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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 15 Apr 2015.


Top mentioned proteins: CAN, AGE, ACID, V1a, HAD
Papers using huntingtin antibodies
A comparison of normalization methods for high density oligonucleotide array data based on variance and bias
Flotte Terence R et al., In Molecular Therapy, 2002
... Intrastriatal rAAV-mediated delivery of anti-huntingtin shRNAs induces partial reversal of disease progression in R6/1 Huntington's disease transgenic mice ...
Modulation of the in situ activity of tissue transglutaminase by calcium and GTP
Johnson Gail V.W. et al., In The Journal of Cell Biology, 1997
... The BamHI–XhoI huntingtin cDNA fragments were also subcloned into the Amersham Pharmacia Biotech and XhoI sites of the pECFP-N1 vector (CLONTECH Laboratories, Inc.) (N-Q18) (pECFP-N1-18Q) ...
Papers on huntingtin
Dysfunctional Dopaminergic Neurones in Mouse Models of Huntington's Disease: A Role for SK3 Channels.
Murphy et al., Milton Keynes, United Kingdom. In Neurodegener Dis, 09 May 2015
BACKGROUND: Huntington's disease (HD) is a late-onset fatal neurodegenerative disorder caused by a CAG trinucleotide repeat expansion in the gene coding for the protein huntingtin and is characterised by progressive motor, psychiatric and cognitive decline.
Cerebrovascular and blood-brain barrier impairments in Huntington's disease: Potential implications for its pathophysiology.
Cicchetti et al., Cambridge, United Kingdom. In Ann Neurol, 09 May 2015
RESULTS: We found mutant huntingtin protein (mHtt) aggregates to be present in all major components of the neurovascular unit of both R6/2 mice and HD patients.
Structure of a single-chain Fv bound to the 17N-terminal amino acids of huntingtin provides insights into pathogenic amyloid formation and suppression.
Dobson et al., Illkirch-Graffenstaden, France. In J Mol Biol, 07 May 2015
The C4 single-chain Fv antibody (scFv), binds to the first 17 residues of huntingtin (HTT(1-17)) and generates substantial protection against multiple phenotypic pathologies in situ and in vivo.
Environmental factors as modulators of neurodegeneration: Insights from gene-environment interactions in Huntington's disease.
Renoir et al., Melbourne, Australia. In Neurosci Biobehav Rev, 10 Apr 2015
UNASSIGNED: Unlike many other neurodegenerative diseases with established gene-environment interactions, Huntington's disease (HD) is viewed as a disorder governed by genetics.
Update on Huntington's disease: advances in care and emerging therapeutic options.
Landwehrmeyer et al., Poznań, Poland. In Parkinsonism Relat Disord, 31 Mar 2015
The authors review recent achievements in HD research and focus on approaches towards disease-modifying therapies, ranging from huntingtin-lowering strategies to improving huntingtin clearance that may be promoted by posttranslational HTT modifications.
Safety, tolerability, and efficacy of PBT2 in Huntington's disease: a phase 2, randomised, double-blind, placebo-controlled trial.
Huntington Study Group Reach2HD Investigators, In Lancet Neurol, Jan 2015
BACKGROUND: PBT2 is a metal protein-attenuating compound that might reduce metal-induced aggregation of mutant huntingtin and has prolonged survival in a mouse model of Huntington's disease.
Characterization of HTT Inclusion Size, Location, and Timing in the zQ175 Mouse Model of Huntington´s Disease: An In Vivo High-Content Imaging Study.
Kwak et al., Hamburg, Germany. In Plos One, Dec 2014
Huntington's disease (HD) is an autosomal dominant neurodegenerative disorder caused by a CAG trinucleotide repeat expansion in the huntingtin gene.
Targeting Hsp90/Hsp70-based protein quality control for treatment of adult onset neurodegenerative diseases.
Lieberman et al., In Annu Rev Pharmacol Toxicol, Dec 2014
Critical target proteins that unfold and aggregate in these diseases, such as the polyglutamine androgen receptor in spinal and bulbar muscular atrophy, huntingtin in Huntington's disease, α-synuclein in Parkinson's disease, and tau in Alzheimer's disease, are client proteins of heat shock protein 90 (Hsp90), and their turnover is regulated by the protein quality control function of the Hsp90/Hsp70-based chaperone machinery.
