HAP1-huntingtin interactions do not contribute to the molecular pathology in Huntington's disease transgenic mice

Autor:	Erich E. Wanker, Christopher A. Ross, Alan H. Sharp, Gillian P. Bates, Hans Lehrach, Fabien Bertaux
Rok vydání:	1998
Předmět:	Genetically modified mouse congenital hereditary and neonatal diseases and abnormalities Huntingtin Transgene Molecular Sequence Data Biophysics Gene Expression Mice Transgenic Nerve Tissue Proteins Biology Biochemistry Transgenic Model HAP1 03 medical and health sciences Mice Structure-Activity Relationship 0302 clinical medicine Huntington's disease Structural Biology mental disorders Genetics medicine Huntingtin Protein Animals Humans Amino Acid Sequence Nuclear protein Cloning Molecular Molecular Biology 030304 developmental biology 0303 health sciences Binding Sites Neurodegeneration Nuclear Proteins Cell Biology medicine.disease Molecular biology nervous system diseases 3. Good health Rats Huntington Disease nervous system Triplet repeat Polyglutamine 030217 neurology & neurosurgery Protein Binding
Zdroj:	FEBS letters. 426(2)
ISSN:	0014-5793
Popis:	HAP1 (huntingtin associated protein) has previously been found to interact with huntingtin (htt) in a glutamine length dependent manner and has been proposed to play a role in the cell specific neurodegeneration observed in Huntington's disease (HD). We have isolated mouse HAP1 (hap1) and have shown that expression is not enriched in areas specifically affected in HD. We have used the yeast two hybrid system to demonstrate that htt amino acids 171–230 are necessary for the hap1-htt binding and that hap1 does not interact with the transgene exon 1 protein in a transgenic model of HD.
Databáze:	OpenAIRE
Externí odkaz:	https://explore.openaire.eu/search/publication?articleId=doi_dedup___::dfa25e46d4c66af8f428600246b979fb https://pubmed.ncbi.nlm.nih.gov/9599014 Zobrazit plný text záznamu Plný text