulari. La modulazione delle loro attività avviene tramite l’aggiunta/rimozione di numerose modificazioni post-traduzionali (MPT), le quali possono comportare anche cambiamenti conformazionali. Le proteine High Mobility Group A (HMGA) sono considerate prototipo delle PID. Esse sono espresse ad alti livelli e giocano funzioni chiave sia durante lo sviluppo embrionale che durante il processo di trasformazione neoplastica. Le proteine della famiglia HMGA (HMGA1a, HMGA1b e HMGA2) appartengono alla super-famiglia delle proteine cromatiniche non istoniche HMG e sono fattori trascrizionali architetturali multifunzionali. L’adattabilità conformazionale e l’intricato pattern di MPT dinamiche e costitutive delle HMGA sono ritenute essere alla base della loro multifunzionalità. In questo lavoro di tesi è stato effettuato uno screening delle MPT a cui sono soggette le HMGA in venti linee cellulari diverse mediante analisi di cromatografia liquida accoppiata alla spettrometria di massa (LC-MS) e si sono evidenziate rilevanti differenze tra i tre diversi membri della famiglia HMGA. Inoltre, concentrandosi sulla poco caratterizzata proteina HMGA2, abbiamo dimostrato mediante mass sequencing che, al pari della proteina HMGA1a, essa è fosforilata sul C-terminale e che tale modificazione comporta un’alterazione delle sue proprietà di legame al DNA. Diversi tipi di tumore esprimono forme tronche delle proteine HMGA mancanti del dominio acidico C-terminale. Dal momento che queste forme sono state dimostrate essere maggiormente oncogeniche rispetto alle controparti a lunghezza completa abbiamo deciso di investigare il ruolo della coda acidica e delle sue fosforilazioni da un punto di vista strutturale. La compattezza e l’accessibilità delle HMGA è stata esplorata sfruttando un approccio innovativo che combina esperimenti di proteolisi limitata e tecniche di spettrometria di massa (MS). Tramite proteolisi limitata, ESI (electrospray ionization)-MS, and IMS (ion mobility separation)-MS abbiamo dimostrato che le HMGA possono assumere una conformazione compatta e che il loro grado di compattezza è dipendente dalla presenza del dominio acidico C-terminale e delle sue fosforilazioni costitutive. Inoltre, analisi LC-MS effettuate dopo saggi enzimatici hanno mostrato come le forme delle HMGA presentanti una delezione della coda acidica C-terminale sono più suscettibili alle MPT, supportando quindi l’idea che la coda acidica sia coinvolta nel mascherare l’accessibilità degli enzimi di modificazione sui siti consensus lungo la sequenza di HMGA. In questo lavoro abbiamo evidenziato differenze macroscopiche riguardanti le MPT che interessano i tre membri della famiglia HMGA e abbiamo fornito i primi dati circa le MPT di HMGA2 in vivo e il loro effetto sul legame al DNA. Le nostre investigazioni strutturali hanno rivelato una relazione struttura/MPT dettata dalla presenza del dominio C-terminale. Questa evidenza, insieme al già noto esito funzionale in vivo della delezione del C-terminale di HMGA, suggerisce un collegamento struttura/funzione tra la coda acidica delle HMGA, le loro MPT, e le loro proprietà oncogeniche.
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Liu, Xiaohu. "Functional and structural study of the AHI-1 SH3 domain, characterization of the BCR-ABL-AHI-1-Dynamin-2 protein complex and investigation of oncogenic roles of dynamin-2 in chronic myeloid leukemia." Thesis, University of British Columbia, 2016. http://hdl.handle.net/2429/60191.
Повний текст джерелаMedicine, Faculty of
Graduate
Helt, Anna-Marija. "Multiple biological activities of the human papillomavirus type 16 E7 oncoprotein contribute to the abrogation of human epithelial cell cycle control /." Thesis, Connect to this title online; UW restricted, 2002. http://hdl.handle.net/1773/11514.
Повний текст джерелаProtopopova, Marina. "Modulation of activity of the tumour suppressor p53 by small molecules and damaged DNA /." Stockholm, 2004. http://diss.kib.ki.se/2004/91-7349-926-9/.
Повний текст джерелаFladvad, Malin. "Structure and function in c-Myc and Grx4 : two key proteins involved in transcriptional activation and oxidative stress /." Stockholm, 2006. http://diss.kib.ki.se/2006/91-7357-007-9/.
Повний текст джерелаHase, Manuela. "Molecular and ultrastructural analysis of Tpr, a nuclear pore complex-attached coiled-coil protein /." Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-525-5/.
Повний текст джерелаYan, Weisi. "Functional proteomic study of Akt reveals novel substrates in translation /." Access full-text from WCMC, 2008. http://proquest.umi.com/pqdweb?did=1619246521&sid=9&Fmt=2&clientId=8424&RQT=309&VName=PQD.
Повний текст джерелаLindström, Mikael. "Functional characterization of the alternative reading frame protein p14ARF /." Stockholm, 2004. http://diss.kib.ki.se/2004/91-7349-917-x.
Повний текст джерелаPääjärvi, Gerd. "Xenobiotics-induced phosphorylations of MDM2 /." Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-951-3/.
Повний текст джерелаCLEMENTI, LETIZIA. "Potenziale ruolo oncogenico della proteina multifunzionale tau." Doctoral thesis, Università degli Studi dell'Aquila, 2022. http://hdl.handle.net/11697/192067.
Повний текст джерелаLeanna, Candice A. "Loss of IkB[alpha]-mediated regulation correlates with increased oncogenicity of mutant c-Rel proteins." free to MU campus, to others for purchase, 1998. http://wwwlib.umi.com/cr/mo/fullcit?p9901255.
Повний текст джерелаTang, Norina Mei Ngon. "Regulation of protein synthesis and induction of oncogenesis by a cellular protein kinase inhibitor /." Thesis, Connect to this title online; UW restricted, 1998. http://hdl.handle.net/1773/11501.
Повний текст джерелаCollins-De, Peyer Laurence. "Screening of a rat thymus and a human hippocampus cDNA library for a novel fyn-related oncogene." Thesis, Hong Kong : University of Hong Kong, 1999. http://sunzi.lib.hku.hk/hkuto/record.jsp?B21253870.
Повний текст джерелаSandberg, Eric M. "Jak2 tyrosine kinase new insights regarding structure, function, and pharmacology /." [Gainesville, Fla.] : University of Florida, 2004. http://purl.fcla.edu/fcla/etd/UFE0006882.
Повний текст джерелаTypescript. Title from title page of source document. Document formatted into pages; contains 118 pages. Includes Vita. Includes bibliographical references.
Chen, Mingzi. "Mos regulation in activating the MAP kinase pathway /." Thesis, Connect to this title online; UW restricted, 1997. http://hdl.handle.net/1773/9195.
Повний текст джерелаLiang, Hongjian [Verfasser]. "Characterization of the oncogenic properties of human papillomavirus E6 proteins / Hongjian Liang." Konstanz : KOPS Universität Konstanz, 2017. http://d-nb.info/1188202790/34.
Повний текст джерела