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Publication : Enhanced cytotoxic T-cell function and inhibition of tumor progression by Mst1 deficiency.

First Author  Yasuda K Year  2016
Journal  FEBS Lett Volume  590
Issue  1 Pages  68-75
PubMed ID  26787462 Mgi Jnum  J:229973
Mgi Id  MGI:5755180 Doi  10.1002/1873-3468.12045
Citation  Yasuda K, et al. (2016) Enhanced cytotoxic T-cell function and inhibition of tumor progression by Mst1 deficiency. FEBS Lett 590(1):68-75
abstractText  Mammalian ste-20 like kinase Mst1 plays important roles during apoptosis, proliferation, cell polarity, and migration. Here, we report a novel role of Mst1 for cytotoxic T-cell responses and tumor suppression. The defect of Mst1 caused decreased levels of FoxO, and promoted cytotoxicity in vitro. Mst1(-/-) cytotoxic T cells also exhibited enhanced T-bet expression that was associated with elevated expression levels of IFNgamma and granzyme B. Moreover, Mst1(-/-) cytotoxic T cells suppressed tumor growth in vivo. The data suggest that Mst1 inhibits cytotoxicity via T-bet suppression by FoxO1 and FoxO3a. Thus, Mst1 is a potential therapeutic target for tumor immunotherapy.
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