Auswahl der wissenschaftlichen Literatur zum Thema „Oncogene Protein p21(ras)“
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Zeitschriftenartikel zum Thema "Oncogene Protein p21(ras)"
Lowe, D. G., und D. V. Goeddel. „Heterologous expression and characterization of the human R-ras gene product“. Molecular and Cellular Biology 7, Nr. 8 (August 1987): 2845–56. http://dx.doi.org/10.1128/mcb.7.8.2845-2856.1987.
Der volle Inhalt der QuelleLowe, D. G., und D. V. Goeddel. „Heterologous expression and characterization of the human R-ras gene product.“ Molecular and Cellular Biology 7, Nr. 8 (August 1987): 2845–56. http://dx.doi.org/10.1128/mcb.7.8.2845.
Der volle Inhalt der QuelleMandanas, RA, DS Leibowitz, K. Gharehbaghi, T. Tauchi, GS Burgess, K. Miyazawa, HN Jayaram und HS Boswell. „Role of p21 RAS in p210 bcr-abl transformation of murine myeloid cells“. Blood 82, Nr. 6 (15.09.1993): 1838–47. http://dx.doi.org/10.1182/blood.v82.6.1838.1838.
Der volle Inhalt der QuelleMandanas, RA, DS Leibowitz, K. Gharehbaghi, T. Tauchi, GS Burgess, K. Miyazawa, HN Jayaram und HS Boswell. „Role of p21 RAS in p210 bcr-abl transformation of murine myeloid cells“. Blood 82, Nr. 6 (15.09.1993): 1838–47. http://dx.doi.org/10.1182/blood.v82.6.1838.bloodjournal8261838.
Der volle Inhalt der QuelleLacal, J. C., A. Cuadrado, J. E. Jones, R. Trotta, D. E. Burstein, T. Thomson und A. Pellicer. „Regulation of protein kinase C activity in neuronal differentiation induced by the N-ras oncogene in PC-12 cells“. Molecular and Cellular Biology 10, Nr. 6 (Juni 1990): 2983–90. http://dx.doi.org/10.1128/mcb.10.6.2983-2990.1990.
Der volle Inhalt der QuelleLacal, J. C., A. Cuadrado, J. E. Jones, R. Trotta, D. E. Burstein, T. Thomson und A. Pellicer. „Regulation of protein kinase C activity in neuronal differentiation induced by the N-ras oncogene in PC-12 cells.“ Molecular and Cellular Biology 10, Nr. 6 (Juni 1990): 2983–90. http://dx.doi.org/10.1128/mcb.10.6.2983.
Der volle Inhalt der QuellePan, B. T., und G. M. Cooper. „Role of phosphatidylinositide metabolism in ras-induced Xenopus oocyte maturation“. Molecular and Cellular Biology 10, Nr. 3 (März 1990): 923–29. http://dx.doi.org/10.1128/mcb.10.3.923-929.1990.
Der volle Inhalt der QuellePan, B. T., und G. M. Cooper. „Role of phosphatidylinositide metabolism in ras-induced Xenopus oocyte maturation.“ Molecular and Cellular Biology 10, Nr. 3 (März 1990): 923–29. http://dx.doi.org/10.1128/mcb.10.3.923.
Der volle Inhalt der QuelleMcCoy, M. S., und R. A. Weinberg. „A human Ki-ras oncogene encodes two transforming p21 proteins“. Molecular and Cellular Biology 6, Nr. 4 (April 1986): 1326–28. http://dx.doi.org/10.1128/mcb.6.4.1326-1328.1986.
Der volle Inhalt der QuelleMcCoy, M. S., und R. A. Weinberg. „A human Ki-ras oncogene encodes two transforming p21 proteins.“ Molecular and Cellular Biology 6, Nr. 4 (April 1986): 1326–28. http://dx.doi.org/10.1128/mcb.6.4.1326.
Der volle Inhalt der QuelleDissertationen zum Thema "Oncogene Protein p21(ras)"
Iritani, Brian Masao. „Control of B lymphocyte development by Ras and Raf /“. Thesis, Connect to this title online; UW restricted, 1997. http://hdl.handle.net/1773/8322.
Der volle Inhalt der QuelleBradbury, Andrew W. „Cyclic AMP binding proteins and ras p21 oncogene expression in human colorectal cancer and mucosa“. Thesis, University of Edinburgh, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.531024.
