Значения термина mutant huntingtin на английском

A possible cross-talk between mutant huntingtin and a-synuclein aggregates has been postulated.

N-terminal cleavage may be linked to mutant huntingtin's role in cell death.

These alterations may increase the susceptibility of striatal neurons to mutant huntingtin-mediated toxicity.

This can be explained as nocodazole inhibits autophagosome-lysosome fusion, a key step in mutant huntingtin exon 1 clearance.

Only mutant huntingtin formed nuclear and cytoplasmic inclusions, which increased with polyglutamine expansion and with time after transfection.

Sequestration of mTOR impairs its kinase activity and induces autophagy, a key clearance pathway for mutant huntingtin fragments.

Addressing the problem at its genetic root by suppressing mutant huntingtin expression is a promising therapeutic strategy for HD.

The protein-protein interactions of mutant huntingtin with transcriptional factors do not constitute conventional and easy targets for drug molecules.

Through a small molecule screening approach, we discovered five structurally distinct compounds that prevent apoptosis induced by mutant huntingtin protein.

Although multiple pathologic mechanisms have been proposed, the exact mechanism by which mutant huntingtin causes neuronal dysfunction is not known.

Here, we have examined the hypothesis that the mutant huntingtin protein may directly interact with the mitochondrion and affect its function.

Neuronal intranuclear inclusions and cytoplasmic aggregates composed of the mutant huntingtin within certain neuronal populations are a characteristic hallmark of HD.

The mutant huntingtin protein-induced MPT pore opening was accompanied by a significant release of cytochrome c, an effect completely inhibited by CSA.

Suppression of the mutant huntingtin gene in cortical output neurons prevents decline in turning and improves alpha, beta, and low-gamma activity in M1.

Neuronal intranuclear inclusions are found in the brains of patients with Huntington's disease and form from the polyglutamine-expanded N-terminal region of mutant huntingtin.

Inhibiting PDI in rat brain cells suppressed the toxicity of mutant huntingtin exon 1 and Aβ peptides processed from the amyloid precursor protein.