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Am J Physiol Lung Cell Mol Physiol (June 22, 2007). doi:10.1152/ajplung.00423.2006
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Submitted on October 26, 2006
Accepted on June 11, 2007

Phosphoinositide 3-kinase is activated by MUC1 but not responsible for MUC1-induced suppression of TLR5 signaling

Kosuke Kato1, Wenju Lu2, Hirofumi Kai3, and K. Chul Kim4*

1 Immunology and Asthma Program, Lovelace Respiratory Research Institute, albuquerque, New Mexico, United States; Department of Molecular Medicine, Kumamoto University, Kumamoto, Japan
2 Department of Medicine, Johns Hopkins University, Baltimore, Maryland, United States
3 Department of Molecular Medicine, Kumamoto University, Kumamoto, Japan
4 Immunology and Asthma Program, Lovelace Respiratory Research Institute, albuquerque, New Mexico, United States

* To whom correspondence should be addressed. E-mail: kckim{at}LRRI.org.

MUC1 is a membrane-tethered mucin-like glycoprotein expressed on the surface of various mucosal epithelial cells as well as hematopoietic cells. Recently we showed that MUC1 suppresses flagellin-induced toll-like receptor (TLR) 5 signaling both in vivo and in vitro through crosstalk with TLR5. In this study, we determined whether phosphoinositide 3-kinase (PI3K), a negative regulator of TLR5 signaling, is involved in the crosstalk between MUC1 and TLR5 using various genetically modified epithelial cell lines. Our results showed that: (a) activation of MUC1 induced recruitment of the PI3K regulatory subunit p85 to the MUC1 cytoplasmic tail (CT) as well as Akt phosphorylation; (b) MUC1-induced Akt phosphorylation required the presence of Tyr20 within the PI3K binding motif of the MUC1 CT; and (c) mutation of Tyr20 or pharmacologic inhibition of PI3K activation failed to block MUC1-induced suppression of TLR5 signaling. We conclude that while PI3K is downstream of MUC1 activation and negatively regulates TLR5 signaling, it is not responsible for MUC1-induced suppression of TLR5 signaling.




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