Results 71 to 80 of about 19,163 (188)
Huntington's disease (HD) is caused by an expanded glutamine tract, which confers a novel aggregation-promoting property on the 350-kDa huntingtin protein.
Francesca Persichetti +6 more
doaj +1 more source
Huntingtin as an Actin Organizer: Structural and Functional Insights
Cytoskeleton, EarlyView.
M. Capizzi, S. Humbert
wiley +1 more source
Frozen in Place: Proximity Labeling Maps Glial Interactomes Across Cell States
Proximity labeling enables cell‐type‐specific and spatially resolved mapping of glial protein networks. Proximity labeling approaches provide insights into glial function under physiological and pathological conditions. ABSTRACT Glial cells, including radial glia, oligodendrocyte precursor cells (OPCs), oligodendrocytes, astrocytes, and microglia, are ...
João Baltar +3 more
wiley +1 more source
The Role of Post-translational Modifications on the Energy Landscape of Huntingtin N-Terminus
Huntington disease is a neurodegenerative disease characterized by a polymorphic tract of polyglutamine repeats in exon 1 of the huntingtin protein, which is thought to be responsible for protein aggregation and neuronal death. The polyglutamine tract is
Havva Yalinca +6 more
doaj +1 more source
Abstract In recent years, the clinical treatment and symptom management of neurological disorders have faced significant challenges due to the high complexity of the nervous system's structure and function. Against this backdrop, physical stimulation techniques have emerged as a vital complementary approach to traditional pharmacological treatments and
Wanying Li, Liqun Chen
wiley +1 more source
Reduced Levels of Proteasome Products in a Mouse Striatal Cell Model of Huntington's Disease.
Huntington's disease is the result of a long polyglutamine tract in the gene encoding huntingtin protein, which in turn causes a large number of cellular changes and ultimately results in neurodegeneration of striatal neurons. Although many theories have
Sayani Dasgupta +6 more
doaj +1 more source
Cell Death in Neurodegenerative Diseases: Molecular Mechanisms and Therapeutic Targets
Regulated cell death pathways, including apoptosis, necroptosis, pyroptosis, ferroptosis, and autophagy‐dependent cell death, interact with mitochondrial dysfunction, proteostasis failure, lysosomal stress, glial remodeling, and neuroinflammation across major neurodegenerative diseases.
Tianjiao Li +3 more
wiley +1 more source
Proteostasis in striatal cells and selective neurodegeneration in Huntington’s disease
Selective neuronal loss is a hallmark of neurodegenerative diseases, including Huntington’s disease (HD). Although mutant huntingtin, the protein responsible for Huntington’s disease, is expressed ubiquitously, a subpopulation of neurons in the striatum ...
Julia eMargulis +4 more
doaj +1 more source
Neurological disorders (NDs) are characterized by substantial loss of specific neurons, with Alzheimer's and Parkinson's diseases being the most frequent NDs and nearly 99% of all “foreign substances” are prohibited from entering the brain by the blood‐brain barrier (BBB) and the blood‐cerebrospinal fluid barrier (CFB).
Nnamdi Ikemefuna Okafor +3 more
wiley +1 more source
Fibrillogenesis of Huntingtin and Other Glutamine Containing Proteins [PDF]
This chapter focuses on the aggregation of glutamine containing peptides and proteins with an emphasis on huntingtin protein, whose aggregation leads to the development of Huntington's disease. The kinetics that leads to the formation of amyloids, the structure of aggregates of various types and the morphological mechanical properties of amyloid ...
Yuri L, Lyubchenko +2 more
openaire +2 more sources

