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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 02 Oct 2014.


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
Localized changes to glycogen synthase kinase-3 and collapsin response mediator protein-2 in the Huntington's disease affected brain.
Crouch et al., Melbourne, Australia. In Hum Mol Genet, Sep 2014
All cases of Huntington's disease (HD) are caused by mutant huntingtin protein (mhtt), yet the molecular mechanisms that link mhtt to disease symptoms are not fully elucidated.
Mechanisms of synaptic dysfunction and excitotoxicity in Huntington's disease.
Raymond et al., Vancouver, Canada. In Drug Discov Today, Jul 2014
Huntington's disease (HD) is an inherited neurodegenerative disorder of movement, mood and cognition, caused by a polyglutamine expansion in the huntingtin (Htt) protein.
Cell-based therapies for Huntington's disease.
Chan et al., Atlanta, United States. In Drug Discov Today, Jul 2014
Current research focuses on genetic suppression of the mutant huntingtin (mHTT) gene and cell replacement therapy of the lost cells in HD.
Cystathionine γ-lyase deficiency mediates neurodegeneration in Huntington's disease.
Snyder et al., Baltimore, United States. In Nature, Jun 2014
Huntington's disease is an autosomal dominant disease associated with a mutation in the gene encoding huntingtin (Htt) leading to expanded polyglutamine repeats of mutant Htt (mHtt) that elicit oxidative stress, neurotoxicity, and motor and behavioural changes.
Identification of novel HSP90α/β isoform selective inhibitors using structure-based drug design. demonstration of potential utility in treating CNS disorders such as Huntington's disease.
Stamos et al., San Diego, United States. In J Med Chem, May 2014
Selective HSP90α/β inhibitors were found to be equipotent to pan-HSP90 inhibitors in promoting the clearance of mutant huntingtin protein (mHtt) in vitro, however with less cellular toxicity.
Curvature enhances binding and aggregation of huntingtin at lipid membranes.
Legleiter et al., Morgantown, United States. In Biochemistry, May 2014
Huntington disease (HD) is a genetic neurodegenerative disease caused by an expanded polyglutamine (polyQ) domain in the first exon of the huntingtin (Htt) protein, facilitating its aggregation.
Study of cholesterol metabolism in Huntington's disease.
Caccia et al., Milano, Italy. In Biochem Biophys Res Commun, May 2014
Huntington's disease (HD) is an autosomal dominant neurodegenerative disorder caused by an abnormal expansion of a CAG repeat in the huntingtin gene.
REST is Present in Human Control and Huntington's Disease Neurons.
Zuccato et al., Pavia, Italy. In Neuropathol Appl Neurobiol, Apr 2014
We also found that REST and huntingtin (HTT) colocalize in human neurons.
14-3-3 and aggresome formation: implications in neurodegenerative diseases.
Zhou et al., Tallahassee, United States. In Prion, Mar 2014
Previously, the 14-3-3 proteins were shown to be indispensable for the formation of aggresomes induced by mutant huntingtin proteins.
Calretinin: from a "simple" Ca(2+) buffer to a multifunctional protein implicated in many biological processes.
Schwaller, Fribourg, Switzerland. In Front Neuroanat, Dec 2013
CR binding to other targets including the pore-forming α1 subunit of the Ca(2+) channel Ca V 2.1, as well as to huntingtin indicates additional Ca(2+) sensor functions besides the well-known Ca(2+)-buffering functions.
Huntington's disease.
Cattaneo et al., Milano, Italy. In Handb Exp Pharmacol, Dec 2013
However, only in Huntington disease (HD) gain- and loss-of-function experiments have mechanistically linked these abnormalities with the genetic defect.In this chapter we will describe how huntingtin protein, whose mutation causes HD, is involved in the physiological control of BDNF synthesis and transport in neurons and how both processes are simultaneously disrupted in HD.
Glutathione peroxidase activity is neuroprotective in models of Huntington's disease.
Giorgini et al., Leicester, United Kingdom. In Nat Genet, Oct 2013
Huntington's disease is a fatal neurodegenerative disorder caused by a CAG repeat expansion encoding a polyglutamine tract in the huntingtin (Htt) protein.
Suppressing aberrant GluN3A expression rescues synaptic and behavioral impairments in Huntington's disease models.
Pérez-Otaño et al., Pamplona, Spain. In Nat Med, Aug 2013
Huntington's disease is caused by an expanded polyglutamine repeat in the huntingtin protein (HTT), but the pathophysiological sequence of events that trigger synaptic failure and neuronal loss are not fully understood.
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.
TRACK-HD Investigators et al., London, United Kingdom. In Lancet Neurol, 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.
Vesicular glycolysis provides on-board energy for fast axonal transport.
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.
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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