Requirement for glycogen synthase kinase-3β in cell survival and NF-κB activation

By K. Hoeflich, Juan Luo, E. Rubie, Ming-Sound Tsao, O. Jin, J. Woodgett. Nature, 2000

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The GSK3 hypothesis of Alzheimer's disease (2008, background): “GSK3b knock-out mice die in utero (Hoeflich et al. 2000), whereas GSK3a knock-out mice are viable and display improved glucose tolerance in response to glucose load and elevated hepatic glycogen storage and insulin sensitivity (MacAulay et al. 2007).”
Glycogen synthase kinase-3 (GSK3): regulation, actions, and diseases (2014, background): “Identifying individual actions of GSK3α and GSK3β was particularly stimulated by the finding that GSK3β knockout mice are embryonically lethal, whereas GSK3α knockout mice are viable, which provided an important demonstration that the two isoforms are not interchangeable (Hoeflich et al., 2000).”
GSK-3: tricks of the trade for a multi-tasking kinase (2003, background): “…pathology – for example, in NIDDM and neurodegenerative diseases (Eldar-Finkelman, 2002) – but it may also be relevant for some of the more recently identified functions of GSK-3, such as its role in activating NF-kB, a well characterized target for anti-inflammatory agents (Hoeflich et al., 2000).”
Glycogen synthase kinase-3 regulates mitochondrial outer membrane permeabilization and apoptosis by destabilization of MCL-1. (2006, background): “To investigate if GSK-3 activity is required for apoptosis induction upon IL-3 withdrawal, we employed small molecule inhibitors of GSK-3 (CHIR-611 and CHIR-911), which inhibit GSK-3a and GSK-3b (Ring et al., 2003; Wagman et al., 2004).”