Der volle Inhalt der QuelleEstrozi, Bruna. „Avaliação anatomoclínica e molecular do melanoma cutâneo em pacientes jovens (idade 18-30 anos)“. Universidade de São Paulo, 2015. http://www.teses.usp.br/teses/disponiveis/5/5144/tde-01042015-144721/.
Der volle Inhalt der QuelleThe incidence of cutaneous melanoma in young adults has dramatically increased in recent years. However, there is scarce data about the clinicopathological and molecular characteristics on the melanomas occurring at this age group. The present study aimed to evaluate 132 patients aged between 18 and 30 years with primary cutaneous melanoma with emphasis on the study of clinical, histopathological characteristics and molecular evaluation of mutations in BRAF, NRAS and KIT genes. Regarding the clinical and histopathological findings, the following results were found: female predominance (61.4%), trunk was the most commonly anatomical site involved (44.3%) and superficial spreading melanoma, was the most common histological type (79.5 %). The V600E mutation in BRAF (BRAFV600E) gene was analyzed in 93 cases, using RT-PCR. It was present in 38.7% (36/93) and statistically related to the vertical growth phase (p = 0.01), mild inflammatory infiltration (p = 0.02) and the presence of intradermal mitosis (p = 0.004). There was, also, strongly evidence of an association with the presence of ulceration (p = 0.05). Worse prognosis was associated with these variables. There was a predominance of BRAFV600E mutation in anatomical regions related to intermittent sun exposure. No cases of melanoma with BRAFV600E mutation showed regression phenomenon (p < 0.05). There was no significant association between BRAFV600E and gender, histological type, Clark level, Breslow thickness, solar elastosis, angiolymphatic and perineural invasion, sattelitosis, coexisting melanocytic nevus and survival. The presence of a mutation in NRAS, by RT-PCR was seen in 3.95% (3/76) of the cases. All these three mutations were of type 61K, occurred in male patients and the head and neck region. BRAFV600E and NRAS mutations, when present, were mutually exclusive. The frequency of KIT mutations, analyzed by sequencing, was 11.1% (3/27). The three mutations identified in this gene were located in exon 9 (G510, G498S and 489I). Concomitant mutations were found between KIT and NRAS and BRAFV600E. Due to the small number of KIT and NRAS mutated cases, it was not possible to establish clinical and histopathological correlations and mutation status in these genes. This study was the first to describe the G510D and G498S mutations in KIT gene in cutaneous melanomas. In the present study, BRAFV600E mutation in cutaneous melanoma of young adults correlated with anatomic and clinical features of worse prognosis compared to wild type
Filho, João Bosco de Oliveira. „Mutação em NRAS causa uma síndrome autoimune linfoproliferativa humana“. Universidade de São Paulo, 2008. http://www.teses.usp.br/teses/disponiveis/5/5144/tde-04112008-174252/.
Der volle Inhalt der QuelleThe p21 RAS subfamily of small GTPases, including KRAS, HRAS, and NRAS, regulates cell proliferation, cytoskeletal organization and other signaling networks, and is the most frequent target of activating mutations in cancer. Activating germline mutations of KRAS and HRAS cause severe developmental abnormalities leading to Noonan, cardio-facial-cutaneous and Costello syndrome, but activating germline mutations of NRAS have not been reported. Autoimmune lymphoproliferative syndrome (ALPS) is the most common genetic disease of lymphocyte apoptosis and causes autoimmunity as well as excessive lymphocyte accumulation, particularly of CD4-, CD8- ab T cells. Mutations in ALPS typically affect Fas-mediated apoptosis, but certain ALPS individuals have no such mutations. We show here that the salient features of ALPS as well as a predisposition to hematological malignancies can be caused by a heterozygous germline Gly13Asp activating mutation of the NRAS oncogene that does not impair Fas-mediated apoptosis. The increase in active, GTP-bound NRAS augmented RAF/MEK/ERK signaling which markedly decreased the pro-apoptotic protein BIM and attenuated intrinsic, nonreceptor-mediated mitochondrial apoptosis. Thus, germline activating mutations in NRAS differ from other p21 Ras oncoproteins by causing selective immune abnormalities without general developmental defects
Driscoll, David R. „The Impact of mTORC2 Signaling on the Initiation and Progression of KRAS-Driven Pancreatic Neoplasias: A Dissertation“. eScholarship@UMMS, 2016. https://escholarship.umassmed.edu/gsbs_diss/821.
