Increased cAMP in monocytes augments notch signaling mechanisms by elevating RBP-J and transducin-like enhancer of split (TLE)

Abstract

Background: Many bacterial pathogens, such as Bacillus anthracis, increase cAMP in monocytes, leading to disruption of immune responses. Results: In human monocytes, cAMP up-regulates transducin-like enhancer of split (TLE) and activates Notch signaling. Conclusion: Our findings demonstrate novel signaling mechanisms used by cAMP to enhance Notch signaling. Significance: This work delineates how cAMP modifies a signaling pathway critical to innate immune responses during infection. © 2013 by The American Society for Biochemistry and Molecular Biology, Inc.