Bibliografías temáticas / Oncogenic protein

Literatura académica sobre el tema "Oncogenic protein"

Autor: Grafiati

Publicado: 11 de marzo de 2023

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Artículos de revistas sobre el tema "Oncogenic protein"

Rodrigues, G. A. y M. Park. "Dimerization mediated through a leucine zipper activates the oncogenic potential of the met receptor tyrosine kinase". Molecular and Cellular Biology 13, n.º 11 (noviembre de 1993): 6711–22. http://dx.doi.org/10.1128/mcb.13.11.6711-6722.1993.

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Oncogenic activation of the met (hepatocyte growth factor/scatter factor) receptor tyrosine kinase involves a genomic rearrangement that generates a hybrid protein containing tpr-encoded sequences at its amino terminus fused directly to the met-encoded receptor kinase domain. Deletion of Tpr sequences abolishes the transforming ability of this protein, implicating this region in oncogenic activation. We demonstrate, by site-directed mutagenesis and coimmunoprecipitation experiments, that a leucine zipper motif within Tpr mediates dimerization of the tpr-met product and is essential for the transforming activity of the met oncogene. By analogy with ligand-stimulated activation of receptor tyrosine kinases, we propose that constitutive dimerization mediated by a leucine zipper motif within Tpr is responsible for oncogenic activation of the Met kinase. The possibility that this mechanism of activation represents a paradigm for a class of receptor tyrosine kinase oncogenes activated by DNA rearrangement is discussed.

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Rodrigues, G. A. y M. Park. "Dimerization mediated through a leucine zipper activates the oncogenic potential of the met receptor tyrosine kinase." Molecular and Cellular Biology 13, n.º 11 (noviembre de 1993): 6711–22. http://dx.doi.org/10.1128/mcb.13.11.6711.

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Cai, Mei, Joseph Amor y Maiyon Park. "Abstract 5834: Examining the potential oncogenic function of septins and their interaction with Chmp1A tumor suppressor in pancreatic cancer". Cancer Research 82, n.º 12_Supplement (15 de junio de 2022): 5834. http://dx.doi.org/10.1158/1538-7445.am2022-5834.

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Abstract Introduction: Chmp1A functions as a tumor suppressor by the activation of ATM and p53 in pancreatic cancer. The nuclear localization signal (NLS) of Chmp1A is required for cell growth inhibition and activation of ATM and p53. Proteomic analysis has identified Septins (a group of GTP-binding proteins) to be associated with the NLS-deleted Chmp1A. Since NLS-deleted Chmp1A promotes cancer cell growth, we hypothesized that Septins may function as oncogenes and that Chmp1A functions as a tumor suppressor partly by inhibiting the oncogenic action of Septin proteins. Objective: To examine whether Septin proteins exhibit oncogenic activity and to investigate whether Chmp1A inhibits the oncogenic function of Septins. Methodology: Using normal pancreatic and cancer cells, we compared Septin transcripts using PCR assays, Septin protein expression using Western blot, and Septin cellular expression using immunocytochemistry. We performed immunohistochemical analysis to examine whether Septin expression is increased in pancreatic cancer tissues compared to corresponding normal tissues. Silencing technology was used to test whether Septin expression is regulated by Chmp1A. Results: Our preliminary data indicates that the transcript and protein of Septins are increased in various pancreatic cancer cell lines compared to normal. Septin protein expression was increased or altered in human pancreatic ductal adenocarcinoma tissues compared to corresponding normal tissues. Additionally, our data implies that Chmp1A negatively regulates Septin expression, since Septin transcripts and proteins are increased when Chmp1A protein is silenced. Summary and future direction: Our data suggests that Septin functions as an oncogene in pancreatic cancer cells and that Chmp1A functions as a tumor suppressor partly by inhibiting the oncogenic action of Septin proteins. For the completion of the project in the future, we plan to confirm the function of Septins by investigating the effect of Septin overexpression on pancreatic cancer cell proliferation. In addition, we will further investigate the interaction between Septins and Chmp1A by examining Septin expression and localization in pancreatic cancer cells that overexpress Chmp1A. Citation Format: Mei Cai, Joseph Amor, Maiyon Park. Examining the potential oncogenic function of septins and their interaction with Chmp1A tumor suppressor in pancreatic cancer [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 5834.

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Longo, Dan L. y Neal Rosen. "Targeting Oncogenic RAS Protein". New England Journal of Medicine 387, n.º 2 (14 de julio de 2022): 184–86. http://dx.doi.org/10.1056/nejme2206831.

