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Title: Dual Mkk4 and Mkk7 Gene Deletion in Adult Mouse Causes an Impairment of Hippocampal Immature Granule Cells
Author: Castro-Torres, Rubén Darío
Olloquequi, Jordi
Ettcheto Arriola, Miren
Caruana, Pablo
Steele, Luke
Leighton, Kyra-Mae
Ureña Bares, Jesús Mariano
Beas Zárate, Carlos
Camins Espuny, Antoni
Verdaguer Cardona, Ester
Auladell i Costa, M. Carme
Keywords: Hipocamp (Cervell)
Proteïnes quinases
Hippocampus (Brain)
Protein kinases
Issue Date: 2-Sep-2021
Publisher: MDPI
Abstract: (1) Background: The c-Jun-NH2-terminal protein kinase (JNK) is a mitogen-activated protein kinase involved in regulating physiological processes in the central nervous system. However, the dual genetic deletion of Mkk4 and Mkk7 (upstream activators of JNK) in adult mice is not reported. The aim of this study was to induce the genetic deletion of Mkk4/Mkk7 in adult mice and analyze their effect in hippocampal neurogenesis. (2) Methods: To achieve this goal, Actin-CreERT2 (Cre+/−), Mkk4flox/flox, Mkk7flox/flox mice were created. The administration of tamoxifen in these 2-month-old mice induced the gene deletion (Actin-CreERT2 (Cre+/−), Mkk4∆/∆, Mkk7∆/∆ genotype), which was verified by PCR, Western blot, and immunohistochemistry techniques. (3) Results: The levels of MKK4/MKK7 at 7 and 14 days after tamoxifen administration were not eliminated totally in CNS, unlike what happens in the liver and heart. These data could be correlated with the high levels of these proteins in CNS. In the hippocampus, the deletion of Mkk4/Mkk7 induced a misalignment position of immature hippocampal neurons together with alterations in their dendritic architecture pattern and maturation process jointly to the diminution of JNK phosphorylation. (4) Conclusion: All these data supported that the MKK4/MKK7-JNK pathway has a role in adult neurogenic activity.
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It is part of: International Journal of Molecular Sciences, 2021, vol. 22, num. 17, p. 9545
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ISSN: 1661-6596
Appears in Collections:Articles publicats en revistes (Bioquímica i Fisiologia)
Articles publicats en revistes (Biologia Cel·lular, Fisiologia i Immunologia)

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