ArticleFEBS letters2016
The PtdIns3-phosphatase MTMR3 interacts with mTORC1 and suppresses its activity.
Article in FEBS letters, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed, 31 citations in OpenAlex.
- Pangenome Reveals Gene Content Variations and Structural Variants Contributing to Pig Characteristics.Genomics, proteomics & bioinformatics · 2025Article
- Recent advances of myotubularin-related (MTMR) protein family in cardiovascular diseases.Frontiers in cardiovascular medicine · 2024Review
- Expression profile of LncRNA ANRIL, miR-186, miR-181a, and MTMR-3 in patients with preeclampsia.Non-coding RNA research · 2023Article
- MicroRNAs as the critical regulators of autophagy-mediated cisplatin response in tumor cells.Cancer cell international · 2023Review
- Transcription factor EB regulates phosphatidylinositol-3-phosphate levels that control lysosome positioning in the bladder cancer model.Communications biology · 2023Article
- BRCA1 mutations in high-grade serous ovarian cancer are associated with proteomic changes in DNA repair, splicing, transcription regulation and signaling.Scientific reports · 2022Article
- SPI1-induced downregulation of FTO promotes GBM progression by regulating pri-miR-10a processing in an m6A-dependent manner.Molecular therapy. Nucleic acids · 2022Article
- Construction of circRNA-related ceRNA networks in longissimus dorsi muscle of Queshan Black and Large White pigs.Molecular genetics and genomics : MGG · 2022Article
- Whole Exome Sequencing in a Population With Severe Congenital Anomalies of Kidney and Urinary Tract.Frontiers in pediatrics · 2022Article
- Condition-dependent functional shift of twoAutophagy · 2021Article
- Tribbles homolog 3-mediated targeting the AKT/mTOR axis in mice with retinal degeneration.Cell death & disease · 2021Article
- Article
- Article
- Lipids in the cell: organisation regulates function.Cellular and molecular life sciences : CMLS · 2018Review
- Macropinocytosis, mTORC1 and cellular growth control.Cellular and molecular life sciences : CMLS · 2018Review
- Gtr/Ego-independent TORC1 activation is achieved through a glutamine-sensitive interaction with Pib2 on the vacuolar membrane.PLoS genetics · 2018Article
- Phosphoinositide conversion in endocytosis and the endolysosomal system.The Journal of biological chemistry · 2018Review
- Regulation of Autophagy through TORC1 and mTORC1.Biomolecules · 2017Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Macroautophagy is a major intracellular degradation system. We previously reported that overexpression of phosphatase-deficient MTMR3, a member of the myotubularin phosphatidylinositol (PI) 3-phosphatase family, leads to induction of autophagy. In this study, we found that MTMR3 interacted with mTORC1, an evolutionarily conserved serine/threonine kinase complex, which regulates cell growth and autophagy in response to environmental stimuli. Furthermore, overexpression of MTMR3 inhibited mTORC1 activity. The N-terminal half of MTMR3, including the PH-G and phosphatase domains, was necessary and sufficient for these effects. Phosphatase-deficient MTMR3 provided more robust suppression of mTORC1 activity than wild-type MTMR3. Furthermore, phosphatase-deficient full length MTMR3 and the phosphatase domain alone were localized to the Golgi. These results suggest a new regulatory mechanism of mTORC1 in association with PI3P.
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.