ArticleNature communications2015
TRPC6 specifically interacts with APP to inhibit its cleavage by γ-secretase and reduce Aβ production.
Article in Nature communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 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.
The trial behind it
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Who cites it
39 citing papers in PubMed, 78 citations in OpenAlex.
- Pyrazole-derived TRPC3 antagonist ameliorates synaptic dysfunctions and memory deficits in Alzheimer's disease models.Molecular psychiatry · 2026Article
- Congenital Hypothyroidism Dysregulates TRPC6 to Mediate Abnormal Dendritic Spine Growth of Hippocampal Neurons.CNS neuroscience & therapeutics · 2025Article
- dCasMINI-mediated therapy rescues photoreceptors degeneration in a mouse model of retinitis pigmentosa.Science advances · 2024Article
- Priestia aryabhattai Improves Soil Environment and Promotes Alfalfa Growth by Enhancing Rhizosphere Microbial Carbon Sequestration Capacity Under Greenhouse Conditions.Current microbiology · 2024Article
- Transient Receptor Potential Channels in the Healthy and Diseased Blood-Brain Barrier.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2024Review
- Transient Receptor Potential Canonical 6 (TRPC6) Channel in the Pathogenesis of Diseases: A Jack of Many Trades.Inflammation · 2023Review
- Role of Calcium Modulation in the Pathophysiology and Treatment of Alzheimer's Disease.International journal of molecular sciences · 2023Review
- The mechanosensitive ion channel Piezo1 modulates the migration and immune response of microglia.iScience · 2023Article
- Mutations in trpγ, the homologue of TRPC6 autism candidate gene, causes autism-like behavioral deficits in Drosophila.Molecular psychiatry · 2022Article
- Chemical genetic activation of the cholinergic basal forebrain hippocampal circuit rescues memory loss in Alzheimer's disease.Alzheimer's research & therapy · 2022Article
- Recurrent moderate hypoglycemia accelerates the progression of Alzheimer's disease through impairment of the TRPC6/GLUT3 pathway.JCI insight · 2022Article
- Regulatory mechanisms of tetramethylpyrazine on central nervous system diseases: A review.Frontiers in pharmacology · 2022Review
- The China Alzheimer Report 2022.General psychiatry · 2022Review
- Ion channels alterations in the forebrain of high-fat diet fed rats.European journal of histochemistry : EJH · 2021Article
- Bilobalide inhibits inflammation and promotes the expression of Aβ degrading enzymes in astrocytes to rescue neuronal deficiency in AD models.Translational psychiatry · 2021Article
- Canonical transient receptor potential channels and their modulators: biology, pharmacology and therapeutic potentials.Archives of pharmacal research · 2021Review
- Functional Importance of Transient Receptor Potential (TRP) Channels in Neurological Disorders.Frontiers in cell and developmental biology · 2021Review
- miR-193a Directly Targets PSEN1 and Inhibits Gastric Cancer Cell Growth, the Activation of PI3K/Akt Signaling Pathway, and the Epithelial-to-Mesenchymal Transition.Journal of oncology · 2021Article
- The Role of TRP Channels and PMCA in Brain Disorders: Intracellular Calcium and pH Homeostasis.Frontiers in cell and developmental biology · 2021Review
- Alterations of the Endoplasmic Reticulum (ER) Calcium Signaling Molecular Components in Alzheimer's Disease.Cells · 2020Review
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Generation of β-amyloid (Aβ) peptide in Alzheimer's disease involves cleavage of amyloid precursor protein (APP) by γ-secretase, a protease known to cleave several substrates, including Notch. Finding specific modulators for γ-secretase could be a potential avenue to treat the disease. Here, we report that transient receptor potential canonical (TRPC) 6 specifically interacts with APP leading to inhibition of its cleavage by γ-secretase and reduction in Aβ production. TRPC6 interacts with APP (C99), but not with Notch, and prevents C99 interaction with presenilin 1 (PS1). A fusion peptide derived from TRPC6 also reduces Aβ levels without effect on Notch cleavage. Crossing APP/PS1 mice with TRPC6 transgenic mice leads to a marked reduction in both plaque load and Aβ levels, and improvement in structural and behavioural impairment. Thus, TRPC6 specifically modulates γ-secretase cleavage of APP and preventing APP (C99) interaction with PS1 via TRPC6 could be a novel strategy to reduce Aβ formation.
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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.