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Neuroscience

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102
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39059
World Ranking
709
National Ranking
398

Genetics

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104
Citations
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645
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327

Medicine

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104
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40214
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Overview

Harry T. Orr is affiliated with the University of Minnesota in the United States. Their research primarily spans the fields of Biochemistry, Genetics and Molecular Biology, and Neuroscience. Within these main fields, they focus on subfields including Molecular Biology, Cellular and Molecular Neuroscience, Neurology, Genetics, and Cognitive Neuroscience.

The scientist's work concentrates on various main topics, notably Genetic Neurodegenerative Diseases, Mitochondrial Function and Pathology, RNA Research and Splicing, Genetics and Neurodevelopmental Disorders, Autism Spectrum Disorder Research, DNA Repair Mechanisms, and Muscle Physiology and Disorders.

Harry T. Orr has contributed to several recent publications, including:

  • Patterns of CAG repeat instability in the central nervous system and periphery in Huntington's disease and in spinocerebellar ataxia type 1, 2020, Human Molecular Genetics
  • Autistic-like behavior and cerebellar dysfunction in Bmal1 mutant mice ameliorated by mTORC1 inhibition, 2022, Molecular Psychiatry
  • Targeting inhibitory cerebellar circuitry to alleviate behavioral deficits in a mouse model for studying idiopathic autism, 2020, Neuropsychopharmacology
  • Consensus Paper: Strengths and Weaknesses of Animal Models of Spinocerebellar Ataxias and Their Clinical Implications, 2021, The Cerebellum
  • Altered Capicua expression drives regional Purkinje neuron vulnerability through ion channel gene dysregulation in spinocerebellar ataxia type 1, 2020, Human Molecular Genetics

Frequent co-authors in Harry T. Orr's publications include Lisa Duvick, Huda Y. Zoghbi, Hillary P. Handler, Praseuth Yang, and Marija Cvetanović.

Common venues for Harry T. Orr's publications include bioRxiv (Cold Spring Harbor Laboratory), Neuron, Human Molecular Genetics, JCI Insight, and The Cerebellum.

Best Publications

  • Expansion of an unstable trinucleotide CAG repeat in spinocerebellar ataxia type 1.

    Harry T. Orr;Ming yi Chung;Sandro Banfi;Thomas J. Kwiatkowski

  • Trinucleotide Repeat Disorders

    Harry T. Orr;Huda Y. Zoghbi

  • Glutamine Repeats and Neurodegeneration

    Huda Y. Zoghbi;Harry T. Orr

  • Genetic linkage evidence for a familial Alzheimer's disease locus on chromosome 14.

    Gerard D. Schellenberg;Thomas D. Bird;Ellen M. Wijsman;Harry T. Orr

  • Ataxin-1 nuclear localization and aggregation: role in polyglutamine-induced disease in SCA1 transgenic mice.

    Ivan A Klement;Pamela J Skinner;Michael D Kaytor;Hong Yi

  • Chaperone suppression of ataxin-1 aggregation and altered subcellular proteasome localization imply protein misfolding in sca1

    Huda Y Zoghbi;Harry T Orr;Donald B Defranco;Michael A Mancini

  • RNAi suppresses polyglutamine-induced neurodegeneration in a model of spinocerebellar ataxia

    Haibin Xia;Qinwen Mao;Steven L Eliason;Scott Q Harper

  • Identification of genes that modify ataxin-1-induced neurodegeneration

    Pedro Fernandez-Funez;Maria Laura Nino-Rosales;Beatrice De Gouyon;Wei Chi She

  • SCA1 transgenic mice: A model for neurodegeneration caused by an expanded CAG trinucleotide repeat

    Eric N Burright;H Brent Clark;Antonio Servadio;Toni Matilla

  • A HUMAN MAJOR HISTOCOMPATIBILITY COMPLEX CLASS I GENE THAT ENCODES A PROTEIN WITH A SHORTENED CYTOPLASMIC SEGMENT

    Daniel E. Geraghty;Beverly H. Koller;Harry T. Orr

  • Major histocompatibility antigens: The human (HLA-A,-B,-C) and murine (H-2K, H-2D) class I molecules

    Hidde L. Ploegh;Harry T. Orr;Jack L. Strominger

  • Ataxin-1 with an expanded glutamine tract alters nuclear matrix-associated structures

    Pamela J. Skinner;Beena T. Koshy;Christopher J. Cummings;Ivan A. Klement

  • Over-expression of inducible HSP70 chaperone suppresses neuropathology and improves motor function in SCA1 mice

    Christopher J. Cummings;Yaling Sun;Puneet Opal;Barbara Antalffy

  • Mutation of the E6-AP Ubiquitin Ligase Reduces Nuclear Inclusion Frequency While Accelerating Polyglutamine-Induced Pathology in SCA1 Mice

    Christopher J Cummings;Eyal Reinstein;Yaling Sun;Barbara Antalffy

  • Evidence for a mechanism predisposing to intergenerational CAG repeat instability in spinocerebellar ataxia type I

    Ming Yi Chung;Laura P.W. Ranum;Lisa A. Duvick;Antonio Servadio

  • Interaction of Akt-Phosphorylated Ataxin-1 with 14-3-3 Mediates Neurodegeneration in Spinocerebellar Ataxia Type 1

    Hung Kai Chen;Hung Kai Chen;Pedro Fernandez-Funez;Summer F. Acevedo;Yung C. Lam

  • Genetic linkage studies suggest that Alzheimer's disease is not a single homogeneous disorder

    P. H. St George-Hyslop;J. L. Haines;L. A. Farrer;R. Polinsky

  • Linkage map of the human major histocompatibility complex including the tumor necrosis factor genes

    Michael C. Carroll;Philip Katzman;Elizabeth M. Alicot;Beverly H. Koller

  • Identification and characterization of the gene causing type 1 spinocerebellar ataxia

    Sandro Banfi;Antonio Servadio;Ming yi Chung;Thomas J. Kwiatkowski

  • Polyglutamine expansion down-regulates specific neuronal genes before pathologic changes in SCA1

    Xi Lin;Barbara Antalffy;Dongcheul Kang;Harry T. Orr

Frequent Co-Authors

Huda Y. Zoghbi
Huda Y. Zoghbi Baylor College of Medicine
Jack L. Strominger
Jack L. Strominger Harvard University
Beverly H. Koller
Beverly H. Koller University of North Carolina at Chapel Hill
Laura P.W. Ranum
Laura P.W. Ranum University of Florida
Peter Parham
Peter Parham Stanford University
Stephen S. Rich
Stephen S. Rich University of Virginia
Juan Botas
Juan Botas Baylor College of Medicine
Hidde L. Ploegh
Hidde L. Ploegh Boston Children's Hospital
Thomas D. Bird
Thomas D. Bird University of Washington
Daniel E. Geraghty
Daniel E. Geraghty Fred Hutchinson Cancer Research Center

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