ArticleJournal of molecular neuroscience : MN2016
Down-Regulated Expression of Liver X Receptor beta in Cortical Lesions of Patients with Focal Cortical Dysplasia.
Article in Journal of molecular neuroscience : MN, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper, 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.
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, 1 synthesis or guideline pooled it, 2 citations in OpenAlex.
- Molecular Signature in Focal Cortical Dysplasia: A Systematic Review of RNA and Protein Data.International journal of molecular sciences · 2025Pooled it
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Focal cortical dysplasia (FCD) is strongly associated with medically intractable epilepsy. Studies suggest that liver X receptor beta (LXRβ) may participate in the pathogenesis of FCD. The present study investigated the expression pattern of LXRβ in FCD and the distribution of LXRβ in different neural precursor cells. Twenty-five surgical specimens from FCD patients and 11 age-matched control samples from autopsies were included in our study. Protein levels and distribution were detected by western blot, immunohistochemistry, and immunofluorescence staining. We found that (1) the level of LXRβ protein was markedly reduced in FCD. (2) LXRβ staining was weaker in the dysplastic cortices of FCD and was mainly observed in neuronal microcolumns, and malformed cells. (3) LXRβ was co-localized with radial glial cells (RGCs) markers and oligodendrocyte precursor cells (OPCs) markers in malformed cells. (4) RGCs marker and OPCs marker were down-regulated while LXRβ downstream factors were up-regulated in FCD specimens. Taken together, our results indicate that LXRβ may interact with β-catenin to regulate the generation of OPCs and the transformation of RGCs. LXRβ therefore potentially contributes to the pathogenesis of FCD.
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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.