ArticleScience signaling2015
Identification of potential drug targets for tuberous sclerosis complex by synthetic screens combining CRISPR-based knockouts with RNAi.
Article in Science signaling, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 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
89 citing papers in PubMed, 145 citations in OpenAlex.
- Multi-omic mapping of Drosophila protein secretomes reveals tissue-specific origins and inter-organ trafficking.Nature communications · 2026Article
- Compensatory action of different types of cis-regulatory elements buffers the striped expression of Drosophila pair-rule genes.Development (Cambridge, England) · 2025Article
- Generation of Monoclonal Cultures from Wolbachia-infected Drosophila melanogaster JW18 Cell Line.Journal of visualized experiments : JoVE · 2025Article
- Inhibition of autophagy as a novel treatment for neurofibromatosis type 1 tumors.Molecular oncology · 2025Article
- Gene model for the ortholog ofmicroPublication biology · 2025Article
- Synthetic guide sequence to generate CRISPR-Cas9 entry strains inmicroPublication biology · 2025Article
- Structure-optimized sgRNA selection with PlatinumCRISPr for efficient Cas9 generation of knockouts.Genome research · 2024Article
- Proximity labeling reveals interactions necessary to maintain the distinct apical domains of Drosophila photoreceptors.Journal of cell science · 2024Article
- Set2 and H3K36 regulate the Drosophila male X chromosome in a context-specific manner, independent from MSL complex spreading.Genetics · 2024Article
- Set2 and H3K36 regulate thebioRxiv : the preprint server for biology · 2024Article
- The ftz upstream element drives late ftz stripes but is not required for regulation of Ftz target genes.Developmental biology · 2024Article
- CRISPR/Cas9 ribonucleoprotein mediated DNA-free genome editing in larch.Forestry research · 2024Article
- Generating CRISPR-edited clonal lines of culturedBiology methods & protocols · 2024Article
- Molecular and functional characterization of the Drosophila melanogaster conserved smORFome.Cell reports · 2023Article
- Quantum biological insights into CRISPR-Cas9 sgRNA efficiency from explainable-AI driven feature engineering.Nucleic acids research · 2023Article
- Article
- Transcriptome profile in Drosophila Kc and S2 embryonic cell lines.G3 (Bethesda, Md.) · 2023Article
- CRISPR/Cas9 Technology for Potato Functional Genomics and Breeding.Methods in molecular biology (Clifton, N.J.) · 2023Article
- CRISPR mediated transactivation in the human disease vector Aedes aegypti.PLoS pathogens · 2023Article
- Article
29 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 2 institutions in 1 country.
Funding
Abstract
The tuberous sclerosis complex (TSC) family of tumor suppressors, TSC1 and TSC2, function together in an evolutionarily conserved protein complex that is a point of convergence for major cell signaling pathways that regulate mTOR complex 1 (mTORC1). Mutation or aberrant inhibition of the TSC complex is common in various human tumor syndromes and cancers. The discovery of novel therapeutic strategies to selectively target cells with functional loss of this complex is therefore of clinical relevance to patients with nonmalignant TSC and those with sporadic cancers. We developed a CRISPR-based method to generate homogeneous mutant Drosophila cell lines. By combining TSC1 or TSC2 mutant cell lines with RNAi screens against all kinases and phosphatases, we identified synthetic interactions with TSC1 and TSC2. Individual knockdown of three candidate genes (mRNA-cap, Pitslre, and CycT; orthologs of RNGTT, CDK11, and CCNT1 in humans) reduced the population growth rate of Drosophila cells lacking either TSC1 or TSC2 but not that of wild-type cells. Moreover, individual knockdown of these three genes had similar growth-inhibiting effects in mammalian TSC2-deficient cell lines, including human tumor-derived cells, illustrating the power of this cross-species screening strategy to identify potential drug targets.
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.