Ganglioside GM1 induces phosphorylation of mutant huntingtin and restores normal motor behavior in Huntington disease mice
about
Ablation of neuronal ceramide synthase 1 in mice decreases ganglioside levels and expression of myelin-associated glycoprotein in oligodendrocytesMouse models of polyglutamine diseases in therapeutic approaches: review and data table. Part II.Fingolimod for the treatment of neurological diseases-state of play and future perspectivesGlycosphingolipid-Protein Interaction in Signal TransductionSerine 421 regulates mutant huntingtin toxicity and clearance in mice.Deletion of the huntingtin proline-rich region does not significantly affect normal huntingtin function in miceBiophysical insights into how surfaces, including lipid membranes, modulate protein aggregation related to neurodegeneration.Defective Sphingosine-1-phosphate metabolism is a druggable target in Huntington's disease.Inhibition of lipid signaling enzyme diacylglycerol kinase epsilon attenuates mutant huntingtin toxicity.Targets for future clinical trials in Huntington's disease: what's in the pipeline?Therapeutic advances in Huntington's Disease.Phosphorylation of mutant huntingtin at serine 116 modulates neuronal toxicity.Differential Anatomical Expression of Ganglioside GM1 Species Containing d18:1 or d20:1 Sphingosine Detected by MALDI Imaging Mass Spectrometry in Mature Rat Brain.Integration-independent Transgenic Huntington Disease Fragment Mouse Models Reveal Distinct Phenotypes and Life Span in Vivo.The emerging role of the first 17 amino acids of huntingtin in Huntington's diseaseSelective histone deacetylase (HDAC) inhibition imparts beneficial effects in Huntington's disease mice: implications for the ubiquitin-proteasomal and autophagy systems.Common disease signatures from gene expression analysis in Huntington's disease human blood and brainA flexible polyglutamine hinge opens new doors for understanding huntingtin functionPolyglutamine domain flexibility mediates the proximity between flanking sequences in huntingtinGenetic manipulations of mutant huntingtin in mice: new insights into Huntington's disease pathogenesis.Promise and Pitfalls of Mitochondrial Replacement for Prevention and Cure of Heritable Neurodegenerative Diseases Caused by Deleterious Mutations in Mitochondrial DNAAntidepressant-Like Effects of GM1 Ganglioside Involving the BDNF Signaling Cascade in Mice.Sphingolipids and brain resident macrophages in neuroinflammation: an emerging aspect of nervous system pathology.Pathogenic role of ganglioside metabolism in neurodegenerative diseases.Pridopidine, a dopamine stabilizer, improves motor performance and shows neuroprotective effects in Huntington disease R6/2 mouse model.Nuclear Lipids in the Nervous System: What they do in Health and Disease.FTY720 (fingolimod) is a neuroprotective and disease-modifying agent in cellular and mouse models of Huntington disease.Proteins Containing Expanded Polyglutamine Tracts and Neurodegenerative Disease.A multifunctional, multi-pathway intracellular localization signal in Huntingtin.Polyglutamine expansion affects huntingtin conformation in multiple Huntington's disease models.The huntingtin N17 domain is a multifunctional CRM1 and Ran-dependent nuclear and cilial export signalNewton, laplace, and the epistemology of systems biology.Identifying therapeutic targets by combining transcriptional data with ordinal clinical measurements.An Automated Home-Cage System to Assess Learning and Performance of a Skilled Motor Task in a Mouse Model of Huntington's DiseaseHuntingtin N17 domain is a reactive oxygen species sensor regulating huntingtin phosphorylation and localization.Motor phenotype is not associated with vascular dysfunction in symptomatic Huntington's disease transgenic R6/2 (160 CAG) miceThe CLIMB (Complex Lipids In Mothers and Babies) study: protocol for a multicentre, three-group, parallel randomised controlled trial to investigate the effect of supplementation of complex lipids in pregnancy, on maternal ganglioside status and subHuntingtin is a scaffolding protein in the ATM oxidative DNA damage response complex.Phosphorylation of huntingtin at residue T3 is decreased in Huntington's disease and modulates mutant huntingtin protein conformation.Glyco-sphingo biology: a novel perspective for potential new treatments in Huntington's disease.
