Upregulation of RIN3 induces endosomal dysfunction in Alzheimer's disease
Abstract Background In Alzheimer's Disease (AD), about one-third of the risk genes
identified by GWAS encode proteins that function predominantly in the endocytic pathways …
identified by GWAS encode proteins that function predominantly in the endocytic pathways …
Dysregulation of Rab5‐mediated endocytic pathways in Alzheimer's disease
W Xu, F Fang, J Ding, C Wu - Traffic, 2018 - Wiley Online Library
Increasing evidence has pointed to that dysregulation of the endo‐lysosomal system is an
early cellular phenotype of pathogenesis for Alzheimer's disease (AD). Rab5, a small …
early cellular phenotype of pathogenesis for Alzheimer's disease (AD). Rab5, a small …
Regional selectivity of rab5 and rab7 protein upregulation in mild cognitive impairment and Alzheimer's disease
Endocytic alterations are one of the earliest changes to occur in Alzheimer's disease (AD),
and are hypothesized to be involved in the selective vulnerability of specific neuronal …
and are hypothesized to be involved in the selective vulnerability of specific neuronal …
The neuronal-specific isoform of BIN1 regulates β-secretase cleavage of APP and Aβ generation in a RIN3-dependent manner
R Bhattacharyya, CAF Teves, A Long, M Hofert… - Scientific Reports, 2022 - nature.com
Genome-wide association studies have identified BIN1 (Bridging integrator 1) and RIN3
(Ras and Rab interactor 3) as genetic risk factors for late-onset Alzheimer's disease (LOAD) …
(Ras and Rab interactor 3) as genetic risk factors for late-onset Alzheimer's disease (LOAD) …
Rab6 is increased in Alzheimer's disease brain and correlates with endoplasmic reticulum stress
W Scheper, JJM Hoozemans… - Neuropathology and …, 2007 - Wiley Online Library
Alzheimer's disease (AD) is characterized by deposits of aggregated proteins. Accumulation
of aggregation‐prone proteins activates protein quality control mechanisms, such as the …
of aggregation‐prone proteins activates protein quality control mechanisms, such as the …
The Alzheimer's gene SORL1 is a regulator of endosomal traffic and recycling in human neurons
S Mishra, A Knupp, MP Szabo, CA Williams… - Cellular and Molecular …, 2022 - Springer
Abstract Background Loss of the Sortilin-related receptor 1 (SORL1) gene seems to act as a
causal event for Alzheimer's disease (AD). Recent studies have established that loss of …
causal event for Alzheimer's disease (AD). Recent studies have established that loss of …
Evidence that the rab5 effector APPL1 mediates APP-βCTF-induced dysfunction of endosomes in Down syndrome and Alzheimer's disease
S Kim, Y Sato, PS Mohan, C Peterhoff… - Molecular …, 2016 - nature.com
Abstract β-Amyloid precursor protein (APP) and its cleaved products are strongly implicated
in Alzheimer's disease (AD). Endosomes are highly active APP processing sites, and …
in Alzheimer's disease (AD). Endosomes are highly active APP processing sites, and …
FGF2 affects Parkinson's disease-associated molecular networks through exosomal Rab8b/Rab31
R Kumar, S Donakonda, SA Müller, K Bötzel… - Frontiers in …, 2020 - frontiersin.org
Ras-associated binding (Rab) proteins are small GTPases that regulate the trafficking of
membrane components during endocytosis and exocytosis including the release of …
membrane components during endocytosis and exocytosis including the release of …
Nurr1 (NR4A2) regulates Alzheimer's disease‐related pathogenesis and cognitive function in the 5XFAD mouse model
The orphan nuclear receptor Nurr1 (also known as NR4A2) is critical for the development
and maintenance of midbrain dopaminergic neurons, and is associated with Parkinson's …
and maintenance of midbrain dopaminergic neurons, and is associated with Parkinson's …
Rab10 phosphorylation is a prominent pathological feature in Alzheimer's disease
Alzheimer's disease (AD) is the leading cause of dementia in the elderly, characterized by
neurofibrillary tangles (NFTs), senile plaques (SPs), and a progressive loss of neuronal cells …
neurofibrillary tangles (NFTs), senile plaques (SPs), and a progressive loss of neuronal cells …