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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Jun 2013.

Huntingtin

huntingtin
Papers using huntingtin antibodies
A comparison of normalization methods for high density oligonucleotide array data based on variance and bias
Supplier
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
Supplier
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
Predictors of phenotypic progression and disease onset in premanifest and early-stage Huntington's disease in the TRACK-HD study: analysis of 36-month observational data.
New
Impact
TRACK-HD Investigators et al., London, United Kingdom. In Lancet Neurol, 31 Jul 2013
METHODS: Individuals without HD but carrying the mutant huntingtin gene (classed as preHD-A if ≥10·8 years and preHD-B if <10·8 years from predicted onset), participants with early HD (classed as HD1 if they had a total functional capacity score of 11-13 and HD2 if they had a score of 7-10), and healthy control individuals were assessed at four study sites in the Netherlands, the UK, France, and Canada.
BDNF-TrkB signaling in striatopallidal neurons controls inhibition of locomotor behavior.
New
Minichiello et al., Edinburgh, United Kingdom. In Nat Commun, 18 Jul 2013
Changes in cortical Bdnf expression levels, and/or impairment in brain-derived neurotrophic factor anterograde transport induced by mutant huntingtin (mHdh) are believed to cause striatopallidal neuron vulnerability in early-stage Huntington's disease.
Unbiased Screen Reveals Ubiquilin-1 and -2 Highly Associated with Huntingtin Inclusions.
New
Giasson et al., Gainesville, United States. In Brain Res, 14 Jul 2013
Using specific ubiquilin-2 antibodies and a series of transgenic mouse models of proteinopathies associated with neurodegenerative disease, we show that ubiquilin-2 preferentially associates with huntingtin polyQ expansion aggregates compared to α-synuclein, tau and several other types of protein inclusions.
Huntington's disease: underlying molecular mechanisms and emerging concepts.
New
Morimoto et al., Evanston, United States. In Trends Biochem Sci, 12 Jul 2013
Huntington's disease (HD) is a progressive neurodegenerative disorder for which no disease modifying treatments exist.
Enhanced Ca(2+)-dependent glutamate release from astrocytes of the BACHD Huntington's disease mouse model.
New
Gray et al., Birmingham, United States. In Neurobiol Dis, 08 Jul 2013
Huntington's disease (HD) causes preferential loss of a subset of neurons in the brain although the huntingtin protein is expressed broadly in various neural cell types, including astrocytes.
Huntington's Disease: The Past, Present, and Future Search for Disease Modifiers.
New
Clabough, Virginia, South Africa. In Yale J Biol Med, 30 Jun 2013
The HD mutation causes a polyglutamine repeat expansion within the N-terminal of the huntingtin (Htt) protein.
Vesicular glycolysis provides on-board energy for fast axonal transport.
New
Impact
Saudou et al., Orsay, France. In Cell, Mar 2013
GAPDH localizes on vesicles via a huntingtin-dependent mechanism and is transported on fast-moving vesicles within axons.
Single-stranded RNAs use RNAi to potently and allele-selectively inhibit mutant huntingtin expression.
New
Impact
Corey et al., Dallas, United States. In Cell, Oct 2012
Mutant huntingtin (HTT) protein causes Huntington disease (HD), an incurable neurological disorder.
Genetic correction of Huntington's disease phenotypes in induced pluripotent stem cells.
New
Impact
Ellerby et al., Novato, United States. In Cell Stem Cell, Sep 2012
Huntington's disease (HD) is caused by a CAG expansion in the huntingtin gene.
Spt4 is selectively required for transcription of extended trinucleotide repeats.
New
Impact
Cheng et al., Taipei, Taiwan. In Cell, Mar 2012
Inhibition of Supt4h, the mammalian ortholog of Spt4, reduced mutant huntingtin protein in neuronal cells and decreased its aggregation and toxicity while not altering overall cellular mRNA synthesis.
Single amino acid and trinucleotide repeats: function and evolution.
Review
Faux, Melbourne, Australia. In Adv Exp Med Biol, 2011
For example, the expansion of the glutamine repeat in huntingtin leads to the debilitating neurodegenerative disease, Huntington's disease.
An in vitro perspective on the molecular mechanisms underlying mutant huntingtin protein toxicity.
Review
Cicchetti et al., Québec, Canada. In Cell Death Dis, 2011
HD is of genetic origin and caused by a mutation in the huntingtin gene.
Lessons learned from the transgenic Huntington's disease rats.
Review
Temel et al., Maastricht, Netherlands. In Neural Plast, 2011
Few years ago, the first transgenic rat model of HD, carrying a truncated huntingtin cDNA fragment with 51 CAG repeats under control of the native rat huntingtin promoter, was introduced.
Hippocampal neurogenesis, cognitive deficits and affective disorder in Huntington's disease.
Review
Hannan et al., Melbourne, Australia. In Neural Plast, 2011
Huntington's disease (HD) is a neurodegenerative disorder caused by a tandem repeat expansion encoding a polyglutamine tract in the huntingtin protein.
Selective neurodegeneration, neuropathology and symptom profiles in Huntington's disease.
Review
Faull et al., Auckland, New Zealand. In Adv Exp Med Biol, 2011
Huntington's disease (HD) is an autosomal dominant inherited neurodegenerative disease caused by a CAG repeat expansion in exon 1 of the Huntington gene (HD) also known as IT15.
Huntingtin is required for mitotic spindle orientation and mammalian neurogenesis.
GeneRIF
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.
GeneRIF
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.
GeneRIF
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.
GeneRIF
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.
GeneRIF
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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