gopubmed logo
find other proteinsAll proteins
GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.


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
Increased Olfactory Bulb BDNF Expression Does Not Rescue Deficits in Olfactory Neurogenesis in the Huntington's Disease R6/2 Mouse.
Guthrie et al., Boca Raton, United States. In Chem Senses, Feb 2016
UNASSIGNED: Huntington's disease (HD) is an inherited neurodegenerative disorder caused by expansion of CAG trinucleotide repeats in the huntingtin gene.
Cytoplasmic protein aggregates interfere with nucleocytoplasmic transport of protein and RNA.
Hipp et al., Martinsried, Germany. In Science, Feb 2016
Here, we analyzed the compartment specificity of aggregate toxicity using artificial β-sheet proteins, as well as fragments of mutant huntingtin and TAR DNA binding protein-43 (TDP-43).
Huntington's Disease: Relationship Between Phenotype and Genotype.
Wu et al., Shanghai, China. In Mol Neurobiol, Feb 2016
It is caused by the dynamic mutation in CAG triplet repeat number in exon 1 of huntingtin (HTT) gene.
PPAR-δ is repressed in Huntington's disease, is required for normal neuronal function and can be targeted therapeutically.
La Spada et al., San Diego, United States. In Nat Med, Jan 2016
Huntington's disease (HD) is a progressive neurodegenerative disorder caused by a CAG trinucleotide repeat expansion in the huntingtin (HTT) gene, which encodes a polyglutamine tract in the HTT protein.
CAMELOT: A machine learning approach for coarse-grained simulations of aggregation of block-copolymeric protein sequences.
Pappu et al., Saint Louis, United States. In J Chem Phys, Jan 2016
We demonstrate the utility of our coarse-graining approach using the block-copolymeric sequence from the exon 1 encoded sequence of the huntingtin protein.
Impaired development of cortico-striatal synaptic connectivity in a cell culture model of Huntington's disease.
Raymond et al., Vancouver, Canada. In Neurobiol Dis, Jan 2016
UNASSIGNED: Huntington's disease (HD) is a genetically inherited neurodegenerative disease caused by a mutation in the gene encoding the huntingtin protein.
Induced Pluripotent Stem Cells in Huntington's Disease: Disease Modeling and the Potential for Cell-Based Therapy.
Wang et al., Wuhan, China. In Mol Neurobiol, Jan 2016
UNASSIGNED: Huntington's disease (HD) is an incurable neurodegenerative disorder that is characterized by motor dysfunction, cognitive impairment, and behavioral abnormalities.
Inhibition of Early Biochemical Defects in Prodromal Huntington's Disease by Simultaneous Activation of Nrf2 and Elevation of Multiple Micronutrients.
Bondy et al., Irvine, United States. In Curr Aging Sci, Dec 2015
Huntington's disease (HD) is a progressive fatal dominant hereditary neurodegenerative disease of the brain, which primarily affects the cortex and the striatum.
α-Synuclein and huntingtin exon 1 amyloid fibrils bind laterally to the cellular membrane.
Melki et al., Gif-sur-Yvette, France. In Sci Rep, Dec 2015
By characterizing the binding properties of aggregates made of α-synuclein or huntingtin exon 1 protein displaying similar composition and structure but different lengths to mammalian cells we demonstrate that in both cases aggregates bind laterally to the cellular membrane, with aggregates extremities displaying little or no role in membrane binding.
Iron neurochemistry in Alzheimer's disease and Parkinson's disease: targets for therapeutics.
Bush et al., Melbourne, Australia. In J Neurochem, Dec 2015
Indeed, many proteins initially characterized in those diseases such as amyloid-β protein, α-synuclein and huntingtin have been linked to iron neurochemistry.
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, 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.
Neural and mesenchymal stem cells in animal models of Huntington's disease: past experiences and future challenges.
Glosman et al., São Paulo, Brazil. In Stem Cell Res Ther, 2014
Huntington's disease (HD) is an inherited disease that causes progressive nerve cell degeneration.
The Neuropathology of Huntington´s disease: classical findings, recent developments and correlation to functional neuroanatomy.
Korf et al., Frankfurt am Main, Germany. In Adv Anat Embryol Cell Biol, 2014
which encodes the mutated protein huntingtin (Htt).
Targeting Hsp90/Hsp70-based protein quality control for treatment of adult onset neurodegenerative diseases.
Lieberman et al., In Annu Rev Pharmacol Toxicol, 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, 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.
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
share on facebooktweetadd +1mail to friends