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The sevenmaker gain‐of‐function mutation in p42 MAP kinase leads to enhanced signalling and reduced sensitivity to dual specificity phosphatase action
Author(s) -
Bott Cynthia M.,
Thorneycroft Simon G.,
Marshall Christopher J.
Publication year - 1994
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(94)00958-9
Subject(s) - phosphatase , kinase , map kinase kinase kinase , mutant , drosophila melanogaster , biology , microbiology and biotechnology , ask1 , mitogen activated protein kinase kinase , mutation , phosphorylation , mitogen activated protein kinase , in vivo , protein kinase a , chemistry , biochemistry , genetics , gene
A mammalian mutant MAP kinase, D319N ERK2, analogous to Drosophila melanogaster sevenmaker (rl sem ) gain‐of‐function mutation was shown to have an increased sensitivity to low levels of signalling in vivo. However, the mutation does not lead to an elevated basal kinase activity and still requires activation by MAP kinase kinase (MAPKK) as does wild type ERK2. This increased responsiveness seen in vivo is not due to an increased ability to phosphorylate substrates but appears to reflect a reduced sensitivity to a MAP kinase phosphatase CL100.

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