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Titolo:
Regulation of alternative splicing of human tau exon 10 by phosphorylationof splicing factors
Autore:
Hartmann, AM; Rujescu, D; Giannakouros, T; Nikolakaki, E; Goedert, M; Mandelkow, EM; Gao, QS; Andreadis, A; Stamm, S;
Indirizzi:
Max Planck Inst Neurobiol, D-82152 Martinsried, Germany Max Planck Inst Neurobiol Martinsried Germany D-82152 rtinsried, Germany Univ Munich, D-80336 Munich, Germany Univ Munich Munich Germany D-80336Univ Munich, D-80336 Munich, Germany Aristotelian Univ Salonika, Sch Chem, Salonika 54006, Greece Aristotelian Univ Salonika Salonika Greece 54006 Salonika 54006, Greece MRC, Mol Biol Lab, Cambridge CB2 2QH, England MRC Cambridge England CB2 2QH , Mol Biol Lab, Cambridge CB2 2QH, England DESY, Max Planck Unit Struct Mol Biol, D-22607 Hamburg, Germany DESY Hamburg Germany D-22607 t Struct Mol Biol, D-22607 Hamburg, Germany Eunice Kennedy Shriver Ctr Mental Retardat Inc, Waltham, MA 02254 USA Eunice Kennedy Shriver Ctr Mental Retardat Inc Waltham MA USA 02254 4 USA
Titolo Testata:
MOLECULAR AND CELLULAR NEUROSCIENCE
fascicolo: 1, volume: 18, anno: 2001,
pagine: 80 - 90
SICI:
1044-7431(200107)18:1<80:ROASOH>2.0.ZU;2-I
Fonte:
ISI
Lingua:
ENG
Soggetto:
PROGRESSIVE SUPRANUCLEAR PALSY; INHERITED DEMENTIA FTDP-17; TRACT-BINDING-PROTEIN; LIGHT-CHAIN-B; MESSENGER-RNA; FRONTOTEMPORAL DEMENTIA; ALZHEIMERS-DISEASE; SR PROTEINS; ANTISENSE OLIGONUCLEOTIDES; GENE-MUTATIONS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
98
Recensione:
Indirizzi per estratti:
Indirizzo: Stamm, S Max Planck Inst Neurobiol, Klopferspitz 18A, D-82152 Martinsried,Germany Max Planck Inst Neurobiol Klopferspitz 18A Martinsried Germany D-82152
Citazione:
A.M. Hartmann et al., "Regulation of alternative splicing of human tau exon 10 by phosphorylationof splicing factors", MOL CELL NE, 18(1), 2001, pp. 80-90

Abstract

Tau is a microtubule-associated protein whose transcript undergoes regulated splicing in the mammalian nervous system. Exon 10 of the gene is an alternatively spliced cassette that is adult-specific and encodes a microtubule-binding domain. Mutations increasing the inclusion of exon 10 result in the production of tau protein which predominantly contains four microtubule-binding repeats and were shown to cause frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17). Here we show that exon 10 usage is regulated by CDC2-like kinases CLK1, 2, 3, and 4 that phosphorylate serine-arginine-rich proteins, which in turn regulate pre-mRNA splicing. Cotransfection experiments suggest that CLKs achieve this effect by releasing specific proteins from nuclear storage sites. Our results show that changing pre-mRNA-processing pathways through phosphorylation could be a new therapeuticconcept for tauopathies.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 20/01/20 alle ore 05:38:30