Der volle Inhalt der QuelleDriscoll, David R. „The Impact of mTORC2 Signaling on the Initiation and Progression of KRAS-Driven Pancreatic Neoplasias: A Dissertation“. eScholarship@UMMS, 2003. http://escholarship.umassmed.edu/gsbs_diss/821.
Der volle Inhalt der QuelleMartins, Carla Pedro. „Cip/Kip proteins in the suppression of murine lymphomagenesis“. [S.l. : Amsterdam : s.n.] ; Universiteit van Amsterdam [Host], 2003. http://dare.uva.nl/document/67628.
Der volle Inhalt der QuelleAlexandre, Cristianne da Silva. „As células linhagem negativa (Lin) de medula óssea atenuam a progressão da doença renal crônica“. Universidade de São Paulo, 2008. http://www.teses.usp.br/teses/disponiveis/5/5148/tde-10032008-150329/.
Der volle Inhalt der QuelleProgressive renal failure continues to be a challenge. The use of bone marrowderived stem cells (SCs) represents a means of meeting that challenge. We used lineage-negative (Lin-) SCs to test the hypothesis that Lin- cell infusion decreases renal injury. Syngeneic Fischer 344 rats were submitted to 5/6 nephrectomy and divided into 3 groups: Nx (untreated); NxSC1 (receiving 2 × 106 Lin- cells on postnephrectomy day 15); and NxSC3 (receiving 2 × 106 Lin- cells on postnephrectomy days 15, 30 and 45). Controls were unoperated/untreated. On postnephrectomy day 60, clearance studies, immunohistochemistry and immunoblotting were performed. Lin- cell infusion effectively reduced postnephrectomy proteinuria, glomerulosclerosis, anemia, renal infiltration of immune cells and monocyte chemoattractant protein-1 protein expression, as well as decreasing the interstitial area. Immunostaining for proliferating cell nuclear antigen showed that, in comparison with controls, Nx rats presented greater cell proliferation, whereas NxSC1 rats and NxSC3 rats presented less cell proliferation than did Nx rats. Protein expression of p21 and VEGF increased after nephrectomy and decreased after Lin- cell infusion. Protein expression of eNOS reduced after nephrectomy and increased after cell infusion. These data suggest that SC treatment ameliorates progressive end-stage renal disease.
Golbert, Lenara. „Implicações do aumento da expressão do proto-oncogene Ras no bócio multinodular“. reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2006. http://hdl.handle.net/10183/7815.
Der volle Inhalt der QuelleMultinodular goiter (MNG) is an enlargement of the thyroid gland and is characterized by heterogeneity in growth and function of thyroid follicular cells. It is a common pathology, with higher prevalence in iodine deficiency areas. Iodine deficiency is the main etiologic factor for MNG. MNG have been considered a true thyroid neoplasm. The pathogenesis of multinodular goiter is not yet clarified. The purpose of this review is to summarize the current knowledge of MNG with respect to the pathology, etiologic and clinical characteristics.
Benisty, Hannah 1986. „Post-transcriptional determinants of RAS protein abundance“. Doctoral thesis, Universitat Pompeu Fabra, 2019. http://hdl.handle.net/10803/668206.
Der volle Inhalt der QuelleEls oncogens KRAS, NRAS i HRAS estan mutats en un terç dels càncers en humans on hi exhibeixen patrons de mutació diferents. Un possible factor que contribueix a aquest biaix de mutació és la variació dels nivells d'expressió de RAS. En aquesta tesi investigo els elements determinants de l'abundància de la proteïna RAS. Primer, examino si el biaix de codó entre els gens RAS i entre gens d'altres famílies implicades en càncer contribueix a les diferències d'expressió, en funció del context cel·lular. Així mateix, descric un programa d'expressió de tRNA que facilita la traducció d'oncogens en cèl·lules proliferatives. En segon lloc, investigo per què mutants oncogènics de RAS tenen una abundància de proteïna més elevada que la RAS salvatge. Així mateix, estudio els mecanismes subjacents responsables d'aquesta variació i més concretament el paper de les interaccions de RAS amb altres proteïnes en la regulació de la seva abundància. Així doncs, aquesta tesi estudia la possible rellevància dels mecanismes de síntesi i degradació de la proteïna RAS en els patrons de mutació en càncer.
