Dr. Sugita’s primary research interest is to understand the molecular mechanisms underpinning exocytosis using neuronal and immune cells with particular emphasis on the roles of Munc18, syntaxin, Munc13, CAPS1 and V-ATPase. To this end, he uses PC12 cells and RBL-2H3 cells as cellular models for neuroendocrince cells and mast cells, respectively, and uses C. elegans as an in vivo model. Moreover, conditional knockout mice are being generated to analyze the function of these proteins in vitro and in vivo. These models will be used to show how Munc18-1 contributes to neuroprotection, thereby explaning why its loss in neurons leads to severe neurodegeneration.
Autoinhibition of Munc18-1 modulates synaptobrevin binding and helps to enable Munc13-dependent regulation of membrane fusion.
Elife. 2017 May 06;6:
Munc18b Increases Insulin Granule Fusion, Restoring Deficient Insulin Secretion in Type-2 Diabetes Human and Goto-Kakizaki Rat Islets with Improvement in Glucose Homeostasis.
EBioMedicine. 2017 Jan 22;:
Curr Biol. 2017 Jan 09;:
ϒ-secretase and LARG mediate distinct RGMa activities to control appropriate layer targeting within the optic tectum.
Cell Death Differ. 2016 Mar;23(3):442-53
Anesthesiology. 2016 Oct;125(4):822-3
Anesthesiology. 2016 Jan 25;
Conformational states of syntaxin-1 govern the necessity of N-peptide binding in exocytosis of PC12 cells and Caenorhabditis elegans.
Mol Biol Cell. 2015 Dec 23;
Chaperoning of closed syntaxin-3 through Lys46 and Glu59 in domain 1 of Munc18 proteins is indispensable for mast cell exocytosis.
J Cell Sci. 2015 May 15;128(10):1946-60
A pivotal role for pro-335 in balancing the dual functions of Munc18-1 domain-3a in regulated exocytosis.
J Biol Chem. 2014 Nov 28;289(48):33617-28
J Neurochem. 2014 Aug;130(4):469-71
Senior Scientist, Krembil Research Institute (Krembil)
Professor, Department of Physiology, University of Toronto