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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 28 Aug 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
Primary cilia and autophagic dysfunction in Huntington's disease.
Bossy-Wetzel et al., Orlando, United States. In Cell Death Differ, 30 Sep 2015
Huntington's disease (HD) is an inherited, neurodegenerative disorder caused by a single-gene mutation: a CAG expansion in the huntingtin (HTT) gene that results in production of a mutated protein, mutant HTT, with a polyglutamine tail (polyQ-HTT).
Inhibition of aggregation of mutant huntingtin by nucleic acid aptamers in vitro and in a yeast model of Huntington's disease.
Roy et al., In Mol Ther, 27 Sep 2015
UNASSIGNED: Elongated polyglutamine stretch in mutant huntingtin (mhtt) correlates well with the pathology of Huntington's disease (HD).
Transcriptional dysregulation of inflammatory/immune pathways after active vaccination against Huntington's disease.
Messer et al., Albany, United States. In Hum Mol Genet, 24 Sep 2015
Huntington's disease (HD), an autosomal dominant disorder triggered by misfolding of huntingtin (HTT) protein with an expanded polyglutamine tract, could also benefit from this approach.
HDAC6 inhibition induces mitochondrial fusion, autophagic flux and reduces diffuse mutant huntingtin in striatal neurons.
Oliveira et al., Porto, Portugal. In Biochim Biophys Acta, 20 Sep 2015
Inhibition of the alpha-tubulin deacetylase HDAC6 has been proposed as a therapeutic strategy for HD, but remains controversial - studies in neurons show improved intracellular transport, whereas studies in cell-lines suggest it may impair autophagosome-lysosome fusion, and reduce clearance of mutant huntingtin (mHtt) and damaged mitochondria (mitophagy).
Environmental factors as modulators of neurodegeneration: insights from gene-environment interactions in Huntington's disease.
Renoir et al., Melbourne, Australia. In Neurosci Biobehav Rev, May 2015
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, 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.
[Gene silencing approaches for the treatment of Huntington's disease].
Déglon et al., Lausanne, Switzerland. In Med Sci (paris), Feb 2015
Huntington's disease is a rare neurodegenerative disease caused by a pathologic CAG expansion in the exon 1 of the huntingtin (HTT) gene.
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.
Delayed identification and diagnosis of Huntington's disease due to psychiatric symptoms.
Correll et al., Brassó, Romania. In Int J Ment Health Syst, Dec 2014
HD is caused by an expanded polyglutamine stretch in the N-terminal part of a 350 kDa protein called huntingtin (HTT).
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.
Transgenic animal models for study of the pathogenesis of Huntington's disease and therapy.
Li et al., Beijing, China. In Drug Des Devel Ther, Dec 2014
Mouse models of HD include transgenic mice, which express N-terminal or full-length mutant huntingtin ubiquitously or selectively in different cell types, and knock-in mice that express full-length mutant Htt at the endogenous level.
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.
Red/ET recombination with chimeric oligonucleotides allows rapid generation of BAC transgenes harboring full-length or truncated huntingtin cDNA.
Kranz et al., Heidelberg, Germany. In Biotechniques, 2012
Huntington's disease (HD) is a fatal neurodegenerative disorder that is caused by a CAG repeat expansion encoding a polyglutamine tract in the huntingtin (htt) gene.
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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