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Intersectin 1 contributes to phenotypes in vivo: implications for Down Syndrome

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Title: Intersectin 1 contributes to phenotypes in vivo: implications for Down Syndrome
Author(s): Hunter, Michael P.; Nelson, Marianela; Kurzer, Michael; Wang, Xuerong; Kryscio, Richard J.; Head, Elizabeth; Pinna, Graziano; O’Bryan, John P.
Subject(s): scaffold protein MAP kinase endocytosis signal transduction neurodegeneration SH3 domain EH domain
Abstract: Intersectin 1 (ITSN1) is a chromosome 21 (HSA21) gene product encoding a multidomain scaffold protein that functions in endocytosis, signal transduction and is implicated in Down Syndrome, Alzheimer’s Disease, and potentially other neurodegenerative diseases through activation of c-Jun N-terminal kinase (JNK). We report for the first time that ITSN1 proteins are elevated in Down Syndrome individuals of varying ages. However, ITSN1 levels decreased in aged Down Syndrome cases with Alzheimer’s Disease-like neuropathology. Analysis of a novel ITSN1 transgenic mouse reveals that ITSN1 overexpression results in a sex-dependent decrease in locomotor activity. This study reveals a link between overexpression of specific ITSN1 isoforms and behavioral phenotypes and has implications for human neurodegenerative diseases such as Down Syndrome and Alzheimer’s Disease.
Issue Date: 2011-10
Publisher: Lippincott, Williams & Wilkins
Citation Info: Hunter MP, Nelson M, Kurzer M, Wang X, Kryscio RJ, Head E, Pinna G, O'Bryan JP. Intersectin 1 contributes to phenotypes in vivo: implications for Down's syndrome. Neuroreport. 2011 Oct 26;22(15):767-72. DOI:10.1097/WNR.0b013e32834ae348
Type: Article
Description: This is a copy of an article published in the NeuroReport © 2011 Lippincott, Williams & Wilkins. Post print version of article may differ from published version. The final publication is available at; DOI: 10.1097/WNR.0b013e32834ae348
ISSN: 1473-558X
Sponsor: Funding for human tissue samples was from UCI ADRC P50 AG16573, NICHD Contract No. N01- HD-4-3368 and NO1-HD-4-3383. M.K. was supported in part by the Craig Fellowship, University of Illinois College of Medicine. This work was supported in part by funding to G. P. from the NIH (MH 085999), to E.H. from the NIH (RO1 HD064993), and to J.P.O from the Intramural Research Program of the NIH, the Foundation Jerome Lejeune, the Department of Defense (PR080428), and the NIH (RO1 HL090651).
Date Available in INDIGO: 2012-09-18

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