Results 101 to 110 of about 25,505 (239)

The Ubiquitin-Proteasome Pathway in Huntington's Disease

open access: yesThe Scientific World Journal, 2008
The accumulation of mutant protein is a common feature of neurodegenerative disease. In Huntington's disease, a polyglutamine expansion in the huntingtin protein triggers neuronal toxicity.
Siddhartha Mitra, Steven Finkbeiner
doaj   +1 more source

Rapid generation of prion disease models using AAV‐delivered PrP variants in knockout mice

open access: yesBrain Pathology, Volume 36, Issue 4, July 2026.
We developed a rapid AAV‐based system to generate prion disease models in weeks rather than months. Following systemic AAV9P31 delivery of modified PrP to knockout mice, we achieved brain‐wide expression and successful propagation of both classical (RML) and atypical (GSS‐A117V) prion strains.
Maitena San‐Juan‐Ansoleaga   +11 more
wiley   +1 more source

HIP1 (huntingtin interactin protein 1) [PDF]

open access: yes, 1998
Review on HIP1 (huntingtin interactin protein 1), with data on DNA, on the protein encoded, and where the gene is ...
Huret, JL, JL Huret
core   +1 more source

Mitochondrial Enzymes Mimetic Ultrasmall Palladium Nanozymes Prevent Senescence and Neurodegeneration Through Metabolic Reprogramming

open access: yesAdvanced Science, Volume 13, Issue 32, 9 June 2026.
Simply constructed polyvinylpyrrolidone (PVP) modified palladium nanoparticles (PdP NPs) as cytochrome c oxidase (CcO) and superoxide dismutase (SOD) mimic are promising multifunctional nanoreactors to boost mitochondrial respiration chain function and refine homeostasis via regulation of mitochondrial dynamics and proteostasis sensor UPRmt, which ...
Wenshu Cong   +8 more
wiley   +1 more source

ALTERED EXPRESSION AND FUNCTIONALITY OF A2A ADENOSINE RECEPTORS IN HUNTINGTON’S DISEASE AND OTHER POLYGLUTAMINE DISORDERS

open access: yes, 2009
Several studies have suggested the possible involvement of A2A adenosine receptors in the pathogenesis of neuronal disorders, including Huntington’s disease.
Vincenzi, Fabrizio
core  

RaptorX structure prediction of huntingtin

open access: yes, 2016
<p>Huntingtin structure-function open lab notebook project.
Toledo-Sherman, Leticia   +7 more
core   +1 more source

Striatal Vulnerability in Huntington’s Disease: Neuroprotection Versus Neurotoxicity

open access: yesBrain Sciences, 2017
Huntington’s disease (HD) is an autosomal dominant neurodegenerative disease caused by the expansion of a CAG trinucleotide repeat encoding an abnormally long polyglutamine tract (PolyQ) in the huntingtin (Htt) protein.
Ryoma Morigaki, Satoshi Goto
doaj   +1 more source

Evolutionary Patterns of the Genes Involved in the Integrity and Segregation of Chromosomes in Sawflies (Hymenoptera: Symphyta)

open access: yesEcology and Evolution, Volume 16, Issue 6, June 2026.
This study identifies and characterizes the genes encoding cohesin and condensin complexes across Symphytan superfamilies, revealing their structural and functional roles with conserved motifs in maintaining genome stability. Phylogenetic analyses indicate that SMC genes originated from ancient duplication events, with notable gene loss (e.g., CAPG2 ...
Ayşe Rümeysa Nalça   +1 more
wiley   +1 more source

INVESTIGATION OF THE HUNTINGTIN-HAP40 INTERACTION IN HUNTINGTON’S DISEASE [PDF]

open access: yes, 2014
Huntington’s disease (HD) is a neurodegenerative disorder caused by the expansion of a polyglutamine tract in the huntingtin protein. The huntingtin protein has many roles in vesicular and endocytic trafficking, which can be modified in HD cells.
Williamson, Jennifer
core  

The Effect of Protein Tagging on Aggregation and Phase Separation

open access: yesJournal of Cellular Biochemistry, Volume 127, Issue 6, June 2026.
ABSTRACT Protein tags are widely used for purification, solubilization, detection, and imaging, yet they can substantially alter protein self‐assembly. This interference is particularly significant for intrinsically disordered proteins and low‐complexity domains, whose aggregation and phase separation are mediated by weak multivalent interactions that ...
Harunobu Saito, Kenji Sugase
wiley   +1 more source

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