P2860
Q24602345-10B4191E-9C1E-48A6-8779-92B30565F410Q27005950-D093843F-0D23-4833-84AB-92805FEACF52Q27026175-D374A64C-2392-4DB3-B426-0C51B7A1A056Q28072827-817E8ED1-EFB9-410C-8827-3164AE255AEAQ30355064-20535CFF-0C2B-4926-946F-0F451EBF94EAQ30425063-CAE1F322-005A-470D-85A5-427A6B38A11FQ30427825-81188AE8-FF99-4B1D-95A7-81F04F24CD47Q33902931-6218DA7E-2022-4955-A9B3-1077F10A7954Q34236510-801CA3CD-77B2-45D1-AED1-D78E2D7936DFQ34435001-8D5CA1B2-FED6-46E2-849F-9B0E9255B93CQ34487604-A4A8312D-29E8-4130-A573-86443AE5A5A5Q35088655-947C04BF-7468-4366-91A3-1B07A1731128Q35863925-15BDFAA1-88E4-470A-B58B-62A724AC3A74Q35905407-13BAE2F3-8783-46BC-ACA6-10E81954F8A3Q36110838-45B2084F-B014-40F8-8BCC-84326F96FC96Q36435854-9501DE8B-DB5F-4D5D-B5CC-1BCD48AECF07Q37141460-73CEAF68-F36D-4204-8E91-27F7B1FF2CD6Q37157263-AAC20C4A-3A7D-4F3C-B088-32B0AD8A85C7Q37157299-1A039A01-E378-4375-81A1-39A86BD7ECC2Q37165188-3F18ED70-48CC-4EC1-B7F2-69B2BB9E8EF5Q37277363-9D2B8E45-73C4-48E7-B12E-023A571A1E3DQ37299377-D58B2A35-B18B-4A4D-B273-65FC80317380Q38147080-9474F4E4-1A71-40C2-9707-03BC3E466B9DQ38218040-0F10DFE1-F387-449E-8F19-C979A87CD930Q38861728-1FEE127B-0244-4CD2-8A41-E79B79AD27A1Q38986890-6FF1D4F0-6091-46DD-A0A9-F8108F927D2DQ39049796-2D5B1A9C-8BCE-457C-963A-3A6363AD8D0CQ39124557-B5E79B87-AA52-46E8-8154-F8027AC54B88Q39358037-A63C6C23-9B8D-48A6-91C1-C687217D7539Q40985899-66941C6E-FE2D-4D26-BCEA-36946CC22F34Q41154714-D945E3A0-9B3F-4E7A-AC5F-64B079C60A91Q41345921-7DC53F85-0AFF-4368-ACA6-1F5B16B4E35FQ41701052-CC75F614-1C10-44BD-876D-29E0880439D8Q41720511-32092279-7A3A-48C3-911C-CC4F45D9B19DQ41731654-06766A08-0362-4F9A-835B-F431529D09D0Q41842714-EBF4B3F2-F7C6-4118-B2D3-C5F7889A31A5Q42650088-1C73B3A5-044A-40D8-BFBA-DFEA2DD1A093Q45299796-C973BC2E-A3A2-4B09-88CD-1E68BFE1B963Q45305618-5837654F-A851-44E9-90F3-39CCA9B96AE6Q47098894-1757892F-F8C9-415B-9087-1195F32FF2F3
P2860
Ganglioside GM1 induces phosphorylation of mutant huntingtin and restores normal motor behavior in Huntington disease mice
description
2012 nî lūn-bûn
@nan
2012 թուականի Փետրուարին հրատարակուած գիտական յօդուած
@hyw
2012 թվականի փետրվարին հրատարակված գիտական հոդված
@hy
2012年の論文
@ja
2012年論文
@yue
2012年論文
@zh-hant
2012年論文
@zh-hk
2012年論文
@zh-mo
2012年論文
@zh-tw
2012年论文
@wuu
name
Ganglioside GM1 induces phosph ...... ior in Huntington disease mice
@ast
Ganglioside GM1 induces phosph ...... ior in Huntington disease mice
@en
type
label
Ganglioside GM1 induces phosph ...... ior in Huntington disease mice
@ast
Ganglioside GM1 induces phosph ...... ior in Huntington disease mice
@en
prefLabel
Ganglioside GM1 induces phosph ...... ior in Huntington disease mice
@ast
Ganglioside GM1 induces phosph ...... ior in Huntington disease mice
@en
P2093
P2860
P50
P356
P1476
Ganglioside GM1 induces phosph ...... ior in Huntington disease mice
@en
P2093
Andrea Ciammola
Jenny Sassone
Joan S Steffan
Melanie Alpaugh
Melanie Horkey
Randy S Atwal
Ray Truant
Simonetta Sipione
P2860
P304
P356
10.1073/PNAS.1114502109
P407
P577
2012-02-13T00:00:00Z