Mice lacking Pin1 develop normally, but are defective in entering cell cycle from G0 arrest
F Fujimori, K Takahashi, C Uchida, T Uchida - Biochemical and biophysical …, 1999 - Elsevier
F Fujimori, K Takahashi, C Uchida, T Uchida
Biochemical and biophysical research communications, 1999•ElsevierThe peptidyl prolil cis/trans isomerase Ess1/Pin1 is essential for mitosis progression in yeast
cells and is hypothesized to perform the same role in mammalian cells. To investigate the
function of Pin1 in mammalian cells, we created mice lacking Pin1. These mice underwent
normal development. Although the embryonic Pin1−/− fibroblasts grew normally, they
proved significantly deficient in their ability to restart proliferation in response to serum
stimulation after G0 arrest. These results suggest that Pin1 is required for cell cycle …
cells and is hypothesized to perform the same role in mammalian cells. To investigate the
function of Pin1 in mammalian cells, we created mice lacking Pin1. These mice underwent
normal development. Although the embryonic Pin1−/− fibroblasts grew normally, they
proved significantly deficient in their ability to restart proliferation in response to serum
stimulation after G0 arrest. These results suggest that Pin1 is required for cell cycle …
The peptidyl prolil cis/trans isomerase Ess1/Pin1 is essential for mitosis progression in yeast cells and is hypothesized to perform the same role in mammalian cells. To investigate the function of Pin1 in mammalian cells, we created mice lacking Pin1. These mice underwent normal development. Although the embryonic Pin1−/− fibroblasts grew normally, they proved significantly deficient in their ability to restart proliferation in response to serum stimulation after G0 arrest. These results suggest that Pin1 is required for cell cycle progression from G0 arrest as well as mitosis progression in normal mammalian cells.
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