Role of the prolyl isomerase Pin1 in protecting against age-dependent neurodegeneration

Nature

Volumn 424, Issue 6948, 2003, Pages 556-561

  Liou, Yih Cherng ^a,g   Sun, Anyang ^a,b   Ryo, Akihide ^a,h   Zhou, Xiao Zhen ^a   Yu, Zhao Xue ^c   Huang, Han Kuei ^d   Uchida, Takafumi ^e   Bronson, Roderick ^f   Bing, Guoying ^b   Li, Xiaojiang ^c   Hunter, Tony ^d   Lu, Kun Ping ^a  

^a HARVARD MEDICAL SCHOOL   (United States)

^b UNIVERSITY OF KENTUCKY   (United States)

^c EMORY UNIVERSITY SCHOOL OF MEDICINE   (United States)

^d SALK INSTITUTE FOR BIOLOGICAL STUDIES   (United States)

^e TOHOKU UNIVERSITY   (Japan)

^f TUFTS UNIVERSITY   (United States)

^g NATIONAL UNIVERSITY OF SINGAPORE   (Singapore)

^h YOKOHAMA CITY UNIVERSITY   (Japan)

Author keywords

[No Author keywords available]

Indexed keywords

BIODIVERSITY; DISEASES; GENETIC ENGINEERING; NEUROLOGY; PATHOLOGY; PROTEINS;

NEUROPATHOLOGY;

ENZYMES;

ISOMERASE; PEPTIDYLPROLYL ISOMERASE PIN1; PROTEIN; UNCLASSIFIED DRUG; NEUROPROTECTIVE AGENT; NIMA INTERACTING PEPTIDYLPROLYL ISOMERASE; NIMA-INTERACTING PEPTIDYLPROLYL ISOMERASE; PEPTIDYLPROLYL ISOMERASE; PHOSPHOPROTEIN; PHOSPHOSERINE; PHOSPHOTHREONINE;

AGE-RELATED DIFFERENCE; BIOLOGY; NEUROLOGY;

ALZHEIMER DISEASE; ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; CONTROLLED STUDY; CORRELATION ANALYSIS; HUMAN; HUMAN CELL; HUMAN TISSUE; KNOCKOUT MOUSE; MOUSE; NERVE CELL NETWORK; NERVE DEGENERATION; NONHUMAN; PREDICTION; PRIORITY JOURNAL; PROTEIN EXPRESSION; TAUOPATHY; AGING; ANIMAL; ANIMAL BEHAVIOR; CHEMISTRY; ELECTRON MICROSCOPY; ENZYMOLOGY; GENE DELETION; GENE EXPRESSION; GENETICS; METABOLISM; MOTOR ACTIVITY; MOUSE MUTANT; NERVE CELL; NEUROFIBRILLARY TANGLE; PATHOLOGY; PATHOPHYSIOLOGY; PHOSPHORYLATION; PHYSIOLOGY; PROTEIN MOTIF; SENILE PLAQUE;

ANIMALIA;

AGING; ALZHEIMER DISEASE; AMINO ACID MOTIFS; ANIMALS; BEHAVIOR, ANIMAL; GENE DELETION; GENE EXPRESSION; HUMANS; MICE; MICE, KNOCKOUT; MICROSCOPY, ELECTRON; MOTOR ACTIVITY; NEUROFIBRILLARY TANGLES; NEURONS; NEUROPROTECTIVE AGENTS; PEPTIDYLPROLYL ISOMERASE; PHOSPHOPROTEINS; PHOSPHORYLATION; PHOSPHOSERINE; PHOSPHOTHREONINE; SENILE PLAQUES; TAUOPATHIES;

EID: 0043069764     PISSN: 00280836     EISSN: None     Source Type: Journal    
DOI: 10.1038/nature01832     Document Type: Article

References (30)

