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Summary

Affiliation: University of Lausanne
Country: Switzerland

Publications

  1. ncbi ER stress activates the NLRP3 inflammasome via an UPR-independent pathway
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    Department of Biochemistry, University of Lausanne, Epalinges, Switzerland
    Cell Death Dis 3:e261. 2012
  2. ncbi The NLRP3 inflammasome in health and disease: the good, the bad and the ugly
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    Department of Biochemistry, University of Lausanne, Epalinges, Switzerland
    Clin Exp Immunol 166:1-15. 2011
  3. ncbi Atherosclerosis in ApoE-deficient mice progresses independently of the NLRP3 inflammasome
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    Department of Biochemistry, University of Lausanne, Epalinges, Switzerland
    Cell Death Dis 2:e137. 2011

Detail Information

Publications3

  1. ncbi ER stress activates the NLRP3 inflammasome via an UPR-independent pathway
    P Menu
    Department of Biochemistry, University of Lausanne, Epalinges, Switzerland
    Cell Death Dis 3:e261. 2012
    ....
  2. ncbi The NLRP3 inflammasome in health and disease: the good, the bad and the ugly
    P Menu
    Department of Biochemistry, University of Lausanne, Epalinges, Switzerland
    Clin Exp Immunol 166:1-15. 2011
    ....
  3. ncbi Atherosclerosis in ApoE-deficient mice progresses independently of the NLRP3 inflammasome
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    Department of Biochemistry, University of Lausanne, Epalinges, Switzerland
    Cell Death Dis 2:e137. 2011
    ..Our results demonstrate that the NLRP3 inflammasome is not critically implicated in atherosclerosis progression in the ApoE mouse model...