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Functional validation of tensin2 SH2-PTB domain by CRISPR/Cas9-mediated genome editing.

The Journal of veterinary medical science (2016-06-02)
Kiyoma Marusugi, Kenta Nakano, Hayato Sasaki, Junpei Kimura, Rieko Yanobu-Takanashi, Tadashi Okamura, Nobuya Sasaki
ZUSAMMENFASSUNG

Podocytes are terminally differentiated and highly specialized cells in the glomerulus, and they form a crucial component of the glomerular filtration barrier. The ICGN mouse is a model of glomerular dysfunction that shows gross morphological changes in the podocyte foot process, accompanied by proteinuria. Previously, we demonstrated that proteinuria in ICR-derived glomerulonephritis mouse ICGN mice might be caused by a deletion mutation in the tensin2 (Tns2) gene (designated Tns2