Ras family of proteins: Cellular function, molecular control, and its role in oncogenesis

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dc.citation.epage373en_US
dc.citation.issueNumber4en_US
dc.citation.spage367en_US
dc.citation.volumeNumber36en_US
dc.contributor.authorTelkoparan, P.en_US
dc.contributor.authorTazebay, U. H.en_US
dc.date.accessioned2016-02-08T09:49:36Z
dc.date.available2016-02-08T09:49:36Z
dc.date.issued2011en_US
dc.departmentDepartment of Molecular Biology and Geneticsen_US
dc.description.abstractSmall 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.en_US
dc.identifier.issn1303-829X
dc.identifier.urihttp://hdl.handle.net/11693/21674
dc.language.isoTurkishen_US
dc.publisherTürk Biyokimya Derneğien_US
dc.source.titleTurkish Journal of Biochemistry [Türk Biyokimya Dergisi]en_US
dc.subjectOncogenesisen_US
dc.subjectRas familyen_US
dc.subjectRasGAPen_US
dc.subjectRasGEFen_US
dc.subjectSmall G-proteinsen_US
dc.titleRas family of proteins: Cellular function, molecular control, and its role in oncogenesisen_US
dc.title.alternativeRas protein ailesi: Hücresel işlevi, moleküler kontrolü, onkogenezdeki rolüen_US
dc.typeArticleen_US
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