ArticleScientific reports2022
HS3ST2 expression induces the cell autonomous aggregation of tau.
Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.
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
9 citing papers in PubMed, 1 synthesis or guideline pooled it, 11 citations in OpenAlex.
- Regulation of autophagy, lipid metabolism, and neurodegenerative pathology by heparan sulfate proteoglycans.Frontiers in genetics · 2022Pooled it
- Synthetic biology for heparin biomanufacturing.Bioresources and bioprocessing · 2026Review
- Integrative multi-omics and machine learning analysis identifies candidate biomarkers associated with mitochondrial quality control in major depressive disorder.Frontiers in psychiatry · 2026Article
- Uric Acid, the End-Product of Purine Metabolism, Mitigates Tau-Related Abnormalities: Comparison with DOT, a Non-Antibiotic Oxytetracycline Derivative.Biomolecules · 2025Article
- A novel TGFβ1-Hs3st2-tau axis regulates tau pathology and synaptic integrity.Frontiers in neuroscience · 2025Article
- Beyond amyloid and tau: rethinking Alzheimer's disease through less explored avenues.Open biology · 2024Review
- Identification of high-performing antibodies for the reliable detection of Tau proteoforms by Western blotting and immunohistochemistry.Acta neuropathologica · 2024Article
- Increased 3-Science advances · 2023Article
- Heparan Sulfate Proteoglycans in Tauopathy.Biomolecules · 2022Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Heparan sulfates have long been known to intracellularly accumulate in Alzheimer's disease neurons, where they colocalize with neurofibrillary tangles made of abnormally phosphorylated and aggregated tau protein. However, the reasons and consequences of the heparan sulfates accumulation in the Alzheimer's cells are not yet well understood. Previously, we showed that the neural heparan sulfate 3-O-sulfotransferase HS3ST2 is critical for the abnormal phosphorylation of tau in Alzheimer's disease-related tauopathy. Using cell models of tauopathy we showed that intracellular 3-O-sulfatated heparan sulfates interact with tau inducing its abnormal phosphorylation. However, it is unknown whether HS3ST2 expression induces the intracellular aggregation of tau in cells. Here, by using replicative pEBV plasmids, we engineered HEK293 cells to stably express HS3ST2 together with human tau carrying or not the P301S mutation. We show that HS3ST2 gain of function induces the cell autonomous aggregation of tau not only in cells expressing tau
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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.