IndraLab

Statements


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"It was recently revealed that PKCtheta, a facilitator of TCR and CD28 induced NFkappaB signaling, binds to CYLD in T cells antagonizing the DUB 's inhibition of NFkappaB and NFAT transactivation."

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"The formation of a direct PKCtheta and CYLD complex appears to regulate the short-term spatial distribution of CYLD, subsequently affecting NFkappaB and NFAT repressional activity of CYLD prior to its MALT1 dependent inactivation."

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"Interestingly, we observed increased activation of PKC-theta and NF-kappaB in CYLD deficient CD8 + T cells, suggesting that the interaction between CYLD and PKC-theta might also lead to the inhibition of PKC-theta-mediated NF-kappaB activation."

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"The different requirement for PKC and the altered kinetics in the mouse system led to the analysis of the stimulation dependent spatial and temporal organization of the PKCtheta and CYLD complex using immunofluorescence microscopy."

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"Alternatively, the existence of a constitutive CYLD and PKCtheta complex might suggest that PKCtheta, which shows activation dependent subcellular translocation, is important for removing CYLD from its NFkappaB related targets and attenuates the negative regulatory function of CYLD, enabling feedback control of NFkappaB activation."

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"demonstrated that PKC-theta interacts with CYLD leading to inhibition of CYLD function."