Results 21 to 30 of about 30,328 (180)
Impaired Nuclear Export of Polyglutamine-Expanded Androgen Receptor in Spinal and Bulbar Muscular Atrophy. [PDF]
, 2019 Spinal and bulbar muscular atrophy (SBMA) is a neuromuscular disease caused by polyglutamine (polyQ) expansion in the androgen receptor (AR). Prior studies have highlighted the importance of AR nuclear localization in SBMA pathogenesis; therefore, in ...
Arnold, Frederick J. +2 more
core +3 more sources
Evidence for gliadin antibodies as causative agents in schizophrenia. [PDF]
, 2010 Antibodies to gliadin, a component of gluten, have frequently been reported in schizophrenia. Highly immunogenic B cell epitopes along its length are homologous to numerous proteins relevant to schizophrenia, including members of the DISC1 interactome ...
Chris J. Carter
core +2 more sources
Sphingomyelin and GM1 Influence Huntingtin Binding to, Disruption of, and Aggregation on Lipid Membranes [PDF]
, 2018 Huntington disease (HD) is an inherited neurodegenerative disease caused by the expansion beyond a critical threshold of a polyglutamine (polyQ) tract near the N-terminus of the huntingtin (htt) protein. Expanded polyQ promotes the formation of a variety
Campbell, Warren A. +5 more
core +4 more sources
Acta Biochimica et Biophysica Sinica, 2023 Nine polyglutamine (polyQ) proteins have already been identified that are considered to be associated with the pathologies of neurodegenerative disorders called polyQ diseases, but whether these polyQ proteins mutually interact and synergize in ...
Hong Jun-Ye +6 more
doaj +1 more source
Aberrant Autophagic Response in The Muscle of A Knock-in Mouse Model of Spinal and Bulbar Muscular Atrophy [PDF]
, 2015 Spinal and bulbar muscular atrophy (SBMA) is characterized by loss of motoneurons and sensory neurons, accompanied by atrophy of muscle cells. SBMA is due to an androgen receptor containing a polyglutamine tract (ARpolyQ) that misfolds and aggregates ...
Aggarwal, Tanya +15 more
core +2 more sources
Activation of p38MAPK contributes to expanded polyglutamine-induced cytotoxicity.
PLoS ONE, 2008 BackgroundThe signaling pathways that may modulate the pathogenesis of diseases induced by expanded polyglutamine proteins are not well understood.Methodologies/principal findingsHerein we demonstrate that expanded polyglutamine protein cytotoxicity is ...
Maria Tsirigotis +4 more
doaj +1 more source
Pathologic polyglutamine aggregation begins with a self-poisoning polymer crystal
eLife, 2023 A long-standing goal of amyloid research has been to characterize the structural basis of the rate-determining nucleating event. However, the ephemeral nature of nucleation has made this goal unachievable with existing biochemistry, structural biology ...
Tej Kandola +13 more
doaj +1 more source
Biology, 2023 Removal of the 5′ cap structure of RNAs (termed decapping) is a pivotal event in the life of cytoplasmic mRNAs mainly catalyzed by a conserved holoenzyme, composed of the catalytic subunit DCP2 and its essential cofactor DCP1.
Fivos Borbolis +6 more
doaj +1 more source
ATXN2-CAG42 sequesters PABPC1 into insolubility and induces FBXW8 in cerebellum of old ataxic knock-in mice [PDF]
, 2012 Spinocerebellar Ataxia Type 2 (SCA2) is caused by expansion of a polyglutamine encoding triplet repeat in the human ATXN2 gene beyond (CAG)31. This is thought to mediate toxic gain-of-function by protein aggregation and to affect RNA processing ...
Auburger, Georg +8 more
core +3 more sources
Frontiers in Molecular Neuroscience, 2017 Spinal and bulbar muscular atrophy (SBMA) is caused by expression of a polyglutamine (polyQ)-expanded androgen receptor (AR). The inefficient nuclear proteasomal degradation of the mutant AR results in the formation of nuclear inclusions containing amino-
Jill M. Yersak +6 more
doaj +1 more source