TY  - INPR
A1  - Ronkina, Natalia
A1  - Schuster-Gossler, Karin
A1  - Hansmann, Florian Heinrich
A1  - Kunze-Schumacher, Heike
A1  - Sandrock, Inga
A1  - Yakovleva, Tatiana
A1  - Lafera, Juri
A1  - Baumgärtner, Wolfgang
A1  - Krueger, Andreas
A1  - Prinz, Immo
A1  - Gossler, Achim
A1  - Kotlyarov, Alexey
A1  - Gaestel, Matthias
T1  - Germline deletion reveals a non-essential role of the atypical MAPK6/ERK3
T2  - bioRxiv
N2  - MAPK6/ERK3 is an atypical member of the MAPKs. An essential role has been suggested by the perinatal lethal phenotype of ERK3 knockout mice carrying a lacZ insertion in exon 2 due to pulmonary disfunction and by defects in function, activation and positive selection of T cells. To study the role of ERK3 in vivo, we generated mice carrying a conditional Erk3 allele with exon3 flanked by LoxP sites. Loss of ERK3 protein was validated after deletion of Erk3 in the female germ line using zona pellucida 3 (Zp3)-cre and a clear reduction of the protein kinase MK5 is detected, providing first evidence for the existence of the ERK3/MK5 signaling complex in vivo. In contrast to the previously reported Erk3 knockout phenotype, these mice are viable and fertile, do not display pulmonary hypoplasia, acute respiratory failure, abnormal T cell development, reduction of thymocyte numbers or altered T cells selection. Hence, ERK3 is dispensable for pulmonary and T-cell functions. The perinatal lethality, lung and T-cell defects of the previous ERK3 knockout mice are likely due to ERK3-unrelated effects of the inserted lacZ-neomycin-resistance-cassette. The knockout mouse of the closely related atypical MAPK ERK4/MAPK4 is also normal suggesting redundant functions of both protein kinases.
Y1  - 2018
UR  - http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/72507
UR  - https://nbn-resolving.org/urn:nbn:de:hebis:30:3-725073
IS  - 467597
ER  -