Cell-specific inhibition of p38alpha as a therapeutic strategy for inflammatory bowel disease
- PMID: 20184972
- PMCID: PMC4414012
- DOI: 10.1053/j.gastro.2010.02.030
Cell-specific inhibition of p38alpha as a therapeutic strategy for inflammatory bowel disease
Conflict of interest statement
Conflicts of interest
The authors disclose no conflicts.
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Comment on
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Distinct effects of p38alpha deletion in myeloid lineage and gut epithelia in mouse models of inflammatory bowel disease.Gastroenterology. 2010 Apr;138(4):1255-65, 1265.e1-9. doi: 10.1053/j.gastro.2010.01.005. Epub 2010 Jan 18. Gastroenterology. 2010. PMID: 20080092 Free PMC article.
References
-
- Sandborn WJ, Feagan BG, Hanauer SB, et al. A review of activity indices and efficacy endpoints for clinical trials of medical therapy in adults with Crohn’s disease. Gastroenterology. 2002;122:512–530. - PubMed
-
- Sands BE, Bank S, Sninsky CA, et al. Preliminary evaluation of safety and activity of recombinant human interleukin 11 in patients with active Crohn’s disease. Gastroenterology. 1999;117:58–64. - PubMed
-
- Schreiber S, Fedorak RN, Nielsen OH, et al. Safety and efficacy of recombinant human interleukin 10 in chronic active Crohn’s disease. Crohn’s Disease IL-10 Cooperative Study Group. Gastroenterology. 2000;119:1461–1472. - PubMed
-
- Ashwell JD. The many paths to p38 mitogen-activated protein kinase activation in the immune system. Nat Rev Immunol. 2006;6:532–540. - PubMed
-
- Lee JC, Laydon JT, McDonnell PC, et al. A protein kinase involved in the regulation of inflammatory cytokine biosynthesis. Nature. 1994;372:739–746. - PubMed
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