ArticleMolecular & cellular proteomics : MCP2010
Quantitative nuclear proteomics identifies mTOR regulation of DNA damage response.
Article in Molecular & cellular proteomics : MCP, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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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.
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Who cites it
22 citing papers in PubMed, 44 citations in OpenAlex.
- Rapamycin reduces DNA damage of in vitro matured oocytes by promoting Rad51-mediated homologous recombination.Reproductive biology and endocrinology : RB&E · 2025Article
- Therapy-induced secretion of spliceosomal components mediates pro-survival crosstalk between ovarian cancer cells.Nature communications · 2024Article
- DNA Damage Response in Cancer Therapy and Resistance: Challenges and Opportunities.International journal of molecular sciences · 2022Review
- Article
- Autophagy-related Proteins in Genome Stability: Autophagy-Dependent and Independent Actions.International journal of biological sciences · 2022Review
- SFPQ Promotes Lung Cancer MalignancyFrontiers in oncology · 2022Article
- Inhibition of Nuclear Pore Complex Formation Selectively Induces Cancer Cell Death.Cancer discovery · 2021Article
- A translational program that suppresses metabolism to shield the genome.Nature communications · 2020Article
- mTORC Inhibitors as Broad-Spectrum Therapeutics for Age-Related Diseases.International journal of molecular sciences · 2018Review
- The mTOR-S6K pathway links growth signalling to DNA damage response by targeting RNF168.Nature cell biology · 2018Article
- R2TP/Prefoldin-like component RUVBL1/RUVBL2 directly interacts with ZNHIT2 to regulate assembly of U5 small nuclear ribonucleoprotein.Nature communications · 2017Article
- mTOR Inhibitors Suppress Homologous Recombination Repair and Synergize with PARP Inhibitors via Regulating SUV39H1 in BRCA-Proficient Triple-Negative Breast Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2016Article
- [Rapamycin decreases irradiation-induced hematopoietic system damage].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2015Article
- Chronic inflammation-related DNA damage response: a driving force of gastric cardia carcinogenesis.Oncotarget · 2015Article
- C-STrap Sample Preparation Method--In-Situ Cysteinyl Peptide Capture for Bottom-Up Proteomics Analysis in the STrap Format.PloS one · 2015Article
- Article
- Regulation of FANCD2 by the mTOR pathway contributes to the resistance of cancer cells to DNA double-strand breaks.Cancer research · 2013Article
- Protein phosphatase 2A and DNA-dependent protein kinase are involved in mediating rapamycin-induced Akt phosphorylation.The Journal of biological chemistry · 2013Article
- The autophagy-senescence connection in chemotherapy: must tumor cells (self) eat before they sleep?The Journal of pharmacology and experimental therapeutics · 2012Article
- ATM kinase is activated by sindbis viral vector infection.Virus research · 2012Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Cellular nutritional and energy status regulates a wide range of nuclear processes important for cell growth, survival, and metabolic homeostasis. Mammalian target of rapamycin (mTOR) plays a key role in the cellular responses to nutrients. However, the nuclear processes governed by mTOR have not been clearly defined. Using isobaric peptide tagging coupled with linear ion trap mass spectrometry, we performed quantitative proteomics analysis to identify nuclear processes in human cells under control of mTOR. Within 3 h of inhibiting mTOR with rapamycin in HeLa cells, we observed down-regulation of nuclear abundance of many proteins involved in translation and RNA modification. Unexpectedly, mTOR inhibition also down-regulated several proteins functioning in chromosomal integrity and up-regulated those involved in DNA damage responses (DDRs) such as 53BP1. Consistent with these proteomic changes and DDR activation, mTOR inhibition enhanced interaction between 53BP1 and p53 and increased phosphorylation of ataxia telangiectasia mutated (ATM) kinase substrates. ATM substrate phosphorylation was also induced by inhibiting protein synthesis and suppressed by inhibiting proteasomal activity, suggesting that mTOR inhibition reduces steady-state (abundance) levels of proteins that function in cellular pathways of DDR activation. Finally, rapamycin-induced changes led to increased survival after radiation exposure in HeLa cells. These findings reveal a novel functional link between mTOR and DDR pathways in the nucleus potentially operating as a survival mechanism against unfavorable growth conditions.
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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.