Mark4 promotes oxidative stress and inflammation via binding to PPARγ and activating NF-κB pathway in mice adipocytes
Author:
Publisher
Springer Science and Business Media LLC
Subject
Multidisciplinary
Link
http://www.nature.com/articles/srep21382.pdf
Reference52 articles.
1. Hurov, J. & Piwnica-Worms, H. The Par-1/MARK Family of Protein Kinases. Cell Cycle 6, 1966–1969 (2007).
2. Naz, F., Anjum, F., Islam, A., Ahmad, F. & Hassan, M. I. Microtubule Affinity-Regulating Kinase 4: Structure, Function and Regulation. Cell Biochem Biophys 67, 485–499 (2013).
3. Hurov, J. B. et al. Loss of the Par-1b/MARK2 polarity kinase leads to increased metabolic rate, decreased adiposity and insulin hypersensitivity in vivo. Proc Natl Acad Sci USA. 104, 5680–5685 (2007).
4. Li, L. & Guan, K. Microtubule-associated Protein/Microtubule Affinity-regulating Kinase 4 (MARK4) Is a Negative Regulator of the Mammalian Target of Rapamycin Complex 1 (mTORC1). J Biol Chem. 288, 703–708 (2013).
5. Rovina, D. et al. Microtubule-associated protein/microtubule affinity-regulating kinase 4 (MARK4) plays a role in cell cycle progression and cytoskeletal dynamics. Eur J Cell Biol. 93, 355–365 (2014).
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