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ALLN is an inhibitor of Calpain 1 (calpain I, Ki = 190 nM), Calpain 2 (calpain II , Ki = 220 nM), cathepsin B (Ki = 150 nM), and cathepsin L (Ki = 500 pM). It inhibits neutral cysteine proteases and proteasome (Ki = 6 μM). It inhibits apoptosis in thymocytes and metamyelocytes. It also inhibits cell cycle progression at the G1/S border and metaphase/anaphase in CHO cells by inhibiting cyclin B degradation. ALLN inhibits the proteolysis of IκBα and IκBβ by the ubiquitin-proteasome complex. Furthermore, it protects against neuronal damage caused by hypoxia and ischemia. ALLN also prevents nitric oxide production by activated macrophages by interfering with transcription of the inducible nitric oxide synthase gene.
See how others have used ALLN. Click on the entry to view the PubMed entry .
PMID: # 25928566 Aslanidis, A. et al. 2015. J Neuroinflammation. 12: -.
PMID: # 25356863 Yoon, S. et al. 2014. Cell Death Dis. 5: e1494.
PMID: # 24068677 Green, SE. et al. 2013. Toxicological sciences : an official journal of the Society of Toxicology. 136: 467-77.
PMID: # 22684109 Zhao, X. et al. 2012. J. Clin. Invest. 122: 2417-27.
PMID: # 16690988 Chambellan, A. et al. 2006. Am. J. Respir. Cell Mol. Biol. 35: 424-35.
PMID: # 15930385 Park, SY. et al. 2005. J Neurosci. 25(22): 5365-5375.
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