Polyglutamine diseases: emerging concepts in pathogenesis and therapy.
about
Machado-Joseph Disease: from first descriptions to new perspectives.Development and application of a DNA microarray-based yeast two-hybrid systemEvo-devo, deep homology and FoxP2: implications for the evolution of speech and language.Improved activities of CREB binding protein, heterogeneous nuclear ribonucleoproteins and proteasome following downregulation of noncoding hsromega transcripts help suppress poly(Q) pathogenesis in fly modelsAnimal models of polyglutamine diseases and therapeutic approachesTau fragmentation, aggregation and clearance: the dual role of lysosomal processingThe Role of Cdkn1A-Interacting Zinc Finger Protein 1 (CIZ1) in DNA Replication and PathophysiologyMouse models of polyglutamine diseases in therapeutic approaches: review and data table. Part II.Huntington's disease cerebrospinal fluid seeds aggregation of mutant huntingtin.Motor Dysfunctions and Neuropathology in Mouse Models of Spinocerebellar Ataxia Type 2: A Comprehensive ReviewCo-chaperone HSJ1a dually regulates the proteasomal degradation of ataxin-3The role of mTOR signaling in Alzheimer diseaseInhibition of mitochondrial protein import by mutant huntingtinInduction of DARPP-32 by brain-derived neurotrophic factor in striatal neurons in vitro is modified by histone deacetylase inhibitors and Nab2Dynamic Sumoylation of a Conserved Transcription Corepressor Prevents Persistent Inclusion Formation during Hyperosmotic StressSmall ubiquitin-like modifier (SUMO) modification of the androgen receptor attenuates polyglutamine-mediated aggregationTherapeutic prospects for spinocerebellar ataxia type 2 and 3.IKK phosphorylates Huntingtin and targets it for degradation by the proteasome and lysosome.The RNA-binding protein ATX-2 regulates cytokinesis through PAR-5 and ZEN-4Hsp70 chaperones and type I PRMTs are sequestered at intranuclear inclusions caused by polyalanine expansions in PABPN1Design of RNAi hairpins for mutation-specific silencing of ataxin-7 and correction of a SCA7 phenotype.Probing the metabolic aberrations underlying mutant huntingtin toxicity in yeast and assessing their degree of preservation in humans and mice.The carboxy-terminal fragment of alpha(1A) calcium channel preferentially aggregates in the cytoplasm of human spinocerebellar ataxia type 6 Purkinje cells.An aggregation sensing reporter identifies leflunomide and teriflunomide as polyglutamine aggregate inhibitors.Interaction with polyglutamine aggregates reveals a Q/N-rich domain in TDP-43.Polyglutamine toxicity is controlled by prion composition and gene dosage in yeast.Expanded ataxin-7 cause toxicity by inducing ROS production from NADPH oxidase complexes in a stable inducible Spinocerebellar ataxia type 7 (SCA7) model.Nicotinamide improves motor deficits and upregulates PGC-1α and BDNF gene expression in a mouse model of Huntington's disease.Altered Ca(2+) signaling in skeletal muscle fibers of the R6/2 mouse, a model of Huntington's diseaseTailor-made RNAi knockdown against triplet repeat disease-causing alleles.Functional interactions as a survival strategy against abnormal aggregationThe expanded amelogenin polyproline region preferentially binds to apatite versus carbonate and promotes apatite crystal elongationHsp40 gene therapy exerts therapeutic effects on polyglutamine disease mice via a non-cell autonomous mechanism.In vivo cell-autonomous transcriptional abnormalities revealed in mice expressing mutant huntingtin in striatal but not cortical neurons.Cytoplasmic location of α1A voltage-gated calcium channel C-terminal fragment (Cav2.1-CTF) aggregate is sufficient to cause cell death.Proceedings of the fourth international conference on central hypoventilation.Structural formation of huntingtin exon 1 aggregates probed by small-angle neutron scattering.Role of inositol 1,4,5-trisphosphate receptors in pathogenesis of Huntington's disease and spinocerebellar ataxiasInteraction with polyglutamine-expanded huntingtin alters cellular distribution and RNA processing of huntingtin yeast two-hybrid protein A (HYPA).Expanded polyglutamine-binding peptoid as a novel therapeutic agent for treatment of Huntington's disease.
P2860
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P2860
Polyglutamine diseases: emerging concepts in pathogenesis and therapy.
description
2007 nî lūn-bûn
@nan
2007 թուականի Հոկտեմբերին հրատարակուած գիտական յօդուած
@hyw
2007 թվականի հոտեմբերին հրատարակված գիտական հոդված
@hy
2007年の論文
@ja
2007年論文
@yue
2007年論文
@zh-hant
2007年論文
@zh-hk
2007年論文
@zh-mo
2007年論文
@zh-tw
2007年论文
@wuu
name
Polyglutamine diseases: emerging concepts in pathogenesis and therapy.
@ast
Polyglutamine diseases: emerging concepts in pathogenesis and therapy.
@en
Polyglutamine diseases: emerging concepts in pathogenesis and therapy.
@nl
type
label
Polyglutamine diseases: emerging concepts in pathogenesis and therapy.
@ast
Polyglutamine diseases: emerging concepts in pathogenesis and therapy.
@en
Polyglutamine diseases: emerging concepts in pathogenesis and therapy.
@nl
prefLabel
Polyglutamine diseases: emerging concepts in pathogenesis and therapy.
@ast
Polyglutamine diseases: emerging concepts in pathogenesis and therapy.
@en
Polyglutamine diseases: emerging concepts in pathogenesis and therapy.
@nl
P356
P1476
Polyglutamine diseases: emerging concepts in pathogenesis and therapy.
@en
P2093
Jieya Shao
Marc I Diamond
P304
P356
10.1093/HMG/DDM213
P478
16 Spec No. 2
P577
2007-10-01T00:00:00Z