ReviewCells2023
Using
Review in Cells, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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
11 citing papers in PubMed, 18 citations in OpenAlex.
- Effect of a Combined Antidepressant Drug Flupentixol-Melitracen on Glucose Level and Expression of Insulin-Like Peptide Genes DILP5 and DILP6 in Drosophila melanogaster.BioMed research international · 2026Article
- Myc and Tor drive growth and cell competition in the regeneration blastema of Drosophila wing imaginal discs.Development (Cambridge, England) · 2025Article
- Decanoic acid extends lifespan and modulates metabolism in models of PLA2G6-associated neurodegeneration.Disease models & mechanisms · 2025Article
- Review
- Loss of Drosophila ribosomal protein S6 kinase II causes mitochondrial dysfunction and cell death.Disease models & mechanisms · 2025Article
- Oncogenic signaling in the Drosophila prostate-like accessory gland activates a pro-tumorigenic program in the absence of proliferation.Disease models & mechanisms · 2025Article
- Review
- Insulin signaling regulates R2 retrotransposon expression to orchestrate transgenerational rDNA copy number maintenance.Nature communications · 2025Article
- Branched-chain amino acids and insulin resistance in type 2 diabetes: from metabolic dysregulation to therapeutic targets.Frontiers in endocrinology · 2025Review
- Undernutrition-induced stunting-like phenotype inNarra J · 2024Article
- Understanding Developmental Cell Death UsingCells · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The evolutionarily conserved target of rapamycin (TOR) serine/threonine kinase controls eukaryotic cell growth, metabolism and survival by integrating signals from the nutritional status and growth factors. TOR is the catalytic subunit of two distinct functional multiprotein complexes termed mTORC1 (mechanistic target of rapamycin complex 1) and mTORC2, which phosphorylate a different set of substrates and display different physiological functions. Dysregulation of TOR signaling has been involved in the development and progression of several disease states including cancer and diabetes. Here, we highlight how genetic and biochemical studies in the model system
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.