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Gambacorti-Passerini, C. "Oncogenic protein tyrosine kinases". Cellular and Molecular Life Sciences 61, n.º 23 (diciembre de 2004): 2895–96. http://dx.doi.org/10.1007/s00018-004-4270-1.

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Saglio, G. y D. Cilloni. "Oncogenic protein tyrosine kinases". Cellular and Molecular Life Sciences 61, n.º 23 (diciembre de 2004): 2897–911. http://dx.doi.org/10.1007/s00018-004-4271-0.

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Jones, A. V. y N. C. P. Cross. "Oncogenic protein tyrosine kinases". Cellular and Molecular Life Sciences 61, n.º 23 (diciembre de 2004): 2912–23. http://dx.doi.org/10.1007/s00018-004-4272-z.

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Kitamura, Y. y S. Hirotab. "Oncogenic protein tyrosine kinases". Cellular and Molecular Life Sciences 61, n.º 23 (diciembre de 2004): 2924–31. http://dx.doi.org/10.1007/s00018-004-4273-y.

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Naoe, T. y H. Kiyoi. "Oncogenic protein tyrosine kinases". Cellular and Molecular Life Sciences 61, n.º 23 (diciembre de 2004): 2932–38. http://dx.doi.org/10.1007/s00018-004-4274-x.

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Pulford, K., L. Lamant, E. Espinos, Q. Jiang, L. Xue, F. Turturro, G. Delsol y S. W. Morris. "Oncogenic protein tyrosine kinases". Cellular and Molecular Life Sciences 61, n.º 23 (diciembre de 2004): 2939–53. http://dx.doi.org/10.1007/s00018-004-4275-9.

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Tesis sobre el tema "Oncogenic protein"

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.

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Human papilloma virus (HPV) is a ubiquitous virus implicated in a growing list of cancers, particularly cervical cancer‐ the second most common cancer among women worldwide. Although persistent infection with high‐risk oncogenic HPVs such as types ‐16 or ‐18 is necessary, additional factors like co‐infection with other viruses can play a role in cancer progression. Protein‐protein interactions play a central role in the infection, survival and proliferation of the virus in the host. Although some interactions of HPV proteins are well characterised, it is essential to discover other key viral interactions to further improve our understanding of the virus and to use this knowledge for the development of newer biomarkers and therapeutics. The aim of this study was to systematically analyse the interactions of HPV‐16 proteins using yeast two‐hybrid (Y2H). To achieve this, a clone collection of the viral proteome was generated by recombinatorial cloning and three independent Y2H screens were performed: (i) Intra‐viral screen to identify interactions among the HPV‐16 proteins; (ii) Inter‐viral screen to identify interactions with proteins of Herpes Simplex Virus (HSV) which is suggested to be a co‐factor; and (iii) Virus‐host screen to identify novel cellular binding partners. The intra‐viral Y2H screen confirmed some of the previously known interactions and also identified binding of the E1 and E7 proteins. Deletion mutagenesis was performed to map the interaction domains to the amino‐terminal 92 amino acids of E1 and carboxy‐terminal CxxC domain of E7. Replication assays suggest a possible repression of E1‐mediated episomal replication by direct binding of E7. The inter‐viral Y2H screen identified interactions of HPV proteins with seventeen HSV‐1 proteins including transcriptional regulator ICP4 and neurovirulance factor ICP34.5. The biological relevance of these interactions in the context of co‐infection is discussed. The virus‐host screen performed against a human cDNA library identified 54 interactions, a subset of which was validated by biochemical pull‐down assays. The functional relevance of an interaction between E7 and a proto‐oncogene spermatogenic leucine zipper protein (SPZ1) was further investigated suggesting a role of SPZ1 in E7‐mediated cell proliferation. The work presented in this thesis identifies several novel interactions of HPV proteins. Future work will involve the in‐depth elucidation of biological relevance of these interactions. In particular, the interactions of E7 with E1 and SPZ1 are of great interest to improve our understanding of the life cycle and pathogenesis of the virus which can be applied for improved strategies of prevention and treatment of malignancies caused by HPV.

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Sumner, Evan T. "Characterizing the Oncogenic Properties of C-terminal Binding Protein". VCU Scholars Compass, 2016. http://scholarscompass.vcu.edu/etd/4153.