Activation and regulation of caspase-6 and its role in neurodegenerative diseases.
Su et al., Key West, United States. In Annu Rev Pharmacol Toxicol, Dec 2014
Cleavage at the caspase-6 site in mutated huntingtin protein is a prerequisite for the development of the characteristic behavioral and neuropathological features of Huntington's disease.
Prion-like transmission of neuronal huntingtin aggregates to phagocytic glia in the Drosophila brain.
Kopito et al., Stanford, United States. In Nat Commun, Dec 2014
We have established a Drosophila model to investigate the role of phagocytic glia in clearance of neuronal mutant huntingtin (Htt) aggregates associated with Huntington disease.
Slowing of neurodegeneration in Parkinson's disease and Huntington's disease: future therapeutic perspectives.
Bezard et al., New York City, United States. In Lancet, Sep 2014
In Huntington's disease, strategies might also be directed at mitochondrial bioenergetics and turnover, the prevention of protein dysregulation, disruption of the interaction between huntingtin and p53 or huntingtin-interacting protein 1 to reduce apoptosis, and interference with expression of mutant huntingtin at both the nucleic acid and protein levels.
Neuronal targets for reducing mutant huntingtin expression to ameliorate disease in a mouse model of Huntington's disease.
Yang et al., Los Angeles, United States. In Nat Med, May 2014
Huntington's disease (HD) is a fatal dominantly inherited neurodegenerative disorder caused by a CAG repeat expansion leading to an elongated polyglutamine stretch in huntingtin.
Skeletal muscle pathology in Huntington's disease.
Mielcarek et al., Poznań, Poland. In Front Physiol, 2013
Huntington's disease (HD) is a hereditary neurodegenerative disorder caused by the expansion of a polyglutamine stretch within the huntingtin protein (HTT).
Ubiquitin-proteasome system involvement in Huntington's disease.
Lucas et al., Madrid, Spain. In Front Mol Neurosci, 2013
Huntington's disease (HD) is a genetic autosomal dominant neurodegenerative disease caused by the expansion of a CAG repeat in the huntingtin (htt) gene.
Possible involvement of self-defense mechanisms in the preferential vulnerability of the striatum in Huntington's disease.
Brouillet et al., Fontenay-aux-Roses, France. In Front Cell Neurosci, 2013
HD is caused by a mutation in the huntingtin gene that consists in a CAG repeat expansion translated into an abnormal poly-glutamine (polyQ) tract in the huntingtin (Htt) protein.
Huntingtin is required for mitotic spindle orientation and mammalian neurogenesis.
Humbert et al., Orsay, France. In Neuron, 2010
The specific disruption of Drosophila huntingtin in neuroblast precursors leads to spindle misorientation; Drosophila huntingtin restores spindle misorientation in mammalian cells.
A genomewide RNA interference screen for modifiers of aggregates formation by mutant Huntingtin in Drosophila.
Perrimon et al., Boston, United States. In Genetics, 2010
a genomewide RNA interference screen for regulators of mutant Htt aggregation
Inactivation of Drosophila Huntingtin affects long-term adult functioning and the pathogenesis of a Huntington's disease model.
Perrimon et al., Boston, United States. In Dis Model Mech, 2009
dHtt is required for maintaining the mobility and long-term survival of adult animals, and for modulating axonal terminal complexity in the adult brain.
Glial cell lineage expression of mutant ataxin-1 and huntingtin induces developmental and late-onset neuronal pathologies in Drosophila models.
Okazawa et al., Tokyo, Japan. In Plos One, 2008
mutant ataxin-1 and huntingtin induce developmental and late-onset neuronal pathologies in Drosophila models
RNAi screening in Drosophila cells identifies new modifiers of mutant huntingtin aggregation.
Nukina et al., Wako, Japan. In Plos One, 2008
genes related to nuclear transport, nucleotide processes, and signaling are modifiers of huntingtin aggregation
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