ArticleFrontiers in molecular neuroscience2025
Tamoxifen attenuates manganese-induced dysregulation of neuronal REST via the genomic ER-
Article in Frontiers in molecular neuroscience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Harnessing the neuroprotective potential of estrogen in Parkinson's disease: an insight into molecular mechanisms and therapeutic approaches.Metabolic brain disease · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
Chronic exposure to elevated levels of manganese (Mn) causes a neurological disorder referred to as manganism, resembling pathological symptoms of Parkinson's disease (PD). The repressor element-1 silencing transcription factor (REST) induces neuroprotection in several neurological disorders, including PD and Mn toxicity. Tamoxifen (TX), a selective estrogen receptor modulator, has been shown to afford neuroprotective effects in various experimental models and increase REST expression via the non-genomic estrogen receptor (ER)/Wnt signaling in Cath. a-differentiated (CAD) neuronal cultures. The present study investigated whether TX enhances REST transcription through the genomic estrogen receptor (ER) pathway in CAD cells, using a combination of Western blotting, quantitative reverse transcription polymerase chain reaction (qRT-PCR), promoter activity assays, chromatin immunoprecipitation, electrophoretic mobility shift assays, and site-directed mutagenesis. The findings showed that the REST promoter sequences contained half-site estrogen response elements (ERE) motifs. The ER-
Indexed as
Identifiers
What OpenQuestion holds
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.