ArticleCell systems2021
Dysregulation of the secretory pathway connects Alzheimer's disease genetics to aggregate formation.
Article in Cell systems, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
13 citing papers in PubMed, 18 citations in OpenAlex.
- Article
- Time-resolved interactome profiling deconvolutes secretory protein quality control dynamics.Molecular systems biology · 2024Article
- Amyloid Precursor Protein: A Regulatory Hub in Alzheimer's Disease.Aging and disease · 2024Review
- Inferring secretory and metabolic pathway activity from omic data with secCellFie.Metabolic engineering · 2024Article
- A Rab6 to Rab11 transition is required for dense-core granule and exosome biogenesis in Drosophila secondary cells.PLoS genetics · 2023Article
- From observational to actionable: rethinking omics in biologics production.Trends in biotechnology · 2023Review
- Large scale microfluidic CRISPR screening for increased amylase secretion in yeast.Lab on a chip · 2023Article
- Dual function of Rab1A in secretion and autophagy: hypervariable domain dependence.Life science alliance · 2023Article
- Graph-based autoencoder integrates spatial transcriptomics with chromatin images and identifies joint biomarkers for Alzheimer's disease.Nature communications · 2022Article
- Harnessing secretory pathway differences between HEK293 and CHO to rescue production of difficult to express proteins.Metabolic engineering · 2022Article
- Neuronal Rubicon Represses Extracellular APP/Amyloid β Deposition in Alzheimer's Disease.Cells · 2022Article
- Article
- Resource allocation in mammalian systems.Biotechnology advancesReview
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Amyloid disorders such as Alzheimer's disease (AD) involve the aggregation of secreted proteins. However, it is largely unclear how secretory-pathway proteins contribute to amyloid formation. We developed a systems biology framework integrating expression data with protein-protein interaction networks to estimate a tissue's fitness for producing specific secreted proteins and analyzed the fitness of the secretory pathway of various brain regions and cell types for synthesizing the AD-associated amyloid precursor protein (APP). While key amyloidogenic pathway components were not differentially expressed in AD brains, we found Aβ deposition correlates with systemic down- and upregulation of the secretory-pathway components proximal to APP and amyloidogenic secretases, respectively, in AD. Our analyses suggest that perturbations from three AD risk loci cascade through the APP secretory-support network and into the endocytosis pathway, connecting amyloidogenesis to dysregulation of secretory-pathway components supporting APP and suggesting novel therapeutic targets for AD. A record of this paper's transparent peer review process is included in the supplemental information.
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Registered trials
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.