High Mobility Group (HMG) A1 proteins are gene regulatory factors whose overexpression is frequently observed in naturally occurring human cancers. Overexpression of transgenic HMGA1 proteins in cells results in neoplastic transformation and promotes progression to malignant cellular phenotypes. The following thesis describes evidence indicating that two likely mechanisms in which the HMGA1a protein promotes malignant changes in cells are through increased sensitivity to activation of the Ras/ERK signaling pathway and by direct regulation of KIT ligand gene expression. These results implicate both HMGA1 as a chemotherapeutic target for Ras/ERK signaling inhibition and plasma KIT ligand as a diagnostic marker for HMGA1-positive carcinomas. In addition, the following thesis will describe the characterization of the HMGA1 mouse gene sequence, its comparison to the human gene, and its importance for generating conditional HMGA1 gene deletion mice. These mice will be important for characterizing the role of HMGA1 in not only the development of cancer, but also, among other biological phenomenon, of embryogenesis and T cell activation.
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Dr. Treff is currently Director of Molecular Biology, RMA of New Jersey, and Assistant Professor, UMDNJ-RWJ Medical School. He completed his PhD at WSU while earning an NIH pre-doctoral fellowship, and obtained NIH funded postdoctoral training in stem cell and reproductive biology at UW-Madison and the EMD-Serono Research Institute.
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Taschenbuch. Zustand: Neu. This item is printed on demand - it takes 3-4 days longer - Neuware -High Mobility Group (HMG) A1 proteins are gene regulatory factors whose overexpression is frequently observed in naturally occurring human cancers. Overexpression of transgenic HMGA1 proteins in cells results in neoplastic transformation and promotes progression to malignant cellular phenotypes. The following thesis describes evidence indicating that two likely mechanisms in which the HMGA1a protein promotes malignant changes in cells are through increased sensitivity to activation of the Ras/ERK signaling pathway and by direct regulation of KIT ligand gene expression. These results implicate both HMGA1 as a chemotherapeutic target for Ras/ERK signaling inhibition and plasma KIT ligand as a diagnostic marker for HMGA1-positive carcinomas. In addition, the following thesis will describe the characterization of the HMGA1 mouse gene sequence, its comparison to the human gene, and its importance for generating conditional HMGA1 gene deletion mice. These mice will be important for characterizing the role of HMGA1 in not only the development of cancer, but also, among other biological phenomenon, of embryogenesis and T cell activation. 132 pp. Englisch. Bestandsnummer des Verkäufers 9783838315065
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Zustand: New. Dieser Artikel ist ein Print on Demand Artikel und wird nach Ihrer Bestellung fuer Sie gedruckt. Autor/Autorin: Treff NathanDr. Treff is currently Director of Molecular Biology, RMA of New Jersey, and Assistant Professor, UMDNJ-RWJ Medical School. He completed his PhD at WSU while earning an NIH pre-doctoral fellowship, and obtained NIH funded. Bestandsnummer des Verkäufers 5412193
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Taschenbuch. Zustand: Neu. nach der Bestellung gedruckt Neuware - Printed after ordering - High Mobility Group (HMG) A1 proteins are gene regulatory factors whose overexpression is frequently observed in naturally occurring human cancers. Overexpression of transgenic HMGA1 proteins in cells results in neoplastic transformation and promotes progression to malignant cellular phenotypes. The following thesis describes evidence indicating that two likely mechanisms in which the HMGA1a protein promotes malignant changes in cells are through increased sensitivity to activation of the Ras/ERK signaling pathway and by direct regulation of KIT ligand gene expression. These results implicate both HMGA1 as a chemotherapeutic target for Ras/ERK signaling inhibition and plasma KIT ligand as a diagnostic marker for HMGA1-positive carcinomas. In addition, the following thesis will describe the characterization of the HMGA1 mouse gene sequence, its comparison to the human gene, and its importance for generating conditional HMGA1 gene deletion mice. These mice will be important for characterizing the role of HMGA1 in not only the development of cancer, but also, among other biological phenomenon, of embryogenesis and T cell activation. Bestandsnummer des Verkäufers 9783838315065
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Taschenbuch. Zustand: Neu. This item is printed on demand - Print on Demand Titel. Neuware -High Mobility Group (HMG) A1 proteins are gene regulatory factors whose overexpression is frequently observed in naturally occurring human cancers. Overexpression of transgenic HMGA1 proteins in cells results in neoplastic transformation and promotes progression to malignant cellular phenotypes. The following thesis describes evidence indicating that two likely mechanisms in which the HMGA1a protein promotes malignant changes in cells are through increased sensitivity to activation of the Ras/ERK signaling pathway and by direct regulation of KIT ligand gene expression. These results implicate both HMGA1 as a chemotherapeutic target for Ras/ERK signaling inhibition and plasma KIT ligand as a diagnostic marker for HMGA1-positive carcinomas. In addition, the following thesis will describe the characterization of the HMGA1 mouse gene sequence, its comparison to the human gene, and its importance for generating conditional HMGA1 gene deletion mice. These mice will be important for characterizing the role of HMGA1 in not only the development of cancer, but also, among other biological phenomenon, of embryogenesis and T cell activation.VDM Verlag, Dudweiler Landstraße 99, 66123 Saarbrücken 132 pp. Englisch. Bestandsnummer des Verkäufers 9783838315065
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Taschenbuch. Zustand: Neu. HMGA1 and Cancer Progression | Molecular Genetics of HMGA1-mediated malignant transformation of breast cancer cells | Nathan Treff | Taschenbuch | 132 S. | Englisch | 2010 | LAP LAMBERT Academic Publishing | EAN 9783838315065 | Verantwortliche Person für die EU: preigu GmbH & Co. KG, Lengericher Landstr. 19, 49078 Osnabrück, mail[at]preigu[dot]de | Anbieter: preigu. Bestandsnummer des Verkäufers 101485328
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