The research in our laboratory focuses on three main topics.
- Neurodegeneration/neuroinflammation and their relationship to apoptosis: Our aim is to study neurodegeneration (acute and chronic) in relation to cell death and survival and the interplay between these processes to neuroinflammation. In previous studies we showed that neuronal activity can promote the survival of neuronal-like cells under stressed condition and studied the association of the Alzheimer's disease-associated proteins, the presenilins, with apoptosis.
- The mechanism of action of pro-apoptotic proteins of the Bcl-2 family: The Bcl-2 family of proteins contains both anti- and pro-apoptotic members. The bcl-x gene encodes a 233-amino-acid protein containing four BH domains and a transmembrane region (Bcl-xL), Bcl-xS; however, as a result of alternative splicing, lacks an internal 63-amino-acid segment that contains the conserved BH1 and BH2 domains. It therefore contains only the BH3 and BH4 domains and the transmembrane region. Our studies showed that Bcl-xS induces apoptosis by mechanism which resembles the action of BH3-only proteins, i.e., it activates Bax and Bak and leads to the perforation of the mitochondria and to the induction of the apoptosome pathway. However, Bcl-xS has also some unique features such as an ability to form homodimers and the unique requirement of Bak for mediating its apoptotic effects in mouse embryonic fibroblasts (MEFs).
- The mechanism whereby the tumor suppressor neurofibromin regulates apoptosis and brain deficits: Neurofibromatosis type 1 (NF1) is characterized by a high incidence of benign and malignant tumors attributed to loss of function of Nf1, which encodes neurofibromin, a tumor suppressor with Ras- GTPase-activating protein (GAP) activity. Neurofibromin deficiency typically causes chronic activation of Ras, considered the major contributor to manifestation of NF1.
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