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The isoform‐specific functions of the c‐Jun N‐terminal Kinases (JNKs): differences revealed by gene targeting
Author(s) -
Bogoyevitch Marie A.
Publication year - 2006
Publication title -
bioessays
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.175
H-Index - 184
eISSN - 1521-1878
pISSN - 0265-9247
DOI - 10.1002/bies.20458
Subject(s) - kinase , gene isoform , biology , gene , immune system , mapk/erk pathway , carcinogenesis , function (biology) , c jun , mitogen activated protein kinase , microbiology and biotechnology , genetics , transcription factor
The c‐Jun N‐terminal kinases (JNKs) are members of the mitogen‐activated protein kinase (MAPK) family. In mammalian genomes, three genes encode the JNK family. To evaluate JNK function, mice have been created with deletions in one or more of three Jnk genes. Initial studies on jnk1 −/− or jnk2 −/− mice have shown roles for these JNKs in the immune system whereas studies on jnk3 −/− mice have highlighted roles for JNK3 in the nervous system. Further studies have highlighted the contributions of JNK1 and/or JNK2 to a range of biological and pathological processes. These include bone remodelling and joint disease, inflammatory and autoimmune diseases, obesity, diabetes, cardiovascular disease, liver disease and tumorigenesis in addition to effects in neurons. These results emphasise the differences in the roles played by JNK isoforms in vivo and suggest that the design of JNK inhibitors for subsequent therapeutic uses may benefit from selective inhibition of individual JNK isoforms. BioEssays 28: 923–934, 2006. © 2006 Wiley periodicals, Inc.