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JCI table of contents: April 22, 2008
Date:4/22/2008

Medical School, Boston, have now determined that nonmutated tau protein and the most frequent form of mutant tau in individuals with FTDP-17 (P301L tau) are regulated differently by the protein Pin1, meaning that mice carrying mutated forms of tau are not likely to model AD very faithfully.

Consistent with previous studies, it was found that elimination of Pin1 in mice enhanced the stability of nonmutated tau protein, whereas overexpression of Pin1 decreased the stability of the protein and suppressed tauopathy in mice engineered to express nonmutated human tau. By contrast, elimination of Pin1 in mice decreased the stability of P301L tau and suppressed tauopathy in mice engineered to express P301L tau, whereas overexpression of Pin1 enhanced tauopathy in P301L tau mice. The authors therefore suggest that therapeutics inducing Pin1 up-regulation might be beneficial for individuals with AD, whereas Pin1 inhibition might be helpful for patients with FTDP-17 due to P301L tau.

TITLE: Pin1 has opposite effects on wild-type and P301L tau stability and tauopathy

AUTHOR CONTACT:
Kun Ping Lu
Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA.
Phone: (617) 667-4143; Fax: (617) 667-0610; E-mail: klu@caregroup.harvard.edu.

MEDIA CONTACT:
Bonnie Prescott
Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA.
Phone: (617) 667-7306; E-mail: bprescot@bidmc.harvard.edu.

View the PDF of this article at: https://www.the-jci.org/article.php?id=34308


VIROLOGY: Uncovering the secret ways of HIV: the HIV protein Nef impairs blood cell development

The generation and function of all types of blood cell are impaired in individuals infected with HIV. HIV i
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