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Dysregulated growth factor signalling is one of the main causes of the haematological malignancies. Rab 7 plays an important role in the trafficking of growth factor receptors. This study was conducted to see whether knockdown of Rab 7 protein affects growth factor receptor signalling. Inhibition of Rab 7 can enhance phosphorylation of ERK 1/2 induced with IGF being stronger and sustainable, while EGF promotes activation of ERK 1/2 but not as strong as IGF. This means that Rab 7 plays an important and crucial role in the regulation of the growth factor receptor trafficking by maintaining…mehr

Produktbeschreibung
Dysregulated growth factor signalling is one of the main causes of the haematological malignancies. Rab 7 plays an important role in the trafficking of growth factor receptors. This study was conducted to see whether knockdown of Rab 7 protein affects growth factor receptor signalling. Inhibition of Rab 7 can enhance phosphorylation of ERK 1/2 induced with IGF being stronger and sustainable, while EGF promotes activation of ERK 1/2 but not as strong as IGF. This means that Rab 7 plays an important and crucial role in the regulation of the growth factor receptor trafficking by maintaining homeostasis of the cell. On the other hand defects or changes in the Rab7 protein by alteration in its gene through internal or external sources, causes derailed growth factor receptor signalling. Rab proteins and associated regulatory factors are frequents targets of mutation and or altered expression in a variety of haematological malignancies. If anything causing change in the Rab 7 either internal or external , responsible for the dysregulated growth factor receptor signalling leading to uncontrolled cell proliferation and ultimately to haematological malignancy.
Autorenporträt
Concluí o meu mestrado de KUT South Korea no programa de Engenharia Eléctrica. O meu trabalho principal centra-se nas energias renováveis, especificamente nas turbinas eólicas DFIG. O meu principal foco é a sua implementação em áreas fora da rede.