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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Ballard, Jimmy D. Larabee, Jason L. Shakir, Salika M. Barua, Soumitra |
| Description | Author Affiliation: Larabee JL ( Department of Microbiology and Immunology, The University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma 73104, USA.) |
| Abstract | In cells of the innate immune system, pathological increases in intracellular cAMP attenuate immune responses and contribute to infections by bacteria such as Bacillus anthracis. In this work, cAMP from B. anthracis edema toxin (ET) is found to activate the Notch signaling pathway in both mouse macrophages and human monocytes. ET as well as a cell-permeable activator of PKA induce Notch target genes (HES1, HEY1, IL2RA, and IL7R) and are able to significantly enhance the induction of these Notch target genes by a Toll-like receptor ligand. Elevated cAMP also resulted in increased levels of Groucho/transducin-like enhancer of Split (TLE) and led to increased amounts of a transcriptional repressor complex consisting of TLE and the Notch target Hes1. To address the mechanism used by ET to activate Notch signaling, components of Notch signaling were examined, and results revealed that ET increased levels of recombinant recognition sequence binding protein at the Jκ site (RBP-J), a DNA binding protein and principal transcriptional regulator of Notch signaling. Overexpression studies indicated that RBP-J was sufficient to activate Notch signaling and potentiate LPS-induced Notch signaling. Further examination of the mechanism used by ET to activate Notch signaling revealed that C/EBP ß, a transcription factor activated by cAMP, helped activate Notch signaling and up-regulated RBP-J. These studies demonstrate that cAMP activates Notch signaling and increases the expression of TLE, which could be an important mechanism utilized by cAMP to suppress immune responses. |
| ISSN | 00219258 |
| e-ISSN | 1083351X |
| Journal | Journal of Biological Chemistry |
| Issue Number | 30 |
| Volume Number | 288 |
| Language | English |
| Publisher | American Society for Biochemistry and Molecular Biology (United States) |
| Publisher Date | 2013-07-26 |
| Publisher Place | United States |
| Access Restriction | Open |
| Subject Keyword | Cyclic AMP Metabolism Immunoglobulin J Recombination Signal Sequence-Binding Protein Monocytes Receptor, Notch1 Repressor Proteins Animals Antigens, Bacterial Pharmacology Bacterial Toxins Basic Helix-Loop-Helix Transcription Factors Genetics Bucladesine Analogs & Derivatives CCAAT-Enhancer-Binding Protein-beta Cell Line Cells, Cultured Gene Expression Drug Effects HEK293 Cells Homeodomain Proteins Immunoblotting Lipopolysaccharides Luciferases Macrophages Mice Mice, Inbred C57BL Cytology Protein Binding Reverse Transcriptase Polymerase Chain Reaction Signal Transduction Research Support, N.I.H., Extramural Biochemistry Molecular Biology |
| Content Type | Text |
| Resource Type | Article |
| Subject | Cell Biology Biochemistry Molecular Biology |
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