ArticleHuman molecular genetics2015
The adipocyte differentiation protein APMAP is an endogenous suppressor of Aβ production in the brain.
Article in Human molecular genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 35 citations in OpenAlex.
- Cortical morphometric similarity patterns and molecular signatures across ischemic stroke recovery.Frontiers in neurology · 2025Article
- A deficiency screen of the 3rd chromosome for dominant modifiers of the Drosophila ER integral membrane protein, Jagunal.G3 (Bethesda, Md.) · 2023Article
- Complexities of JC Polyomavirus Receptor-Dependent and -Independent Mechanisms of Infection.Viruses · 2022Review
- A multi-omics study to characterize the transdifferentiation of human dermal fibroblasts to osteoblast-like cells.Frontiers in molecular biosciences · 2022Article
- Neurotranscriptomic changes associated with chick-directed parental care in adult non-reproductive Japanese quail.Scientific reports · 2021Article
- APMAP Promotes Epithelial-Mesenchymal Transition and Metastasis of Cervical Cancer Cells by Activating the Wnt/β-catenin Pathway.Journal of Cancer · 2021Article
- Synapse type-specific proteomic dissection identifies IgSF8 as a hippocampal CA3 microcircuit organizer.Nature communications · 2020Article
- Adipocyte Plasma Membrane Protein (APMAP) promotes JC Virus (JCPyV) infection in human glial cells.Virology · 2020Article
- Genetic and environmental determinants of variation in the plasma lipidome of older Australian twins.eLife · 2020Article
- Identification of adipocyte plasma membrane-associated protein as a novel modulator of human cytomegalovirus infection.PLoS pathogens · 2019Article
- The APMAP interactome reveals new modulators of APP processing and beta-amyloid production that are altered in Alzheimer's disease.Acta neuropathologica communications · 2019Article
- APMAP interacts with lysyl oxidase-like proteins, and disruption ofFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017Article
- Metabolic relationship between diabetes and Alzheimer's Disease affected by Cyclo(His-Pro) plus zinc treatment.BBA clinical · 2017Review
- Caspase-3 and GFAP as early markers for apoptosis and astrogliosis in shRNA-induced hippocampal cytotoxicity.The Journal of experimental biology · 2017Article
- High-Throughput Single-Cell Derived Sphere Formation for Cancer Stem-Like Cell Identification and Analysis.Scientific reports · 2016Article
- The acquisition of novel N-glycosylation sites in conserved proteins during human evolution.BMC bioinformatics · 2015Article
- Is γ-secretase a beneficial inactivating enzyme of the toxic APP C-terminal fragment C99?The Journal of biological chemistryReview
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The deposition of amyloid-beta (Aβ) aggregates in the brain is a major pathological hallmark of Alzheimer's disease (AD). Aβ is generated from the cleavage of C-terminal fragments of the amyloid precursor protein (APP-CTFs) by γ-secretase, an intramembrane-cleaving protease with multiple substrates, including the Notch receptors. Endogenous modulation of γ-secretase is pointed to be implicated in the sporadic, age-dependent form of AD. Moreover, specifically modulating Aβ production has become a priority for the safe treatment of AD because the inhibition of γ-secretase results in adverse effects that are related to impaired Notch cleavage. Here, we report the identification of the adipocyte differentiation protein APMAP as a novel endogenous suppressor of Aβ generation. We found that APMAP interacts physically with γ-secretase and its substrate APP. In cells, the partial depletion of APMAP drastically increased the levels of APP-CTFs, as well as uniquely affecting their stability, with the consequence being increased secretion of Aβ. In wild-type and APP/ presenilin 1 transgenic mice, partial adeno-associated virus-mediated APMAP knockdown in the hippocampus increased Aβ production by ∼20 and ∼55%, respectively. Together, our data demonstrate that APMAP is a negative regulator of Aβ production through its interaction with APP and γ-secretase. All observed APMAP phenotypes can be explained by an impaired degradation of APP-CTFs, likely caused by an altered substrate transport capacity to the lysosomal/autophagic system.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.