Results 81 to 90 of about 19,163 (188)
UBL3 Interacts with PolyQ-Expanded Huntingtin Fragments and Modifies Their Intracellular Sorting
Background/Objectives: UBL3 (Ubiquitin-like 3) is a protein that plays a crucial role in post-translational modifications, particularly in regulating protein transport within small extracellular vesicles. While previous research has predominantly focused
Soho Oyama +19 more
doaj +1 more source
Detection of alpha-rod protein repeats using a neural network and application to huntingtin.
A growing number of solved protein structures display an elongated structural domain, denoted here as alpha-rod, composed of stacked pairs of anti-parallel alpha-helices.
Gareth A Palidwor +10 more
doaj +1 more source
The DNA/RNA autophagy protein SIDT2 as a novel neuropathological hallmark in Huntington disease
SIDT2‐immunoreactive inclusions are observed in the striatum, cerebral cortex, and hypothalamus in HD cases with different Vonsattel grades, and the frequency of SIDT2‐immunoreactive inclusions is associated with longer CAG repeats in the huntingtin gene.
Sanaz Gabery +17 more
wiley +1 more source
Neuronal cell death in HD is believed to be largely a dominant cell-autonomous effect of the mutant huntingtin protein. We previously developed an inducible PC12 cell model which expresses an N-terminal huntingtin fragment with an expanded poly Q repeat (
Wenfei Wang +5 more
doaj +1 more source
Reduction of mutant huntingtin accumulation and toxicity by lysosomal cathepsins D and B in neurons
Background Huntington's disease is caused by aggregation of mutant huntingtin (mHtt) protein containing more than a 36 polyQ repeat. Upregulation of macroautophagy was suggested as a neuroprotective strategy to degrade mutant huntingtin.
Ouyang Xiaosen +3 more
doaj +1 more source
Therapeutic nano‐drug delivery systems interact with cellular mitochondria in a multitude of ways. While the complexity of such interactions disrupts the mitochondrial electron transport chain and increases reactive oxygen species production, thereby contributing to nanoparticle toxicity, they also present unique theranostic opportunities in diseases ...
Sourav Bhattacharjee
wiley +1 more source
Abstract INTRODUCTION Blood‐based biomarkers are essential for early detection, monitoring, and therapeutic development in Alzheimer's disease (AD) and related dementia (ADRD), but current assays lack brain cell specificity and sensitivity to low‐abundant proteins.
Ashish Kumar +10 more
wiley +1 more source
The power of many: when genetics met yeasts and high‐throughput
ABSTRACT In recent years, complex technological capabilities have evolved, driven by the need to solve complex and integrative biological questions through global analyses. New equipment allows the scaling up and automation of processes which previously were carried out on a very limited scale.
Víctor A. Tallada, Víctor Carranco
wiley +1 more source
Two lateral mouse brain sagittal sections labeled, respectively, for Lypd1 (A) and Kcnab3 (B). (A) Lypd1 labels positively cortical Layers 2 and 5 (less heavily), but only at limbic mesocortical sites, forming the limbic ring that separates the unlabeled isocortex (IsoCx) from the unlabeled hippocampal and olfactory allocortex (Hi, Sub, ERh; OlfCx ...
Luis Puelles, Elena Garcia‐Calero
wiley +1 more source
Huntingtin Interacting Proteins Are Genetic Modifiers of Neurodegeneration
Huntington's disease (HD) is a fatal neurodegenerative condition caused by expansion of the polyglutamine tract in the huntingtin (Htt) protein. Neuronal toxicity in HD is thought to be, at least in part, a consequence of protein interactions involving mutant Htt.
Linda S Kaltenbach +20 more
openaire +4 more sources

