Phhoscholation Of JNK Phosphorylation

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Activator protein-1 (AP-1) is a transcription factor made up of a number of proteins such as c-Jun, mentioned above, which forms a complex with others such as c-fos and is an important substrate of JNK phosphorylation playing a role in regulation of gene expression relating to a number of cytokines (Gius et al, 1999; Johnson and Lapadat, 2002; Weston and Davis, 2007). The c-Jun can arrange into homodimers with itself but only occurs when c-fos is not present and it can also arrange into a heterodimer with c-fos (Halazonetis et al, 1988). Phosphorylation by JNK on c-Jun occurs at the N-terminal in the activation domain at serine 63 and serine 73 and creates the ability for precision in signal transduction from the membrane into the…show more content…
UV radiation can produce apoptosis in cells however it was shown through c-Jun wildtype and c-Jun null mutants in varying quantities of UV that mouse fibroblast cells lacking c-Jun had greater levels of cell death. This occurrence could be seen with a number of the different UV quantities and over many time points and was confirmed to be apoptosis through DNA end-labelling assays. The paper suggested that the c-Jun could represent a checkpoint stopping growth and allowing DNA repair or it could act to help initiate production of genes that inhibit cell death. Apoptosis may be inhibited by JNK and c-Jun but a second cellular response suggests they may stimulate this method of cell death (Leppä and Bohmann, 1999). One study showed that JNK1 initiation rose quickly when in the presence of both a low and high quantity of UV-C radiation (Chen et al, 1996). They created JNK1 overexpression Jurkat cells, which did not actually overexpress the JNK but did show varying results to the wildtype. Through the use of flow cytometry, they showed that in all but one of the overexpressing samples when exposed to radiation, apoptosis occurred, with samples that had greater initiation of JNK also having higher sensitivity to cell death by radiation suggesting a link between initiation of JNK and radiation-induced apoptosis. Cell death by both UV-C and radiation was blocked by mutants with the
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