1. Selkoe, D. J. The cell biology of β-amyloid precursor protein and presenilin in Alzheimer's disease. Trends Cell Biol. 8, 447-453 (1998).
2. Mandelkow, E. M. & Mandelkow, E. Tau in Alzheimer's disease. Trends Cell Biol. 8, 425-427 (1998).
3. Lee, V. M., Goedert, M. & Trojanowski, J. Q. Neurodegenerative tauopathies. Annu. Rev. Neurosci. 24, 1121-1159 (2001).
4. Wong, P. C., Cai, H., Borchelt, D. R. & Price, D. L. Genetically engineered mouse models of neurodegenerative diseases. Nature Neurosci. 5, 633-639 (2002).
5. Ishihara, T. et al. Age-dependent emergence and progression of a tauopathy in transgenic inice overexpressing the shortest human tau isoform. Neuron 24, 751-762 (1999).
6. Lewis, J. et al. Neurofibrillary tangles, amyotrophy and progressive motor disturbance in mice expressing mutant (P301L) tau protein. Nature Genet. 25, 402-405 (2000).
7. Gotz, J., Chen, E, Barmettler, R. & Nitsch, R. M. Tau filament formation in transgenic mice expressing P301L tau. J. Biol. Chem. 276, 529-534 (2001).
8. Lewis, J. et al. Enhanced neurofibrillary degeneration in transgenic mice expressing mutant tau and APP. Science 293, 1487-1491 (2001).
9. Gotz, J., Chen, F., van Dorpe, J. & Nitsch, R. M. Formation of neurofibrillary tangles in P3011 tau transgenic mice induced by Aβ42 fibrils. Science 293, 1491-1495 (2001).
10. Allen, B. et al. Abundant tau filaments and nonapoptotic neurodegeneration in transgenic mice expressing human P301S tau protein. J. Neurosci. 22, 9340-9351 (2002).
11. Bancher, C. et al. Accumulation of abnormally phosphorylated tau precedes the formation of neurofibrillary tangles in Alzheimer's disease. Brain Res. 477, 90-99 (1989).
12. Preuss, U. & Mandelkow, E. M. Mitotic phosphorylation of tau protein in neuronal cell lines resembles phosphorylation in Alzheimer's disease. Eur. J. Cell Biol. 76, 176-184 (1998).
13. Vincent, I., Zheng, J. H., Dickson, D. W., Kress, Y. & Davies, P. Mitotic phosphoepitopes precede paired helical filaments in Alzheimer's disease. Neurobiol. Aging 19, 287-296 (1998).
14. Lu, K. P., Liou, Y. C. & Vincent, I. Proline-directed phosphorylation and isomerization in mitotic regulation and in Alzheimer's disease. BioEssays 25, 174-181 (2003).
15. Lu, K. P., Hanes, S. D. & Hunter, T. A human peptidyl-prolyl isomerase essential for regulation of mitosis. Nature 380, 544-547 (1996).
16. Yaffe, M. B. et al. Sequence-specific and phosphorylation-dependent proline isomerization: a potential mitotic regulatory mechanism. Science 278, 1957-1960 (1997).
17. Lu, K. P., Liou, Y. C. & Zhou, X. Z. Pinning down the proline-directed phosphorylation signaling. Trends Cell Biol. 12, 164-172 (2002).
18. Lu, P. J., Wulf, G., Zhou, X. Z., Davies, P. & Lu, K. P. The prolyl isomerase Pin1 restores the function of Alzheimer-associated phosphorylated tau protein. Nature 399, 784-788 (1999).
19. Zhou, X. Z. et al. Pin1-dependent prolyl isomerization regulates dephosphorylation of Cdc25C and tau proteins. Mol. Cell 6, 873-883 (2000).
20. Holzer, M. et al. Inverse association of Pin1 and tau accumulation in Alzheimer's disease hippocampus. Acta Neuropathol. 104, 471-481 (2002).
21. Davies, D. C., Horwood, N., Isaacs, S. L. & Mann, D. M. The effect of age and Alzheimer's disease on pyramidal neuron density in the individual fields of the hippocampal formation. Acta Neuropathol. 83, 510-517 (1992).
22. Liou, Y. C. et al. Loss of Pin1 function in the mouse resembles the cyclin D1-null phenotypes. Proc. Natl Acad. Sci. USA 99, 1335-1340 (2002).
23. Husseman, J. W., Nochlin, D. & Vincent, I. Mitotic activation: a convergent mechanism for a cohort of neurodegenerative diseases. Neurobiol. Aging 21, 815-828 (2000).
24. Kins, S. et al. Reduced protein phosphatase 2A activity induces hyperphosphorylation and altered compartmentalization of tau in transgenic mice. J. Biol. Chem. 276, 38193-38200 (2001).
25. Wolozin, B. L., Pruchnicki, A., Dickson, D. W. & Davies, P. A neuronal antigen in the brains of Alzheimer patients. Science 232, 648-650 (1986).
26. Lee, V. M., Balin, B. J., Otvos, L. Jr & Trojanowski, J. Q. A68: a major subunit of paired helical filaments and derivatized forms of normal Tau. Science 251, 675-678 (1991).
27. Gordon-Krajcer, W., Yang, L. & Ksiezak-Reding, H. Conformation of paired helical filaments blocks dephosphorylation of epitopes shared with fetal tau except Ser199/202 and Ser202/Thr205. Brain Res. 856, 163-175 (2000).
28. Fujimori, F., Takahashi, K., Uchida, C. & Uchida, T. Mice lacking Pin1 develop normally, but are defective in entering cell cycle from G90) arrest. Biochem. Biophys. Res. Commun 265, 658-663 (1999).
29. Patrick, G. N. et al. Conversion of p35 to p25 deregulates Cdk5 activity and promotes neurodegeneration. Nature 402, 615-622 (1999).
30. Lucas, J. J. et al. Decreased nuclear β-catenin, tau hyperphosphorylation and neurodegeneration in GSK-3β conditional transgenic mice. EMBO J. 20, 27-39 (2001).