Rebecca L. Kow
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View article: Tri-snRNP activity modulates tauopathy phenotypes
Tri-snRNP activity modulates tauopathy phenotypes Open
Alzheimer’s disease (AD) and other tauopathies are neurodegenerative disorders with devastating consequences for cognition and memory. Pathogenic accumulation of tau can be modeled in Caenorhabditis elegans, which recapitulate human neurod…
View article: TMEM106B C‐terminal fragments aggregate and drive neurodegenerative proteinopathy in transgenic Caenorhabditis <i>elegans</i>
TMEM106B C‐terminal fragments aggregate and drive neurodegenerative proteinopathy in transgenic Caenorhabditis <i>elegans</i> Open
INTRODUCTION Genetic variation in the lysosomal and transmembrane protein 106B (TMEM106B) modifies risk for several neurodegenerative disorders, especially frontotemporal lobar degeneration (FTLD). The C‐terminal (CT) domain of TMEM106B oc…
View article: TMEM106B C-terminal fragments aggregate and drive neurodegenerative proteinopathy
TMEM106B C-terminal fragments aggregate and drive neurodegenerative proteinopathy Open
Genetic variation in the lysosomal and transmembrane protein 106B (TMEM106B) modifies risk for a diverse range of neurodegenerative disorders, especially frontotemporal lobar degeneration (FTLD) with progranulin (PGRN) haplo-insufficiency,…
View article: Sut-6/NIPP1 modulates tau toxicity
Sut-6/NIPP1 modulates tau toxicity Open
Neurodegenerative diseases exhibiting the pathological accumulation of tau such as Alzheimer’s disease and related disorders still have no disease-modifying treatments and the molecular mechanisms of neurodegeneration remain unclear. To di…
View article: SPOP loss of function protects against tauopathy
SPOP loss of function protects against tauopathy Open
The pathological accumulation of the microtubule binding protein tau drives age-related neurodegeneration in a variety of disorders, collectively called tauopathies. In the most common tauopathy, Alzheimer’s disease (AD), the accumulation …
View article: Loss of aly/ALYREF suppresses toxicity in both tau and TDP-43 models of neurodegeneration
Loss of aly/ALYREF suppresses toxicity in both tau and TDP-43 models of neurodegeneration Open
View article: Loss of Aly/ALYREF Suppresses Toxicity in Both Tau and TDP-43 Models of Neurodegeneration
Loss of Aly/ALYREF Suppresses Toxicity in Both Tau and TDP-43 Models of Neurodegeneration Open
Background Neurodegenerative diseases with tau pathology, or tauopathies, include Alzheimer’s Disease and related dementia disorders. Previous work has shown that loss of the poly(A) RNA-binding protein gene sut2/MSUT2 strongly suppressed …
View article: Distinct Poly(A) nucleases have differential impact on sut-2 dependent tauopathy phenotypes.
Distinct Poly(A) nucleases have differential impact on sut-2 dependent tauopathy phenotypes. Open
Aging drives pathological accumulation of proteins such as tau, causing neurodegenerative dementia disorders like Alzheimer's disease. Previously we showed loss of function mutations in the gene encoding the poly(A) RNA binding protein SUT…
View article: Activity of the poly(A) binding protein MSUT2 determines susceptibility to pathological tau in the mammalian brain
Activity of the poly(A) binding protein MSUT2 determines susceptibility to pathological tau in the mammalian brain Open
The poly(A) RNA binding proteins MSUT2 and PABPN1 regulate the accumulation of pathological tau in two mouse models of tauopathy.
View article: DOPA Decarboxylase Modulates Tau Toxicity
DOPA Decarboxylase Modulates Tau Toxicity Open
Loss of the DDC bas-1 reduced tau-induced toxicity in a C. elegans model of tauopathy, while loss of no other dopamine or serotonin synthesis genes tested had this effect. Because loss of activity upstream of DDC could reduce suppression o…