IKK-β links inflammation to obesity-induced insulin resistance
By M. C. Arkan, A. Hevener, F. Greten, S. Maeda, Zhi-wei Li, J. Long, A. Wynshaw-Boris, G. Poli, Jerrold M. Olefsky, M. Karin. Nature Medicine, 2005
1,139 citations recorded by the source corpus.
Subfields: Cancer Research, Epidemiology, Physiology
View Paper: https://www.semanticscholar.org/paper/40903773da8cdd52b8b8b1051d59d5671091eb5b
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Citations in the corpus
- Molecular and metabolic mechanisms of insulin resistance and β-cell failure in type 2 diabetes (2008, background): “However, mice in which IKKβ is selectively knocked out in myeloid cells remain globally insulin sensitiv”
- Innate immunity gone awry: linking microbial infections to chronic inflammation and cancer. (2006, background): “However, recent studies based on selective inactivation of the classical NF-kB pathway in myeloid cells suggest that migratory macrophages may be the major source of proinflammatory cytokines in obesity-induced insulin resistance (Arkan et al., 2005).”
- Type 2 diabetes as an inflammatory disease (2011, background): “Many of the metabolic stresses that promote insulin resistance and T2D also activate the inflammation- and stress-induced kinases IκB kinase-β (IKKβ) and JUN N-terminal kinase (JNK”