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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 01 Mar 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
Selective striatal mtDNA depletion in end-stage Huntington's disease R6/2 mice.
Orth et al., Ulm, Germany. In Exp Neurol, 12 Mar 2015
UNASSIGNED: In Huntington's disease (HD) striatum and cortex seem particularly vulnerable.
The JAK/STAT3 Pathway Is a Common Inducer of Astrocyte Reactivity in Alzheimer's and Huntington's Diseases.
Escartin et al., Fontenay-aux-Roses, France. In J Neurosci, 11 Mar 2015
Inhibition of the JAK/STAT3 pathway within reactive astrocytes also increased the number of huntingtin aggregates, a neuropathological hallmark of HD, but did not influence neuronal death.
Neonatal iron supplementation potentiates oxidative stress, energetic dysfunction and neurodegeneration in the R6/2 mouse model of Huntington's disease.
Fox et al., Laramie, United States. In Redox Biol, 11 Mar 2015
UNASSIGNED: Huntington's disease (HD) is a progressive neurodegenerative disorder caused by a CAG repeat expansion that encodes a polyglutamine tract in huntingtin (htt) protein.
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.
Update on Huntington's disease: Advances in care and emerging therapeutic options.
Landwehrmeyer et al., Poznań, Poland. In Parkinsonism Relat Disord, Jan 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.
Detection of ubiquitinated huntingtin species in intracellular aggregates.
Reits et al., Amsterdam, Netherlands. In Front Mol Neurosci, Dec 2014
Huntington's disease (HD) is one of nine diseases caused by an expanded polyQ repeat within the affected protein and is hallmarked by intracellular inclusion bodies composed of aggregated N-terminal huntingtin (Htt) fragments and other sequestered proteins.
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.
Neferine Attenuates the Protein Level and Toxicity of Mutant Huntingtin in PC-12 Cells via Induction of Autophagy.
Law et al., Aomen, Macao. In Molecules, Dec 2014
Furthermore, by overexpressing huntingtin with 74 CAG repeats (EGFP-HTT 74) in PC-12 cells, neferine reduces both the protein level and toxicity of mutant huntingtin through an autophagy-related gene 7 (Atg7)-dependent mechanism.
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.
Proteostasis in striatal cells and selective neurodegeneration in Huntington's disease.
Finkbeiner et al., San Francisco, United States. In Front Cell Neurosci, 2013
Although mutant huntingtin, the protein responsible for HD, is expressed ubiquitously, a subpopulation of neurons in the striatum is the first to succumb.
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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