Goda Snieckute
Postdoc
Cells have the capacity to cope with external stress. They do so by activating signaling cascades that result in the appropriate biological response. The MAP kinase p38-signaling pathway is essential for stress response and is activated by different stressors such as UV light, inflammatory cytokines and osmotic stress. p38 is activated through a signal transduction cascade by upstream MAP2 and MAP3 kinases.
Solar radiation emits UV light that is primarily responsible for causing damage and cancer in exposed skin. In mice it has been shown that p38 inhibition protects animals from several detrimental effects of acute UV irradiation, namely apoptosis, inflammation, and a hyperproliferation response. We have shown that the upstream MAP3 kinase ZAK is required for p38 activation upon UV radiation.
For my PhD thesis my main aim is to elucidate a physiological role of the ZAK MAP3 kinase in UV-induced skin inflammation and sunburn formation.
In our laboratory, we have established ZAK deficient mice that I challenge with UV irradiation and decipher macroscopic as well as microscopic changes in the animal. In addition, I look for biological markers of skin inflammation, p38 activation and apoptotic cells. Finally, I will investigate if UV-ZAK-p38 mediated inflammatory signalling contributes to skin cancer development. We hope that upstream inactivation of the pathway will have therapeutic value for people suffering from excessive and acute sunburns.
ID: 33146755
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Alternative Translation Initiation Generates a Functionally Distinct Isoform of the Stress-Activated Protein Kinase MK2
Research output: Contribution to journal › Journal article › Research › peer-review
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93
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Insulin-induced serine 22 phosphorylation of retinoid X receptor alpha is dispensable for adipogenesis in brown adipocytes
Research output: Contribution to journal › Journal article › Research › peer-review
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59
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ZAKβ is activated by cellular compression and mediates contraction-induced MAP kinase signaling in skeletal muscle
Research output: Contribution to journal › Journal article › Research › peer-review
Published