Interleukin-1β enhances FasL-induced caspase-3/-7 activity without increasing apoptosis in primary mouse hepatocytes.
Saved in:
| Title: | Interleukin-1β enhances FasL-induced caspase-3/-7 activity without increasing apoptosis in primary mouse hepatocytes. |
|---|---|
| Authors: | Lutz A; Department of Pharmaceutical Biology and Biotechnology, Albert Ludwigs University Freiburg, Freiburg, Germany., Sanwald J; Institute for System Dynamics, University of Stuttgart, Stuttgart, Germany., Thomas M; Dr. Margarete Fischer-Bosch Institute of Clinical Pharmacology, Stuttgart, Germany., Feuer R; Institute for System Dynamics, University of Stuttgart, Stuttgart, Germany., Sawodny O; Institute for System Dynamics, University of Stuttgart, Stuttgart, Germany., Ederer M; Institute for System Dynamics, University of Stuttgart, Stuttgart, Germany., Borner C; Institute of Molecular Medicine and Cell Research, Albert Ludwigs University Freiburg, Freiburg, Germany; Spemann Graduate School of Biology and Medicine (SGBM), Albert Ludwigs University Freiburg, Freiburg, Germany; Bioss - Centre for Biological Signaling Studies, Albert Ludwigs University Freiburg, Freiburg, Germany., Humar M; Department of Pharmaceutical Biology and Biotechnology, Albert Ludwigs University Freiburg, Freiburg, Germany., Merfort I; Department of Pharmaceutical Biology and Biotechnology, Albert Ludwigs University Freiburg, Freiburg, Germany; Spemann Graduate School of Biology and Medicine (SGBM), Albert Ludwigs University Freiburg, Freiburg, Germany. |
| Source: | PloS one [PLoS One] 2014 Dec 31; Vol. 9 (12), pp. e115603. Date of Electronic Publication: 2014 Dec 31 (Print Publication: 2014). |
| Publication Type: | Journal Article; Research Support, Non-U.S. Gov't |
| Journal Info: | Publisher: Public Library of Science Country of Publication: United States NLM ID: 101285081 Publication Model: eCollection Cited Medium: Internet ISSN: 1932-6203 (Electronic) Linking ISSN: 19326203 NLM ISO Abbreviation: PLoS One Subsets: MEDLINE |
| Database: | MEDLINE Ultimate |
Be the first to leave a comment!
