Results 51 to 60 of about 30,328 (180)

Restoration from polyglutamine toxicity after free electron laser irradiation of neuron-like cells [PDF]

open access: yes, 2019
学位記番号 ...
Mohara, Miho   +2 more
core  

Intrabodies Binding the Proline-Rich Domains of Mutant Huntingtin Increase Its Turnover and Reduce Neurotoxicity [PDF]

open access: yes, 2008
Although expanded polyglutamine (polyQ) repeats are inherently toxic, causing at least nine neurodegenerative diseases, the protein context determines which neurons are affected.
Bugg, Charles W.   +5 more
core   +2 more sources

QBP1 Peptide as a Potential Anti‐Amyloidogenic Therapy for Type 2 Diabetes: An In Vitro Study

open access: yesAdvanced Science, EarlyView.
The anti‐amyloidogenic peptide QBP1 effectively halts human islet amyloid polypeptide (hIAPP) aggregation, preventing the formation of toxic β‐structured intermediates. Through a combination of biophysical assays, molecular dynamics, and cell‐based studies, QBP1 is shown to preserve β‐cell viability and metabolic homeostasis, positioning it as a ...
María M. Tejero‐Ojeda   +8 more
wiley   +1 more source

Protein Aggregates and Polyglutamine Tracts In Neurodegenerative Disease [PDF]

open access: yes, 2018
The incidence of neurodegenerative diseases such as Alzheimer\u27s Disease, Parkinson\u27s Disease, Huntington\u27s Disease and other Polyglutamine Diseases is projected to dramatically increase throughout the developed world, and yet the pathology of ...
Mack, John
core   +1 more source

Quantification of mutant huntingtin protein in cerebrospinal fluid from Huntington's disease patients. [PDF]

open access: yes, 2015
Quantification of disease-associated proteins in the cerebrospinal fluid (CSF) has been critical for the study and treatment of several neurodegenerative disorders; however, mutant huntingtin protein (mHTT), the cause of Huntington's disease (HD), is at ...
Andreas Weiss   +16 more
core   +1 more source

Spinocerebellar Ataxia Type 2 [PDF]

open access: yes, 2012
1. Introduction: The autosomal dominant cerebellar ataxias (ADCA) are a clinically, pathologically and genetically heterogeneous group of neurodegenerative disorders caused by degeneration of cerebellum and its afferent and efferent connections.
Auburger, Georg   +3 more
core   +1 more source

Alogliptin Reduces Oxidative Stress in Cardiomyocytes and Ameliorates Diabetic Cardiomyopathy via the AURKB/NLGN2 Signaling

open access: yesThe Kaohsiung Journal of Medical Sciences, EarlyView.
ABSTRACT Diabetic cardiomyopathy (DCM) is a common complication of diabetes mellitus. This study investigated the effects of alogliptin on DCM and its underlying mechanisms. A DCM model was constructed and treated with alogliptin. Downstream targets of alogliptin were screened using bioinformatics analysis.
Li‐Jing Jiao   +7 more
wiley   +1 more source

miR-1 coordinately regulates lysosomal v-ATPase and biogenesis to impact proteotoxicity and muscle function during aging

open access: yeseLife, 2021
Muscle function relies on the precise architecture of dynamic contractile elements, which must be fine-tuned to maintain motility throughout life. Muscle is also plastic, and remodeled in response to stress, growth, neural and metabolic inputs.
Isabelle Schiffer   +10 more
doaj   +1 more source

The replicative lifespan-extending deletion of SGF73 results in altered ribosomal gene expression in yeast. [PDF]

open access: yes, 2017
Sgf73, a core component of SAGA, is the yeast orthologue of ataxin-7, which undergoes CAG-polyglutamine repeat expansion leading to the human neurodegenerative disease spinocerebellar ataxia type 7 (SCA7).
Garza, Renee M   +6 more
core   +2 more sources

Modulation of the Stress Granule Component Carhsp1 Mitigates Disease‐Associated Deficits in Spinocerebellar Ataxia Type 3 Mouse Models

open access: yesMovement Disorders, EarlyView.
Abstract Background Spinocerebellar ataxia type 3 (SCA3) is a polyglutamine (polyQ) neurogenerative disorder that results from CAG trinucleotide repeat expansions in the ATXN3 gene, leading to toxic protein aggregate formation and cellular pathway dysfunction.
Tiago Moreira‐Gomes   +9 more
wiley   +1 more source

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