ArticleScientific data2018
High content screen for identifying small-molecule LC3B-localization modulators in a renal cancer cell line.
Article in Scientific data, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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
3 citing papers in PubMed, 7 citations in OpenAlex.
- Autophagy profiling in single cells with open source CellProfiler-based image analysis.Autophagy · 2023Article
- Chemical Biology Strategies to Study Autophagy.Frontiers in cell and developmental biology · 2018Review
- Inhibiting Autophagy in Renal Cell Cancer and the Associated Tumor Endothelium.Cancer journal (Sudbury, Mass.)Review
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 at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Forms of selective autophagy have now been recognized to regulate flux in many intracellular processes. Specific pathways and functions have been identified for mitophagy, ERphagy, and other selective autophagies; yet there is no consensus in whether and how autophagy regulates protein maintenance in and around the nucleus. Such processes are of interest for potential degradation of DNA and nuclear envelope proteins in various disease states. The mechanistic details of such nucleus-related autophagic processes remain elusive due to the lack of chemical or genetic regulators to manipulate and follow the process in vitro. Here, we describe a high content screen from which we identified small chemical compounds that can modulate the localization of the autophagy marker MAP1LC3B (LC3) in renal carcinoma cells. We also describe a pipeline designed for the execution and analysis of high content screens. The chemical tools discerned from this screen will allow for the deeper exploration of the mechanism, regulation, and molecular targets of nuclear-localized LC3 in perturbed cellular states.
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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.