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Endocrine/metabolic disease


Calcium calmodulin-dependent protein kinase IIg (CAMK2G)

Mouse studies suggest inhibiting CAMK2G could help improve hyperglycemia and insulin sensitivity in patients with type 2 diabetes. CAMK2G stimulates glucagon-induced, calcium-mediated hepatic glucose production. In three mouse models of obesity and type 2 diabetes, liver-specific inactivation of Camk2g improved blood glucose response and decreased hepatic glucose production and blood insulin levels compared with no Camk2g inactivation. In mouse livers, Camk2g inactivation enhanced insulin signaling through MAP kinase-activated protein kinase 2 (MAPKAPK2; MK2)-mediated activation of the eukaryotic translation initiator factor 2a kinase 3 (EIF2AK3; PERK) branch of the unfolded protein response. Next steps include developing inhibitors of MK2 and testing them in animal models of diabetes.
The authors have cofounded Tabomedex Biosciences LLC to develop MK2 inhibitors licensed from Columbia University.

SciBX 7(1); doi:10.1038/scibx.2014.16
Published online Jan. 9, 2014

Patent application filed by Columbia University; additional application in preparation covering unpublished MK2 inhibitors; licensed by Tabomedex Biosciences

Ozcan, L. et al. Cell Metab.; published online Nov. 21, 2013;
Contact: Ira Tabas, Columbia University, New York, N.Y.
Contact: Lale Ozcan, same affiliation as above