Mihail Iordanov, Ph.D.
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The question of whether an individual cell lives or dies is of paramount importance not only for the cell itself, but also for the multicellular organism that harbors it. Our research is oriented towards the understanding of the mechanisms of cell survival and programmed cell death (apoptosis) in specific cell types. For instance, one major project focuses on the signal transduction events that underlie the pro-survival and pro-apoptotic responses of human keratinocytes (the main cell type of the epidermis) to ultraviolet (UV) radiation, a relevant human skin carcinogen. We apply a plethora of molecular and cellular approaches to investigate the involvement of signaling proteins (e.g. receptors for growth factors and cytokines, GTPases, kinases, phosphatases, and transcription factors) in mediating the decisions of keratinocytes to survive or to commit cell suicide following exposure to UV. One example of a particular signaling pathway we investigate is the UV-induced regulation of the Ras GTPases and their downstream effectors, the extracellular signal-regulated kinases ERK1 and ERK2. Another major project focuses on the roles played by the stress-activated protein kinases JNK1 and JNK2 in the protective responses to toxic electrophilic compounds that challenge the cellular antioxidant defenses and cause oxidative stress. These compounds are either environmental pollutants (e.g. arsenic) or drug metabolites produced inside cells by cellular drug-activating enzymes. Our research may lead to the development of novel strategies for counteracting the harmful impact of important environmental pollutants and human.
"Proximal giant neurofilamentous axonopathy in mice genetically engineered to resist calpain and caspase cleavage of Î±-II spectrin,"
"An epidermotypic model of interface dermatitis reveals individual functions of fas ligand and gamma interferon in hypergranulosis, cytoid body formation, and gene expression,"
"Doxorubicin and daunorubicin induce processing and release of interleukin-1Î² through activation of the NLRP3 inflammasome,"
"ZAK is required for doxorubicin, a novel ribotoxic stressor, to induce SAPK activation and apoptosis in HaCaT cells,"
"Th17 cytokines stimulate CCL20 expression in keratinocytes in vitro and in vivo: Implications for psoriasis pathogenesis,"