Published: October 23, 2010Received: May 13, 2010Available on J-STAGE: October 23, 2010Accepted: July 12, 2010
Advance online publication: October 07, 2010
Revised: -
The phenotypes of mice lacking peptidyl prolyl cis/trans isomerase Pin1 (Pin1−⁄−) indicated that deficient Pin1 might be related to a variety of diseases. We created TAT-Pin1, a fusion protein of human immunodeficiency virus 1 trans-activator of transcription factor with Pin1. Treatment of HeLa cells with TAT-Pin1 increased the ratio of the S phase. Moreover, TAT-Pin1 restored the proliferating function of Pin1−⁄− mouse embryonic fibroblasts which cannot restart proliferation after G0 arrest. These results indicate that TAT-Pin1 is useful in studying the functions of Pin1 and can be developed as a macromolecular drug for diseases related to Pin1 loss.
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