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

Fabien Bertaux; Alan H. Sharp; Christopher A. Ross; Hans Lehrach; Gillian P. Bates; Erich Wanker

doi:10.1016/S0014-5793(98)00352-4

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

Fabien Bertaux, Alan H. Sharp, Christopher A. Ross, Hans Lehrach, Gillian P. Bates, Erich Wanker

School of Medicine

Research output: Contribution to journal › Article › peer-review

28 Scopus citations

Abstract

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.

Original language	English (US)
Pages (from-to)	229-232
Number of pages	4
Journal	FEBS Letters
Volume	426
Issue number	2
DOIs	https://doi.org/10.1016/S0014-5793(98)00352-4
State	Published - Apr 17 1998

Keywords

HAP1
Huntington's disease
Polyglutamine
Triplet repeat

ASJC Scopus subject areas

Biophysics
Structural Biology
Biochemistry
Molecular Biology
Genetics
Cell Biology

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10.1016/S0014-5793(98)00352-4

Cite this

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

abstract = "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.",

keywords = "HAP1, Huntington's disease, Polyglutamine, Triplet repeat",

author = "Fabien Bertaux and Sharp, {Alan H.} and Ross, {Christopher A.} and Hans Lehrach and Bates, {Gillian P.} and Erich Wanker",

note = "Funding Information: This work was supported by grants from the European Community, the Wellcome Trust, the Deutsche Forschungsgemeinschaft, the National Institutes of Health (NS16375 to C.R.), the Hereditary Disease Foundation and the Huntington's Disease Society of America.",

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T1 - HAP1-huntingtin interactions do not contribute to the molecular pathology in Huntington's disease transgenic mice

AU - Bertaux, Fabien

AU - Sharp, Alan H.

AU - Ross, Christopher A.

AU - Lehrach, Hans

AU - Bates, Gillian P.

AU - Wanker, Erich

N1 - Funding Information: This work was supported by grants from the European Community, the Wellcome Trust, the Deutsche Forschungsgemeinschaft, the National Institutes of Health (NS16375 to C.R.), the Hereditary Disease Foundation and the Huntington's Disease Society of America.

PY - 1998/4/17

Y1 - 1998/4/17

N2 - 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.

AB - 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.

KW - HAP1

KW - Huntington's disease

KW - Polyglutamine

KW - Triplet repeat

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JO - FEBS Letters

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

Abstract

Keywords

ASJC Scopus subject areas

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