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Full-Text Articles in Molecular Biology
Erk3 Negatively Regulates The Il-6/Stat3 Signaling Via Socs3, Astha Shakya
Erk3 Negatively Regulates The Il-6/Stat3 Signaling Via Socs3, Astha Shakya
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Mitogen activated protein kinases (MAPKs) are Ser/Thr kinases that relay the extracellular signal into intracellular responses and regulate several biological responses. They are classified into conventional MAPKs and atypical MAPKs. Extracellular signal regulated kinase 3 (ERK3) is an atypical MAPK that has a single phospho-acceptor site (Ser 189) in its activation motif instead of the canonical Thr-Xaa-Tyr (TXY) motif of conventional MAPK like ERK1/2. ERK3 comprises of a unique C terminal tail and a central C34 domain that further distinguishes it from ERK1/2. Moreover, compared to ERK1/2, much less is known about the upstream activators and the downstream targets of …
Role Of Erk3 In Regulating Rhogdi1-Paks Signaling Axis, Hitham Abdulrahman Aldharee
Role Of Erk3 In Regulating Rhogdi1-Paks Signaling Axis, Hitham Abdulrahman Aldharee
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Extracellular signal-regulated kinase 3 (ERK3) is an atypical protein kinase of the mitogen-activated protein kinase (MAPK) family. In comparison to well-investigated ERK1/2 (classical) MAPKs, much less has been discovered about ERK3 signaling and its cellular functions. Recent studies have shown that ERK3 is overexpressed in various types of cancers such as lung cancer and breast cancer and that ERK3 promotes cancer cell migration and invasion. How ERK3 regulates cancer cell motility and invasiveness, however, is still largely unknown. RhoGTPases, including Rho, Cdc42 and Rac1, play critical roles in regulating cell motility and invasiveness through activating downstream effectors such as p21-activated …
Mdm2 Amplification In Nih3t3l1 Preadipocytes Leads To Mdm2 Elevation In Terminal Adipogenesis, Vaughn Litteral
Mdm2 Amplification In Nih3t3l1 Preadipocytes Leads To Mdm2 Elevation In Terminal Adipogenesis, Vaughn Litteral
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The p53 protein is a tumor suppressor protein that is mutated or non-functional in nearly all cancers. The Mdm2 protein has the ability to functionally inactivate p53 and these two proteins have been studied extensively in the context of cellular proliferation. In this study, expression of the murine double minute 2 (mdm2) gene was examined in the mouse NIH3T3L1 cell line. Under the proper conditions, the immortalized NIH3T3L1 cells have the ability to differentiate from fibroblasts to adipocytes (Green et al., 1975). This well characterized cell line provides an excellent model to study mdm2 in differentiation. While evaluating the regulation …