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The paralogous C-terminal binding proteins (CtBP) 1 and 2 are evolutionarily conserved transcriptional coregulators that target and disrupt the expression of several genes essential for multiple cellular processes critical to regulating tumor formation. CtBP’s ability to govern the transcription of genes necessary for apoptosis, tumor suppression, invasion/migration and EMT gives rise to its oncogenic activities. Both isoforms of CtBP are found to be overexpressed in cancers including colorectal, pancreatic, ovarian, and breast, with higher levels correlating to lower overall median survival. Although multiple lines of evidence suggest CtBP plays a role in tumorigenesis, it has never been formally characterized as an oncogene. For this reason, the goal of this dissertation was to design a set of experiments to determine the transforming ability of CtBP2 in vitro using both murine and human fibroblast and in vivo using the Apcmin/+ mouse model of cancer. Specifically, we demonstrate that overexpression of CtBP2 alone can drive transformation of NIH3T3 cells leading to loss of contact inhibition, increased x invasion/migration, and anchorage independent growth. In addition, CtBP2 was found to cooperate with the large T-antigen (LT) component of the simian virus 40 (SV40) to lead to transformation of murine embryonic fibroblasts (MEFs) and with both LT and small T-antigen (ST) to induce migration/invasion and anchorage-independent growth in BJ human foreskin fibroblasts. To confirm the role of Ctbp2 in a mouse tumor model with Ctbp overexpression, we bred Apcmin/+ mice to Ctbp2 heterozygous (Ctbp2+/-) mice, which otherwise live normal lifespans. CtBP is a known target of the APC tumor suppressor and is thus stabilized in APC mutated human colon cancers and is found in high levels in Apcmin/+ polyps. Remarkably, removing an allele of Ctbp2 doubled the median survival of Apcmin/+ mice (P <0.001) and reduced polyp formation to near undetectable levels. These data suggest the importance of CtBP2 in driving cellular transformation and identify it as a potential target for prevention or therapy in APC mutant backgrounds.

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Dubé, 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.

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Protein tyrosine phosphatase 1B (PTP1B) is a ubiquitously expressed enzyme that is involved in multiple signaling pathways. Biochemical and substrate trapping studies have implicated PTP1B in the dephosphorylation of various tyrosine kinases, including the EGFR, PDGFR, IR, IGF-IR, JAK2, p210Bcr-Abl, and Src. Of particular interest, gene-targeting studies in mice have established PTP1B as a critical physiological regulator of metabolism by attenuating insulin and leptin signaling. Indeed, PTP1B null mice exhibit resistance to diet-induced diabetes and obesity. Although PTP1B is involved in signaling pathways that contribute to oncogenesis, PTP1B null mice do not develop spontaneous tumors. Therefore, my doctoral research focuses on identifying the physiological significance of PTP1B in these pathways. Our laboratory has previously demonstrated that PTP1B modulates leptin signaling via the tyrosine kinase JAK2. Accordingly, I have shown that PTP1B dephosphorylates JAK2 in a growth hormone (GH)-dependent manner, thus negatively regulating GH signaling and downstream effectors such as STAT3 and STAT5. Consequently, mice lacking PTP1B remain sensitive to GH action after starvation. In addition, I showed that the absence of PTP1B could improve glycemia during streptozotocin-induced type 1 diabetes. In the second part of my research, I have elucidated the mechanism for the previously reported decreased ERK activation in PTP1B null fibroblasts. I demonstrated that Ras activity is reduced in these cells, which is due to increased p120RasGAP expression and p62Dok hyperphosphorylation. Both of these molecules negatively regulate Ras activity by promoting the intrinsic GTPase activity of Ras, leading to decreased ERK activation. Finally, I developed a mouse model of cancer to study the role of PTP1B in tumorigenesis. Since the majority of cancers harbor mutations in p53, I generated p53/PTP1B double null mice. In the absence of p53, PTP1B heterozygous

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Quill, Lee. "Fragment-based screening of the oncogenic protein tyrosine phosphatase SHP2". Thesis, University of Birmingham, 2017. http://etheses.bham.ac.uk//id/eprint/7425/.

