ArticleNeuropathology : official journal of the Japanese Society of Neuropathology2012
Non-invasive detection of spatio-temporal activation of SBE and NFAT5 promoters in transgenic reporter mice following stroke.
Article in Neuropathology : official journal of the Japanese Society of Neuropathology, 2012. 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, 2 citations in OpenAlex.
- NFAT5: a stress-related transcription factor with multiple functions in health and disease.Cell stress · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The characterization of molecular responses following cerebral ischemia-induced changes in animal models capable of undergoing real-time analysis is an important goal for stroke research. In this study, we use transgenic mice to examine the activation of two different promoters in a firefly luciferase reporter mouse analyzable through a non-invasive bioluminescent imaging system. In the first model, we examine the middle cerebral artery occlusion (MCAO)-induced activation of Smad-binding elements (SBE), a downstream target of Smad 1/2/3 transcription factors, in which SBEs regulate the expression of the fluc reporter. We observed that MCAO induces a bilateral activation (i.e., both ipsilateral and contralateral brain hemispheres) of the SBE-luc reporter with a peak at 24 h. In the second model, we examined MCAO-induced activation of the osmolarity-sensitive promoter nuclear factor of activated T-cell 5 (NFAT5) and identified a peak reporter expression 72 h post-MCAO in the ipsilateral but not contralateral hemisphere. In each of these models, the assessment of post-MCAO fluc-expression provided both a quantitative measure (i.e., radiance in photons/sec/cm(2) /steradian) as well as qualitative localization of the molecular response following focal ischemic injury.
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.