Knockout of the c-Jun N-terminal Kinase 2 aggravates the development of mild chronic dextran sulfate sodium colitis independently of expression of intestinal cytokines TNFα, TGFB1, and IL-6
Author(s) -
Sabine Kersting,
Reinecke,
Hilgert,
Janot,
Elisabeth Haarmann,
Albrecht,
Mueller,
Herdegen,
Mittelkoetter,
Uhl,
Chromik
Publication year - 2013
Publication title -
journal of inflammation research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.656
H-Index - 33
ISSN - 1178-7031
DOI - 10.2147/jir.s36415
Subject(s) - tumor necrosis factor alpha , colitis , proinflammatory cytokine , inflammatory bowel disease , immunology , inflammation , knockout mouse , interleukin , medicine , cytokine , receptor , disease
The c-Jun N-terminal kinases (JNKs) are involved in signal transduction of inflammatory bowel diseases. The aim of this study was to examine the function of JNKs by using a low-dose dextran sulfate sodium (DSS) model in JNK1 knockout mice (Mapk8-/-), JNK2 knockout mice (Mapk9-/-), and wild-type controls (WT1, WT2).
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