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Protein tyrosine phosphatases represent a family of signalling enzymes with emerging therapeutic potential. The cytoplasmic protein tyrosine phosphatase SHP2, encoded by the PTPN11 gene, plays a central role in the activation of downstream signalling events at multiple growth factor and cytokine receptors, and was the first oncogenic protein tyrosine phosphatase to be discovered. Aberrant SHP2 signalling underlies the pathology of numerous developmental disorders such as Noonan and LEOPARD syndrome, and is a known driver of breast cancer and myeloproliferative disease. To gain a deeper insight into ligand interactions with the SHP2 catalytic domain in solution, NMR backbone resonance assignments of the 34 KDa SHP2 catalytic domain were determined and utilised in conjunction with 15N-1H HSQC NMR spectroscopy to map the structurally undisclosed binding site of the previously reported SHP2 inhibitor, NSC-87877. In addition, use of a fragment-based screening approach to accelerate the discovery of novel SHP2 inhibitors has enabled the identification of two novel and distinct chemical scaffolds, both of which now serve as validated chemical precursors for the development of more potent SHP2 lead inhibitors.

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Tse, 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.

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Cen, 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.

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徐智 y 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.

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Xu, 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.

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Marchetti, 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.

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The regulation of human DNA replication operates via the time-programmed activation and deactivation of approximately 30,000 replication origins distributed along the genome. A multi-protein replicative complex recognizes and assembles onto each origin; this determines the local unwinding of the origin DNA and the start of two oppositely moving replicative forks. The mechanism that governs the selection of a specific DNA sequence as human (and, more generally, metazoan) origin, in the course of G1 phase of the cell-cycle, is still poorly understood. The lack of DNA-sequence consensus among well-characterized replication origins, together with the little bindingspecificity displayed by the Origin Recognition Complex, suggest that origin selection might rather be determined by local chromatin structures and/or accessory targeting proteins. With regard to the latter possibility, it was interesting to find out that three homeotic proteins, namely HOXC13, HOXC10, and HOXA13 display a specific affinity for a DNA fragment corresponding to the sequence covered by the Replicative Complex of the human Lamin B2 replication origin. In the study conducted during this Ph.D. program, the possible role of homeotic proteins in origin function was explored by investigating the involvement of a selected homeotic protein, namely HOXC13, within the replicative complexes in living human cells. To this purpose, recent advances in biophysical microscopy technologies were exploited to study in vivo the localization, dynamics, and interactions of HOXC13 protein in the context of DNA replication regulation. The data reported in this thesis demonstrate that HOXC13 indeed participates in origin function. The protein is a stable component of early replicating chromatin, as it displays stable chromatin binding in correspondence to the nuclear areas where replication foci of early S phase are collected. This peculiar behavior is driven by the homeodomain and relies mainly on the conserved homeodomain arginine-5 anchoring to the DNA minor groove. Furthermore, HOXC13 displays unambiguous affinity for origin sequences and for selected replicative-complex proteins. The close proximity of HOXC13 to both Cdc6 and ORC2 proteins measured in living cells proves that the homeotic protein is involved in direct protein-protein interactions within the replicative-complex; not unexpectedly, such interactions are modulated in a cell-cycle dependent fashion that is consistent with origin function. These observations are not restricted to a single origin, but rather appear to have a general significance in the nuclear architecture of DNA replication; nor are they restricted to a single homeotic protein, as the HOXC13 exerts its function via highly conserved homeodomain residues. Hence, this dissertation argues that the homeoproteins functionally contribute in a general manner, dependent on their chromatin-binding properties, to the specification of origins, likely the early replicating ones. In this view, HOX proteins, probably in the context of a multi-protein homeotic effector, contribute to recruit and stabilize the replicative complexes onto early replicating origins, in presence of specific chromatin and topological configurations. Considering that HOXC13, involved in development and differentiation, is also an oncoprotein, the data presented in this thesis, besides offering an indication for the basis of origin selection, hint at the homeotic proteins as actors in the cross-talk between development and DNA replication regulation.

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Green, 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.

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Libros sobre el tema "Oncogenic protein"

Ludlow, John W. Tumor suppressors: Involvement in human diseases, viral protein interactions, and growth regulation. Austin: R.G. Landes, 1994.

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B, Murphy Peter y Clarke Jason R, eds. Oncogene proteins. New York: Nova Biomedical Books, 2008.

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H, Malloy Artur y Carson Earl C, eds. Oncogene proteins. New York: Nova Science Publishers, 2008.

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Guinivan, Phyllis. Selected abstracts on oncogene protein products. Bethesda, MD: U.S. Dept. of Health and Human Services, Public Health Service, National Institutes of Health, International Cancer Research Data Bank, National Cancer Institute, 1987.

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Collum, Robert Gerard. Studies on the structure and function of N-m y c. [New York]: [Columbia University], 1992.

