Intrabody gene therapy ameliorates motor, cognitive, and neuropathological symptoms in multiple mouse models of Huntington's disease.
about
The P42 peptide and Peptide-based therapies for Huntington's diseaseDeveloping stem cell therapies for juvenile and adult-onset Huntington's diseaseEngineering humoral immunity as prophylaxis or therapyThe role of ALFY in selective autophagyTransgenic animal models for study of the pathogenesis of Huntington's disease and therapyMouse models of polyglutamine diseases: review and data table. Part IIntrabodies as neuroprotective therapeuticsMouse models of polyglutamine diseases in therapeutic approaches: review and data table. Part II.Assessment of motor function, sensory motor gating and recognition memory in a novel BACHD transgenic rat model for huntington disease.Sudden death due to paralysis and synaptic and behavioral deficits when Hip14/Zdhhc17 is deleted in adult mice.Mice lacking caspase-2 are protected from behavioral changes, but not pathology, in the YAC128 model of Huntington disease.Mutant huntingtin fragments form oligomers in a polyglutamine length-dependent manner in vitro and in vivo.Functional identification of an aggression locus in the mouse hypothalamusA fully humanized transgenic mouse model of Huntington disease.Physico-chemical determinants of soluble intrabody expression in mammalian cell cytoplasm.Intrastriatal transplantation of adenovirus-generated induced pluripotent stem cells for treating neuropathological and functional deficits in a rodent model of Huntington's disease.Perturbation with intrabodies reveals that calpain cleavage is required for degradation of huntingtin exon 1Cystamine and intrabody co-treatment confers additional benefits in a fly model of Huntington's disease.Systemic delivery of P42 peptide: a new weapon to fight Huntington's disease.Bifunctional anti-huntingtin proteasome-directed intrabodies mediate efficient degradation of mutant huntingtin exon 1 protein fragments.Differential nuclear localization of complexes may underlie in vivo intrabody efficacy in Huntington's disease.Nicotinamide improves motor deficits and upregulates PGC-1α and BDNF gene expression in a mouse model of Huntington's disease.Capsid serotype and timing of injection determines AAV transduction in the neonatal mice brain.A huntingtin peptide inhibits polyQ-huntingtin associated defectsTau aggregation and its interplay with amyloid-β.Gene therapy in mouse models of huntington disease.Interaction with polyglutamine-expanded huntingtin alters cellular distribution and RNA processing of huntingtin yeast two-hybrid protein A (HYPA).Assessment of motor balance and coordination in mice using the balance beamPolyglutamine- and temperature-dependent conformational rigidity in mutant huntingtin revealed by immunoassays and circular dichroism spectroscopyReductions in behavioral deficits and neuropathology in the R6/2 mouse model of Huntington's disease following transplantation of bone-marrow-derived mesenchymal stem cells is dependent on passage number.The Aggregation Inhibitor Peptide QBP1 as a Therapeutic Molecule for the Polyglutamine Neurodegenerative Diseases.Mutant huntingtin's interaction with mitochondrial protein Drp1 impairs mitochondrial biogenesis and causes defective axonal transport and synaptic degeneration in Huntington's disease.AAV9 delivering a modified human Mullerian inhibiting substance as a gene therapy in patient-derived xenografts of ovarian cancerIBC's 22nd Annual Antibody Engineering and 9th Annual Antibody Therapeutics International Conferences and the 2011 Annual Meeting of The Antibody Society, December 5-8, 2011, San Diego, CA.A single-chain variable fragment intrabody prevents intracellular polymerization of Z α1-antitrypsin while allowing its antiproteinase activityThe emerging role of the first 17 amino acids of huntingtin in Huntington's diseaseTranscriptional dysregulation of inflammatory/immune pathways after active vaccination against Huntington's diseaseBifunctional Anti-Non-Amyloid Component α-Synuclein Nanobodies Are Protective In Situ.Effects of the combined treatment of bone marrow stromal cells with mild exercise and thyroid hormone on brain damage and apoptosis in a mouse focal cerebral ischemia model.Methylene blue modulates huntingtin aggregation intermediates and is protective in Huntington's disease models
P2860
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P2860
Intrabody gene therapy ameliorates motor, cognitive, and neuropathological symptoms in multiple mouse models of Huntington's disease.
description
2009 nî lūn-bûn
@nan
2009 թուականի Հոկտեմբերին հրատարակուած գիտական յօդուած
@hyw
2009 թվականի հոտեմբերին հրատարակված գիտական հոդված
@hy
2009年の論文
@ja
2009年学术文章
@wuu
2009年学术文章
@zh-cn
2009年学术文章
@zh-hans
2009年学术文章
@zh-my
2009年学术文章
@zh-sg
2009年學術文章
@yue
name
Intrabody gene therapy amelior ...... odels of Huntington's disease.
@ast
Intrabody gene therapy amelior ...... odels of Huntington's disease.
@en
type
label
Intrabody gene therapy amelior ...... odels of Huntington's disease.
@ast
Intrabody gene therapy amelior ...... odels of Huntington's disease.
@en
prefLabel
Intrabody gene therapy amelior ...... odels of Huntington's disease.
@ast
Intrabody gene therapy amelior ...... odels of Huntington's disease.
@en
P2093
P2860
P1476
Intrabody gene therapy amelior ...... odels of Huntington's disease.
@en
P2093
Amber L Southwell
Paul H Patterson
P2860
P304
13589-13602
P356
10.1523/JNEUROSCI.4286-09.2009
P407
P577
2009-10-01T00:00:00Z