Bücher zum Thema "Oncogene Protein p21(ras)"
Vivo, Immaculata De. Mutated ras P21 in chemical carcinogenesis of vinyl chloride-exposed workers. 1993, 1993.
Den vollen Inhalt der Quelle findenBuchteile zum Thema "Oncogene Protein p21(ras)"
Yiagnisis, M., K. Papadimitriou und D. A. Spandidos. „Human Thyroid Neoplasms Express ras p21 Protein at High Levels“. In ras Oncogenes, 47–49. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4757-1235-3_8.
Der volle Inhalt der Quellede Gunzburg, Jean, Rebecca Riehl und Robert A. Weinberg. „Identification of a Protein Interacting with ras-p21- by Chemical Cross-Linking“. In ras Oncogenes, 281–85. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4757-1235-3_37.
Der volle Inhalt der QuelleWillumsen, Berthe M., und Douglas R. Lowy. „P21 ras Transforming Protein: Significance of the Carboxy Terminus“. In RNA Tumor Viruses, Oncogenes, Human Cancer and AIDS: On the Frontiers of Understanding, 25–40. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4613-2583-3_3.
Der volle Inhalt der QuellePizon, V., P. Chardin, I. Lerosey und A. Tavitian. „The rap Proteins : GTP Binding Proteins Related to p21 ras with a Possible Reversion Effect on ras Transformed Cells“. In ras Oncogenes, 83–91. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4757-1235-3_13.
Der volle Inhalt der QuelleMarshall, M. S., M. D. Schaber, U. S. Vogel, W. S. Hill, A. S. Ng, E. M. Scolnick, R. A. F. Dixon, I. S. Sigal und J. B. Gibbs. „The ras Oncogene Protein“. In Molecular Mechanisms of Hormone Action, 85–91. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-75022-9_10.
Der volle Inhalt der QuelleLeftheris, K., T. Kline, W. Lau, L. Mueller, V. S. Goodfellow, M. K. DeVirgilio, Y. H. Cho et al. „Tetrapeptide based inhibitors of p21 ras protein farnesyl transferase“. In Peptides, 622–24. Dordrecht: Springer Netherlands, 1994. http://dx.doi.org/10.1007/978-94-011-0683-2_205.
Der volle Inhalt der QuelleTeruya, Kiichiro, Sanetaka Shirahata, Takahiro Yano, Junko Watanabe, Kiyohiko ki Se, Kazuhiro Osada, Hirofumi Tachibana, Hideya Ohashi und Hiroki Murakami. „RAS Oncogene Enhances the Various Recombinant Protein Productivities of BHK-21 Cells Regulated by the CMV Promoter“. In Animal Cell Technology: Developments Towards the 21st Century, 91–95. Dordrecht: Springer Netherlands, 1995. http://dx.doi.org/10.1007/978-94-011-0437-1_15.
Der volle Inhalt der QuelleAgnantis, N. J., A. Pintzas, A. Kakkanas, P. Markoulatos und D. A. Spandidos. „Expression of the ras Oncogene p 21 Protein in Human Breast Tumors and in Several Benign Conditions Using the Y13 259 Monoclonal Antibody“. In Fundamental Problems in Breast Cancer, 323–25. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4613-2049-4_36.
Der volle Inhalt der QuelleDonato, Armando Di, Shiv K. Srivastava und Juan Carlos Lacal. „Analysis of the Biochemical and Biological Activities of Deletion Mutants of the H-Ras P21 Protein Suggest That Gap is an Essential Component of Its Effector Function“. In The Guanine — Nucleotide Binding Proteins, 179–90. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4757-2037-2_17.
Der volle Inhalt der QuelleWittinghofer, Alfred, und Alfonso Valencia. „Three-dimensional structure of Ras and Ras-related proteins“. In Guidebook to the Sinall GTPases, 20–29. Oxford University PressOxford, 1995. http://dx.doi.org/10.1093/oso/9780198599456.003.0003.
Der volle Inhalt der QuelleKonferenzberichte zum Thema "Oncogene Protein p21(ras)"
Pirogova, Elena, Vuk Vojisavljevic und Irena Cosic. „Prediction of protein active and/or binding site using time-frequency analysis: Application to ras oncogene proteins“. In 2012 ISSNIP Biosignals and Biorobotics Conference: Biosignals and Robotics for Better and Safer Living (BRC). IEEE, 2012. http://dx.doi.org/10.1109/brc.2012.6222173.
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