Kctd13 deletion reduces synaptic transmission via increased RhoA

Christine Ochoa Escamilla, Irina Filonova, Angela K. Walker, Zhong X. Xuan, Roopashri Holehonnur, Felipe Espinosa, Shunan Liu, Summer B. Thyme, Isabel A. López-García, Dorian B. Mendoza, Noriyoshi Usui, Jacob Ellegood, Amelia J. Eisch, Genevieve Konopka, Jason P. Lerch, Alexander F. Schier, Haley E. Speed and Craig M. Powell ()
Additional contact information
Christine Ochoa Escamilla: University of Texas Southwestern Medical Center
Irina Filonova: University of Texas Southwestern Medical Center
Angela K. Walker: University of Texas Southwestern Medical Center
Zhong X. Xuan: University of Texas Southwestern Medical Center
Roopashri Holehonnur: University of Texas Southwestern Medical Center
Felipe Espinosa: University of Texas Southwestern Medical Center
Shunan Liu: University of Texas Southwestern Medical Center
Summer B. Thyme: Harvard University
Isabel A. López-García: University of Texas Southwestern Medical Center
Dorian B. Mendoza: University of Texas Southwestern Medical Center
Noriyoshi Usui: University of Texas Southwestern Medical Center
Jacob Ellegood: Mouse Imaging Centre (MICe), Hospital for Sick Children
Amelia J. Eisch: University of Texas Southwestern Medical Center
Genevieve Konopka: University of Texas Southwestern Medical Center
Jason P. Lerch: Mouse Imaging Centre (MICe), Hospital for Sick Children
Alexander F. Schier: Harvard University
Haley E. Speed: University of Texas Southwestern Medical Center
Craig M. Powell: University of Texas Southwestern Medical Center

Nature, 2017, vol. 551, issue 7679, 227-231

Abstract: Experimental evidence that global Kctd13 reduction leads to increased RhoA levels that reduce synaptic transmission, implicating RhoA as a potential therapeutic target for neuropsychiatric disorders associated with copy-number variants that include KCTD13.

Date: 2017
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DOI: 10.1038/nature24470

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