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Carlos, Lacal Juan y McCormick Frank 1950-, eds. The Ras superfamily of GTPases. Boca Raton: CRC Press, 1993.

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Davis, Jeremy R. Oncoproteins: Types and detection. Hauppauge, N.Y: Nova Science, 2011.

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Pierre, Hainaut y Wiman Klas, eds. 25 years of p53 research. Dordrecht: Springer, 2005.

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Alexander, Tsygankov, ed. Cbl proteins. New York: Nova Science Publishers, 2008.

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Kellie, Stuart. Tyrosine kinases and neoplastic transformation. Austin: R.G. Landes, 1994.

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Capítulos de libros sobre el tema "Oncogenic protein"

Seldin, David C. y Esther Landesman-Bollag. "The Oncogenic Potential of CK2". En Protein Kinase CK2, 292–304. Oxford, UK: John Wiley & Sons, Inc., 2013. http://dx.doi.org/10.1002/9781118482490.ch10.

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Disis, Mary L., Helga Bernhard, Julie R. Gralow, Susan L. Hand, Sandra R. Emery, Emanuel Calenoff y Martin A. Cheever. "Immunity to the HER-2/neu Oncogenic Protein". En Ciba Foundation Symposium 187 - Vaccines Against Virally Induced Cancers, 198–211. Chichester, UK: John Wiley & Sons, Ltd., 2007. http://dx.doi.org/10.1002/9780470514672.ch13.

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Sawyer, T. K., R. S. Bohacek, W. C. Shakespeare, C. A. Metcalf, Y. Wang, R. Sundaramoorthi, T. Keenan, S. Narula y D. C. Dalgarno. "SMART Drug Design: Novel Phosphopeptide and ATP Mimetic-Based Small Molecule Inhibitors of the Oncogenic Protein Kinase pp60src (Src)". En Proteomics and Protein-Protein Interactions, 219–53. Boston, MA: Springer US, 2005. http://dx.doi.org/10.1007/0-387-24532-4_11.

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Yamamoto, Tadashi, Tetsu Akiyama, Kentaro Semba, Yuji Yamanashi, Kazushi Inoue, Yukinori Yamada, Jun Sukegawa y Kumao Toyoshima. "Oncogenic Potential and Normal Function of the Proto-Oncogenes Encoding Protein-Tyrosine Kinases". En Antimutagenesis and Anticarcinogenesis Mechanisms II, 321–39. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4615-9561-8_28.

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Benveniste, Etty N., G. Kenneth Gray y Braden C. McFarland. "Protein Kinase CK2 and Dysregulated Oncogenic Inflammatory Signaling Pathways". En Protein Kinase CK2 Cellular Function in Normal and Disease States, 259–80. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-14544-0_15.

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Bargmann, C. I., D. F. Stern, J. Drebin, A. Schechter y R. A. Weinberg. "Analysis of the neu-Encoded Protein and Its Mechanism of Oncogenic Activation". En Cell Cycle and Oncogenes, 63–68. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-71686-7_7.

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Li, S. C., C. M. Deber y S. E. Shoelson. "Glu-mediated dimerization of the transmembrane region of the oncogenic neu protein". En Peptides, 757–59. Dordrecht: Springer Netherlands, 1994. http://dx.doi.org/10.1007/978-94-011-0683-2_251.

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Byun, Wan Gi. "Identification of Small-Molecule Inhibitors of Oncogenic Lin28–Let-7 Interaction". En Discovery of Small-Molecule Modulators of Protein–RNA Interactions for Treating Cancer and COVID-19, 7–52. Singapore: Springer Nature Singapore, 2022. http://dx.doi.org/10.1007/978-981-19-7814-2_2.

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Jones, Janet E. y Juan Carlos Lacal. "Ras Proteins as Potential Activators of Protein Kinase C Function". En ras Oncogenes, 105–18. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4757-1235-3_16.

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Burck, Kathy B., Edison T. Liu y James W. Larrick. "src and Related Protein Kinases". En Oncogenes, 133–55. New York, NY: Springer New York, 1988. http://dx.doi.org/10.1007/978-1-4612-3718-1_7.

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Actas de conferencias sobre el tema "Oncogenic protein"

Smith, Matthew A., Richard Hall, Scott Haake, Jiannong Li y Eric B. Haura. "Abstract 3502: Proximity ligation assays reveal protein-protein interactions associated with oncogenic signaling and drug sensitivity." En Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-3502.

