We are studying the mechanisms by which mutations in
sodium channel genes result in seizures in patients with
epileptic encephalopathy. More than 100 mutations have
been identified in the SCN8A gene, many of which change
the biophysical properties of the channel and result in
neuronal hyperactivity. We have generated two mouse models
by knock-in of patient mutations. These models are being used to
probe mechanisms and to test therapies. We are using our new
conditional model of patient mutation R1872W to dissect pathogenesis
in different classes of neurons and at different stages of development.
Projects involve assessment of molecular and behavioral effects
of expressing this gain-of-function mutation in vivo, as well as
characterization of new patient mutations.
The lab currently includes two research track faculty,
postdoctoral fellow, graduate student, lab manager,
technician, and several undergraduates. The postdoctoral position is available
immediately and is funded for five years by an NIH R01 Grant.
Please email your CV and contact information for references to firstname.lastname@example.org.
recent Ph. D. degree, expertise in neuroscience; experience with mouse genetics an advantage.
Publications from thesis research required.
If you have questions, email email@example.com or
call (202) 962-4000.
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