دورية أكاديمية
Ras family of proteins: Cellular function, molecular control, and its role in oncogenesis [Ras protein ailesi: Hücresel i̇şlevi, moleküler kontrolü, onkogenezdeki rolü]
| العنوان: | Ras family of proteins: Cellular function, molecular control, and its role in oncogenesis [Ras protein ailesi: Hücresel i̇şlevi, moleküler kontrolü, onkogenezdeki rolü] |
|---|---|
| المؤلفون: | Telkoparan P., Tazebay, U.H. |
| المصدر: | Turkish Journal of Biochemistry |
| سنة النشر: | 2011 |
| المجموعة: | Bilkent University: Institutional Repository |
| مصطلحات موضوعية: | Oncogenesis, Ras family, RasGAP, RasGEF, Small G-proteins, guanine nucleotide exchange factor, guanosine triphosphatase activating protein, guanosine triphosphate, Ras protein, article, carcinogenesis, cell differentiation, cell division, cell function, cell proliferation, cell structure, conformational transition, controlled study, cytoplasm, gene expression, gene mutation, genetic code, human, oncogene ras, phosphorylation, protein hydrolysis, protein interaction, protein protein interaction, protein transport |
| الوصف: | Small GTPases belonging to Ras family of proteins have key roles in regulating nearly every aspect of cell biology, such as cell division, cellular differentiation, vesicular transport and localization of cargo proteins, cell morphology, and gene expression. Depending on the extracellular signals, Ras family members oscillate between GTP-bound (active) and GDP-bound (inactive) conformations, and in the active form they interact with downstream effector molecules, leading to conformational changes in those effectors. As a result, extracellular signals trigger cellular responses, by means of initiation of a phosphorylation cascade. Functional cycles of Ras family of proteins include interactions with GTPase Activating Proteins (GAPs), and with Guanine Nucleotide Exchange Factors (GEFs) that regulate these small GTPases. GAP proteins activate intrinsic GTP hydrolysis activities of these small G-proteins, and convert active Ras-GTP to inactive Ras-GTP. On the other hand, GEF proteins interact with inactivated Ras-GDP molecules, and convert those inactivated molecules back to activated Ras-GTP, by triggering dissociation of GDP, and reassociation of Ras with GTP which is found at higher concentrations as compared to GDP in the cell cytoplasm. It is well known that mutations in Ras that block these molecules in GTP-bound forms by impairing GTP hydrolysis activity could trigger an uncontrolled and aberrant cellular proliferation. This type of mutations in Ras genes causing uncontrolled activation of the protein, are found in approximately 30% of human cancers overall, and they indicate the significance of mutations in genes encoding Ras family members in cellular proliferation related to de novo oncoge-nesis in human. |
| نوع الوثيقة: | article in journal/newspaper |
| وصف الملف: | application/pdf |
| اللغة: | English Turkish |
| تدمد: | 1303829X |
| العلاقة: | http://hdl.handle.net/11693/21674Test |
| الإتاحة: | http://hdl.handle.net/11693/21674Test |
| رقم الانضمام: | edsbas.7DBBEF48 |
| قاعدة البيانات: | BASE |
| تدمد: | 1303829X |
|---|