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Enbo Ma
Besides its clinical importance, O2 deprivation (hypoxia)
stimulates vascularization and angiogenesis during both normal embryonic
development and tumor formation. Therefore, understanding the molecular
mechanisms underlying hypoxic vascularization or tissue damage is
important both clinically and biologically.
Our genetic and molecular studies revealed that dADAR (Drosophila
adenosine deaminase acting on RNA) plays an important role in neuronal
tolerance to O2 lack. We are using use the combination
of molecular and biochemical approaches to dissect signal pathways
and molecular mechanism of dADAR in neuronal tolerance to lack of
O2.
Our long term aims and objectives are to dissect the signaling pathways
by which cells, especially neurons, sense or respond to O2
deprivation. Eventually we hope to manipulate mammalian cells, especially
neurons, to increase their tolerance to hypoxia for prolonging neuronal
survival or preventing cellular damage caused by hypoxia.
Selected Publications
Ma, E., Macrae, I.J., Kirsch, J.F., and Doudna, J.A. (2008)
Autoinhibition of human dicer by its internal helicase domain.
J. Mol. Biol. Epub ahead of print.
(360KB .pdf)
Macrae, I.J., Ma, E., Zhou, M., Robinson, C.V. and Doudna, J.A. (2008)
In vitro reconstitution of the human RISC-loading complex.
PNAS 105, 512-517.
(1.8MB .pdf)
Chen, L., Lullo, D.J., Ma, E., Celniker, S.E., Rio, D.C. and Doudna, J.A. (2005)
Identification and analysis of U5 snRNA variants in Drosophila.
RNA 11, 1473-7.
(268KB .pdf)
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