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Garcia, Laura A. Lopez, Maria E. Gierisch y Beat W. Schäfer. "Abstract A68: Posttranslational modifications of the oncogenic fusion protein EWS/FLI1". En Abstracts: AACR Special Conference: Pediatric Cancer at the Crossroads: Translating Discovery into Improved Outcomes; November 3-6, 2013; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.pedcan-a68.

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Burslem, George. "Abstract NG06: Addressing scaffolding roles of oncogenic kinases with targeted protein degradation". En Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-ng06.

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Li, Ming, Webster Cavenee y Frank Furnari. "Abstract 1193: Guanylate binding protein-1, a novel oncogenic gene in glioblastoma". En 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.am2011-1193.

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Schwentner, Raphaela, Maximilian O. Kauer, Sven Bilke, Gunhild Jug, Robert L. Walker, Paul S. Meltzer y Heinrich Kovar. "Abstract 4968: Modes of co-factor recruitment by an oncogenic fusion protein". En Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-4968.

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Hovhannisyan, Grant Henry y Ashot Vardan Marqaryan. "Abstract C213: Protein interaction analysis of mll-aff4 and mll-fel oncogenic fusion proteins using data mining approach." En Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Oct 19-23, 2013; Boston, MA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1535-7163.targ-13-c213.

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Dang, Hien T., Lucy Knight, Yotsawat Pomyen y Xin Wei Wang. "Abstract 4468: Oncogenic activation of the RNA binding protein AGO2 in hepatocellular carcinoma". En Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-4468.

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"Protein design and crystallization trials for constitutively active CysLT2R with oncogenic L129Q mutation". En Bioinformatics of Genome Regulation and Structure/Systems Biology (BGRS/SB-2022) :. Institute of Cytology and Genetics, the Siberian Branch of the Russian Academy of Sciences, 2022. http://dx.doi.org/10.18699/sbb-2022-166.

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Walensky, Loren D. "Abstract SY06-03: Stapled helical peptides to dissect and target oncogenic protein interactions." En Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-sy06-03.

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Angeles, Christina V., Markus Hafner, Nicholas D. Socci, Penelope DeCarolis, Thomas Tuschl y Samuel Singer. "Abstract 3100: The RNA-binding protein insulin-like growth factor 2 mRNA-binding protein 3 is oncogenic in liposarcoma". En Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-3100.

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Informes sobre el tema "Oncogenic protein"

Freeman, Michael R. The Oncogenic Palmitoyi-Protein Network in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, marzo de 2014. http://dx.doi.org/10.21236/ada610716.

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Freeman, Michael R. The Oncogenic Palmitoyl-Protein Network in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, marzo de 2013. http://dx.doi.org/10.21236/ada604582.

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Freeman, Michael R. The Oncogenic Palmitoyl-Protein Network in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, marzo de 2011. http://dx.doi.org/10.21236/ada544483.

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Yang, Zeng-Quan. Histone Code Modulation by Oncogenic PWWP-Domain Protein in Breast Cancers. Fort Belvoir, VA: Defense Technical Information Center, agosto de 2014. http://dx.doi.org/10.21236/ada611736.

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Yang, Zeng-Quan. Histone Code Modulation by Oncogenic PWWP-domain Protein in Breast Cancers. Fort Belvoir, VA: Defense Technical Information Center, junio de 2012. http://dx.doi.org/10.21236/ada564161.

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Yang, Zeng-Quan. Histone Code Modulation by Oncogenic PWWP-domain Protein in Breast Cancers. Fort Belvoir, VA: Defense Technical Information Center, junio de 2013. http://dx.doi.org/10.21236/ada584664.

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Yang, Zeng-Quan. Histone Code Modulation by Oncogenic PWWP-Domain Protein in Breast Cancers. Fort Belvoir, VA: Defense Technical Information Center, junio de 2010. http://dx.doi.org/10.21236/ada547591.

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Byers, Stephen W. Targeting of Oncogenic Proteins for Intracellular Degradation. Fort Belvoir, VA: Defense Technical Information Center, julio de 2002. http://dx.doi.org/10.21236/ada421110.

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Byers, Stephen. Targeting of Oncogenic Proteins for Intracellular Degradation. Fort Belvoir, VA: Defense Technical Information Center, julio de 2000. http://dx.doi.org/10.21236/ada391534.

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Byers, Stephen W. Targeting of Oncogenic Proteins for Intracellular Degradation (97breast). Fort Belvoir, VA: Defense Technical Information Center, julio de 1999. http://dx.doi.org/10.21236/ada390580.

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