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Tandem Repeats in Genes, Proteins, and Disease

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Cover of 'Tandem Repeats in Genes, Proteins, and Disease'

Table of Contents

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    Book Overview
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    Chapter 1 Longitudinal Imaging and Analysis of Neurons Expressing Polyglutamine-Expanded Proteins
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    Chapter 2 Atomic Force Microscopy Assays for Evaluating Polyglutamine Aggregation in Solution and on Surfaces
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    Chapter 3 Morphometric Analysis of Huntington's Disease Neurodegeneration in Drosophila.
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    Chapter 4 Size analysis of polyglutamine protein aggregates using fluorescence detection in an analytical ultracentrifuge.
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    Chapter 5 A Method for the Incremental Expansion of Polyglutamine Repeats in Recombinant Proteins
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    Chapter 6 Tandem Repeats in Genes, Proteins, and Disease
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    Chapter 7 Characterizing social behavior in genetically targeted mouse models of brain disorders.
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    Chapter 8 PCR Amplification and Sequence Analysis of GC-Rich Sequences: Aristaless-Related Homeobox Example
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    Chapter 9 Challenges of “Sticky” Co-immunoprecipitation: Polyalanine Tract Protein–Protein Interactions
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    Chapter 10 Molecular Pathology of Polyalanine Expansion Disorders: New Perspectives from Mouse Models
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    Chapter 11 Yeast as a platform to explore polyglutamine toxicity and aggregation.
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    Chapter 12 Immuno-based Detection Assays to Quantify Distinct Mutant Huntingtin Conformations in Biological Samples.
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    Chapter 13 Modeling and Analysis of Repeat RNA Toxicity in Drosophila
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    Chapter 14 Analyzing Modifiers of Protein Aggregation in C. elegans by Native Agarose Gel Electrophoresis.
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    Chapter 15 Kinetic Analysis of Aggregation Data
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    Chapter 16 Tandem Repeats in Genes, Proteins, and Disease
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    Chapter 17 Detecting Soluble PolyQ Oligomers and Investigating Their Impact on Living Cells Using Split-GFP
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    Chapter 18 Cell Biological Approaches to Investigate Polyglutamine-Expanded AR Metabolism
Attention for Chapter 7: Characterizing social behavior in genetically targeted mouse models of brain disorders.
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Chapter title
Characterizing social behavior in genetically targeted mouse models of brain disorders.
Chapter number 7
Book title
Tandem Repeats in Genes, Proteins, and Disease
Published in
Methods in molecular biology, January 2013
DOI 10.1007/978-1-62703-438-8-7
Pubmed ID
Book ISBNs
978-1-62703-437-1, 978-1-62703-438-8
Authors

Burrows, Emma L, Hannan, Anthony J, Emma L. Burrows, Anthony J. Hannan

Editors

Danny M. Hatters, Anthony J. Hannan

Abstract

Fragile X syndrome, the leading inherited cause of mental retardation and autism spectrum disorders worldwide, is caused by a tandem repeat expansion in the FMR1 (fragile X mental retardation 1) gene. It presents with a distinct behavioral phenotype which overlaps significantly with that of autism. Emerging evidence suggests that tandem repeat polymorphisms (TRPs) might also play a key role in modulating disease susceptibility for a range of common polygenic disorders, including the broader autism spectrum of disorders (ASD) and other forms of psychiatric illness such as schizophrenia, depression, and bipolar disorder [1]. In order to understand how TRPs and associated gene mutations mediate pathogenesis, various mouse models have been generated. A crucial step in such functional genomics is high-quality behavioral and cognitive phenotyping. This chapter presents a basic behavioral battery for standardized tests for assaying social phenotypes in mouse models of brain disorders, with a focus on aggression.

Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 13 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Netherlands 1 8%
Unknown 12 92%

Demographic breakdown

Readers by professional status Count As %
Researcher 10 77%
Student > Master 7 54%
Student > Ph. D. Student 6 46%
Student > Bachelor 3 23%
Professor 3 23%
Other 7 54%
Readers by discipline Count As %
Neuroscience 11 85%
Psychology 11 85%
Agricultural and Biological Sciences 6 46%
Medicine and Dentistry 5 38%
Biochemistry, Genetics and Molecular Biology 1 8%
Other 1 8%