A novel pharmacological target to counteract loss-of-function in KCNQ2/3-linked epilepsy disorders
In collaboration with the Giraldez and de la Rosa labs at Universidad de La Laguna, Tenerife, we help to uncover the ability of SGK1.1, the neuronal isoform of the serum and glucocorticoids-regulated kinase 1, to increase activity of KCNQ2/3 loss-of-function mutants, providing another potential molecular target for pharmacological rescue of neuronal M-current.
Activation of SGK1.1 Upregulates the M-current in the Presence of Epilepsy Mutations
Elva Martin-Batista1, Rían W. Manville2, Belinda Rivero-Pérez1, David Bartolomé-Martín1, Diego Alvarez de la Rosa1, Geoffrey W. Abbott2 and Teresa Giraldez1*
1Departamento de Ciencias Medicas Basicas and Instituto de Tecnologias Biomedicas, Universidad de La Laguna, San Cristóbal de La Laguna, Spain
2Bioelectricity Laboratory, Department of Physiology and Biophysics, School of Medicine, University of California, Irvine, Irvine, CA, United States
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