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Research Focus: The regulation of cytoplasmic dynein by Lis1 and Ndel1 in development and disease.
Cells exhibit an array of behaviors that require movement - they establish polarity, divide, migrate, and undergo morphological changes necessary for specific functions. Molecular motors are emerging as critical components of many of these processes, and as such are likely to be tightly regulated. Indeed, several human diseases have been linked to problems with motor proteins. Cytoplasmic dynein is a microtubule-associated ATPase active during mitosis, migration, and intracellular transport. Our lab focuses on two gene products, Lis1 and Ndel1, that interact with cytoplasmic dynein. Loss or mutation of one allele of the Lis1 gene causes a severe human developmental brain malformation known as type 1 lissencephaly (smooth brain). It is likely that lissencephaly is the result of altered dynein activity, but this has not been directly established. Moreover, there are many unanswered questions concerning how, when, where, and why Lis1 influences dynein behavior. The same is true for Ndel1, which binds to both Lis1 and dynein, as well as to microtubules directly. Our lab is interested in answering these questions. We are also trying to determine if and how Lis1 and Ndel1 behaviors are modified by specific kinase signaling pathways. Finally, we are examining crosstalk between Lis1 and Ndel1 and other molecules that have been linked to dynein function. |
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607 Coker Life Sciences 700 Sumter St Columbia, SC 29208
Phone: 803-777-3020 Lab: 803-777-3016 Fax: 803-777-4002 |
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