K. Kegel

发表

Early and Progressive Accumulation of Reactive Microglia in the Huntington Disease Brain

P G Bhide, M. DiFiglia, T. Hashikawa, 2001, Journal of neuropathology and experimental neurology.

Huntingtin Expression Stimulates Endosomal–Lysosomal Activity, Endosome Tubulation, and Autophagy

M. DiFiglia, Manho Kim, N. Aronin, 2000, The Journal of Neuroscience.

Lysosomal proteases are involved in generation of N-terminal huntingtin fragments

M. DiFiglia, P. Detloff, Z. Qin, 2006, Neurobiology of Disease.

AlphaB-crystallin protects glial cells from hypertonic stress.

T. Iwaki, J. Goldman, K. Kegel, 1996, The American journal of physiology.

Optimization of an HTRF Assay for the Detection of Soluble Mutant Huntingtin in Human Buffy Coats: A Potential Biomarker in Blood for Huntington Disease

H. D. Rosas, M. DiFiglia, S. Hersch, 2010, PLoS currents.

Polyglutamine expansion in huntingtin increases its insertion into lipid bilayers.

M. DiFiglia, E. Wanker, W. Goldmann, 2009, Biochemical and biophysical research communications.

Polyglutamine expansion in huntingtin alters its interaction with phospholipids

M. DiFiglia, N. Aronin, E. Sapp, 2009, Journal of neurochemistry.

Reagents that block neuronal death from Huntington’s disease also curb oxidative stress

M. DiFiglia, E. Sapp, K. Kegel, 2012, Neuroreport.

Pro-caspase-8 Is Predominantly Localized in Mitochondria and Released into Cytoplasm upon Apoptotic Stimulation*

M. DiFiglia, K. Kikly, Z. Qin, 2001, The Journal of Biological Chemistry.

The regulation of N-terminal Huntingtin (Htt552) accumulation by Beclin1

M. DiFiglia, Z. Qin, Jun-chao Wu, 2012, Acta Pharmacologica Sinica.

Assessment of chloroquine treatment for modulating autophagy flux in brain of WT and HD mice.

D. Marchionini, C. Dominguez, H. Birch, 2014, Journal of Huntington's disease.

Multiple phenotypes in Huntington disease mouse neural stem cells

D. Irimia, S. Sinha, S. Zeitlin, 2012, Molecular and Cellular Neuroscience.

Aberrant Rab11-Dependent Trafficking of the Neuronal Glutamate Transporter EAAC1 Causes Oxidative Stress and Cell Death in Huntington's Disease

N. Aronin, E. Sapp, Marian DiFiglia, 2010, The Journal of Neuroscience.

Mutant huntingtin and glycogen synthase kinase 3‐β accumulate in neuronal lipid rafts of a presymptomatic knock‐in mouse model of Huntington's disease

N. Aronin, E. Sapp, K. Chase, 2010, Journal of neuroscience research.

Autophagy regulates the processing of amino terminal huntingtin fragments.

L. Thompson, Z. Qin, N. Aronin, 2003, Human molecular genetics.

Huntingtin Is Present in the Nucleus, Interacts with the Transcriptional Corepressor C-terminal Binding Protein, and Represses Transcription*

J. Nevins, Z. Qin, N. Aronin, 2002, The Journal of Biological Chemistry.

Huntingtin Associates with Acidic Phospholipids at the Plasma Membrane*

M. Hayden, W. Goldmann, Z. Qin, 2005, Journal of Biological Chemistry.

Huntingtin Bodies Sequester Vesicle-Associated Proteins by a Polyproline-Dependent Interaction

M. Hayden, E. Wanker, Z. Qin, 2004, The Journal of Neuroscience.

Single-step detection of mutant huntingtin in animal and human tissues: a bioassay for Huntington's disease.

H. D. Rosas, D. Housman, S. Hersch, 2009, Analytical biochemistry.

αB‐crystallin regulates intermediate filament organization in situ

James E. Goldman, L. Hurwitz, J. Goldman, 2000 .

Huntingtin cleavage product A forms in neurons and is reduced by gamma-secretase inhibitors

Dimitri Krainc, D. Curtis, D. Krainc, 2010, Molecular Neurodegeneration.

Caspase 3-cleaved N-terminal fragments of wild-type and mutant huntingtin are present in normal and Huntington's disease brains, associate with membranes, and undergo calpain-dependent proteolysis

Z. Qin, N. Aronin, E. Sapp, 2001, Proceedings of the National Academy of Sciences of the United States of America.

Striatal synaptosomes from Hdh140Q/140Q knock-in mice have altered protein levels, novel sites of methionine oxidation, and excess glutamate release after stimulation.

S. Shaffer, S. Kwak, K. Green, 2013, Journal of Huntington's disease.

Mutant Huntingtin Impairs Vesicle Formation from Recycling Endosomes by Interfering with Rab11 Activity

Kevin Fogarty, Lawrence M. Lifshitz, Clive Standley, 2009, Molecular and Cellular Biology.

Elevated NADPH oxidase activity contributes to oxidative stress and cell death in Huntington's disease.

M. Frosch, E. Sapp, K. Kegel, 2013, Human molecular genetics.

Triplicate Repeats: Huntington’s disease

J. Cha, K. Kegel, 2009 .

Disruption of Rab11 activity in a knock-in mouse model of Huntington's disease

N. Aronin, E. Sapp, K. Chase, 2009, Neurobiology of Disease.

Native Mutant Huntingtin in Human Brain

A. Young, J. Vonsattel, N. Wexler, 2012, The Journal of Biological Chemistry.

A function of huntingtin in guanine nucleotide exchange on Rab11

Z. Qin, S. Zeitlin, N. Aronin, 2008, Neuroreport.

Autophagy regulates the processing of amino terminal huntingtin fragments.

L. Thompson, N. Aronin, A. Kazantsev, 2003, Human molecular genetics.

Mutant Huntingtin Impairs Vesicle Formation from Recycling Endosomes by Interfering with Rab11 Activity

Lawrence M. Lifshitz, K. Fogarty, R. Tuft, 2009, Molecular and Cellular Biology.

Mutant huntingtin and glycogen synthase kinase 3‐β accumulate in neuronal lipid rafts of a presymptomatic knock‐in mouse model of Huntington's disease

N. Aronin, E. Sapp, K. Chase, 2010, Journal of neuroscience research.

EARLY INCREASE IN THE NADPH-OXIDASE (NOX2) ACTIVITY CONTRIBUTES TO OXIDATIVE STRESS AND NEURODEGENERATION IN HUNTINGTON'S DISEASE

N. Aronin, E. Sapp, K. Kegel, 2011 .