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Phosphorylation Of Cdk2 At Threonine 39 By Akt Facilitates Cyclin-Cdk2 Activation, Thiago Bezerra Gaspar Carvalho Da Silva
Phosphorylation Of Cdk2 At Threonine 39 By Akt Facilitates Cyclin-Cdk2 Activation, Thiago Bezerra Gaspar Carvalho Da Silva
Open Access Dissertations
Cdk2 importantly regulates G1 progression. Cdk2 activation requires cyclin binding and phosphorylation at T160 by CAK. Here we describe a novel Cdk2 site whose Akt dependent phosphorylation appears to facilitate cyclin-Cdk2 assembly Cdk2 bears a Akt consensus motif containing threonine 39 (T39) immediately preceding the PSTAIRE helix. Cellular Cdk2 co-precipitated with Akt and Akt phosphorylated Cdk2 in vitro. Treatment of quiescent cells with serum leads to activation of the Akt pathway, followed by phosphorylation of Cdk2T39. This phosphorylation preceded the formation of cyclin-Cdk2 complexes and the phosphorylation at Cdk2T160. PI3K inhibition caused cyclin E dissociation from Cdk2, loss of CAK …
Balancing Effector And Regulatory T Cell Responses In Cancer And Autoimmunity, Taylor H. Schreiber
Balancing Effector And Regulatory T Cell Responses In Cancer And Autoimmunity, Taylor H. Schreiber
Open Access Dissertations
Activation of immunity to self-antigens is the goal in cancer immunotherapy, whereas blocking such responses is the goal in autoimmune disease. Thus, it is not surprising that investigation into cancer immunotherapy might also produce insights for the treatment of autoimmune disease. Heat shock protein, gp96, based therapies lead to the robust activation of CD8+ cytotoxic T cells that can slow tumor growth in 60-70% of mice, but only lead to the elimination of tumors in 30-40% of animals. The primary goal of the current studies was to understand why vaccination with a secreted gp96 vaccine was not efficacious in a …
Activation Of Non-Muscle Myosin Iib Helps Mediate Tnf-Alpha Cell Death Signaling, Patrick G. Flynn
Activation Of Non-Muscle Myosin Iib Helps Mediate Tnf-Alpha Cell Death Signaling, Patrick G. Flynn
Open Access Dissertations
TNF-alpha can stimulate a variety of kinases with the ability to activate non-muscle myosin II. As a result, increases in actin filament formation and actomyosin contractility (AMC) have been reported in response to TNF-alpha. These events are thought to play an important role in mediating TNF-alpha induced apoptosis but how they do so is unclear. In this study we prevented non-muscle myosin II activation in response to TNF-alpha by treating cells with the myosin light chain kinase (MLCK) inhibitor ML-7 or through isoform specific siRNA knockdown of myosin IIA and IIB. We found that treatment with ML-7 or knockdown of …