ArticleFrontiers in aging neuroscience2018
TRPC1 Deletion Causes Striatal Neuronal Cell Apoptosis and Proteomic Alterations in Mice.
Article in Frontiers in aging neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Role of TRPC1 in the pathogenesis of depression induced by traumatic brain injury.Frontiers in neuroscience · 2026Article
- Loss of endothelial TRPC1 aggravates metabolic dysfunction in obesity via disrupting adipose tissue homeostasis.Frontiers in molecular biosciences · 2025Article
- Transient Receptor Potential (TRP) Channels in Pain, Neuropsychiatric Disorders, and Epilepsy.International journal of molecular sciences · 2023Review
- TRPC1 promotes the genesis and progression of colorectal cancer via activating CaM-mediated PI3K/AKT signaling axis.Oncogenesis · 2021Article
- Review
- Transient Receptor Potential Channels as an Emerging Target for the Treatment of Parkinson's Disease: An Insight Into Role of Pharmacological Interventions.Frontiers in cell and developmental biology · 2020Review
Corrections and comments
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Authors and funding
11 authors.
Funding
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Abstract
Transient receptor potential channel 1 (TRPC1) is widely expressed throughout the nervous system, while its biological role remains unclear. In this study, we showed that TRPC1 deletion caused striatal neuronal loss and significantly increased TUNEL-positive and 8-hydroxy-2'-deoxyguanosine (8-OHdG) staining in the striatum. Proteomic analysis by two-dimensional fluorescence difference gel electrophoresis (2D-DIGE) coupled with mass spectrometry (MS) revealed a total of 51 differentially expressed proteins (26 increased and 25 decreased) in the stratum of TRPC1 knockout (TRPC1
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