Requirement for glycogen synthase kinase-3beta in cell survival and NF-kappaB activation.

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

722 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/ac52b4d224ae92fa52525323cec0eebc13e5b5f6

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1. K. Guan
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Citations in the corpus

• Tumor necrosis factor signaling (2003, background): “not thought to be involved in TNF signalling, also exert reduced NF-kB-dependent transcription, but normal nuclear translocation and DNA binding in response to TNF, suggesting a role of these kinases in p65 transactivation, also.(68,114)”
• 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).”
• 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).”
• Functional redundancy of GSK-3α and GSK-3β in wnt/β-catenin signaling shown by using an allelic series of embryonic stem cell lines (2007, background): “We have previously characterized mice lacking GSK-3β (Hoeflich et al. 2000).”
• TSC2 integrates Wnt and energy signals via a coordinated phosphorylation by AMPK and GSK3 to regulate cell growth. (2006, background): “It is worth noting that GSK3a still exists in the GSK3b / MEF cells (Hoeflich et al., 2000) and likely contributes to the cellular energy response.”
• Role of tau protein in both physiological and pathological conditions. (2004, unknown): “knock-out mice die during embryonic life (135).”
• Glycogen synthase kinase-3β mediates convergence of protection signaling to inhibit the mitochondrial permeability transition pore (2004, unknown): “However, deletion of the GSK-3 β gene results in developmental arrest and embryonic lethality, thus showing that endogenous GSK-3 α signaling is unable to compensate and rescue the GSK-3 β –null mice (21).”
• 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).”
• Antioxidative and Anti-Inflammatory Properties of Cannabidiol (2019, background): “ Oxidative modifications play an  important role  in  the  functioning  of  redox‐sensitive  transcription  factors  (including Nrf2  and  the  nuclear  factor  kappa  B  (NFκB).”
• The complexity of NF-κB signaling in inflammation and cancer (2013, background): “It could be shown that GSK-3β has a modulating role for the NF-κB signaling pathway, as it seems to facilitate NF-κB function through post-transcriptional regulation of the NF-κB complex [125].”