The DOI matches its Crossref record; 26 of the 26 references it cites were found in a registry or an index.
Spatial Coupling of mTOR and Autophagy Augments Secretory Phenotypes
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A cellular compartment allows simultaneous protein synthesis and degradation.
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In the citing paper
“Interestingly, OIS is associated with accumulation of autolysosome compartments, where a Rag GTPase-dependent sequestration of mTOR correlates with enhanced autophagosome formation as well as cytokine production (Narita et al. 2011).”
From Cellular senescence and its effector programs (2014) · cites this paper as Narita et al. 2011
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Accordingly, the ULK activity state may thus reflect its role in these processes [780-786].”
From Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition) 1 (2021) · cites this paper as [782]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“We recently showed that the subcellular localization of autophagy and mTOR might play a key role for the simultaneous activation of anabolic and catabolic processes during senescence (Narita et al. 2011).”
From Cellular senescence and its effector programs (2014) · cites this paper as Narita et al. 2011
In the citing paper
“macro-autophagy (hereafter referred to as autophagy)—a tightly regulated major lysosomal degradation pathway (27–30)—has been implicated in establishing the SASP through the target of rapamycin (TOR) autophagy spatial coupling compartment (TASCC).”
From The DNA damage response induces inflammation and senescence by inhibiting autophagy of GATA4. (2015) · cites this paper as [32]
In the citing paper
“Our results indicate that autophagy is both a negative and a positive regulator of senescence, resolving apparently contradictory reports in the literature (31–33, 44).”
From The DNA damage response induces inflammation and senescence by inhibiting autophagy of GATA4. (2015) · cites this paper as [32]
In the citing paper
“Autophagy is dynamically activated during OIS and facilitates the synthesis of interleukin 6 (IL-6) and IL-8, major components of the SASP 58,59 .”
From Inside and out: the activities of senescence in cancer (2014) · cites this paper as [58]
In the citing paper
“The mTOR–autophagy spatial coupling compartment (TASCC), which is close to the nucleus, is highly enriched in mTOR and keeps mTOR away from the autophagy machinery, located away from the TASCC, to avoid its inactivation.”
From Mechanisms and Regulation of Cellular Senescence (2021) · cites this paper as [246]
In the citing paper
“This paradoxical outcome is possible through the spatiotemporal sub-compartmentalization of mTOR and autophagy that allows their simultaneous activation [246].”
From Mechanisms and Regulation of Cellular Senescence (2021) · cites this paper as [246]
In the citing paper
“These amino acids are then used by mTOR to support the increased biosynthetic demand during the acquisition of the OIS phenotype [246].”
From Mechanisms and Regulation of Cellular Senescence (2021) · cites this paper as [246]
In the citing paper
“Conversely, selective autophagy, for instance of GATA4 that accumulates during senescence induction [160], can prevent senescence [160,246].”
From Mechanisms and Regulation of Cellular Senescence (2021) · cites this paper as [246]
In the citing paper
“In the TASCC, mTOR is closely associated with lysosomes/autolysosomes that generate a high flux of recycled amino acids and other metabolites.”
From Mechanisms and Regulation of Cellular Senescence (2021) · cites this paper as [246]
In the citing paper
“TASCCs provide cells with a mechanism for simultaneous activation of anabolic and catabolic processes, which facilitates mTOR-controlled synthesis of secretory proteins with sources of energy or building blocks provided by constitutive autophagy”
From Autophagy in kidney homeostasis and disease (2020) · cites this paper as [53]
In the citing paper
“podocytes form TOR–autophagy spatial coupling compartments (TASCCs), which are distinct cytoplasmic compartments enriched for mTORC1 that include autolysosomes but largely exclude autophagosomes”
From Autophagy in kidney homeostasis and disease (2020) · cites this paper as [53]
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Metadata
- Authors
- Narita, M., Young, A. R. J., Arakawa, S., Samarajiwa, S. A., Nakashima, T., Yoshida, S., Hong, S., Berry, L. S., Reichelt, S., Ferreira, M., Tavaré, S., Inoki, K., Shimizu, S., & Narita, M.
- Affiliations
- Cancer Research UK (GB)
- Tokyo Medical and Dental University (JP)
- University of Cambridge (GB)
- University of Michigan (US)
- Corresponding author
- Narita, Masako
- Young, Andrew R. J.
- Narita, Masashi
- ORCID
- Venue
- Science
- Published
- 2011-05-20
- Volume
- 332
- Issue
- 6032
- Pages
- 966-970
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- PMC
- PMC3426290
- OpenAlex
- W1965493795
- Cited by
- 594
- References
- 26
- Citations by year
- 2026: 30 · 2025: 26 · 2024: 41 · 2023: 40 · 2022: 52 · 2021: 50 · 2020: 39 · 2019: 38 · 2018: 36 · 2017: 28 · 2016: 37 · 2015: 31 · 2014: 36 · 2013: 44 · 2012: 45
- FWCI
- 35.04
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Science (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (DK083491)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Autophagy in Disease and Therapy
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Cellular transport and secretion
- Keywords
- mTOR, autophagy, spatial coupling, Golgi apparatus, lysosomes, Ras-induced senescence, Rag GTPases, amino acid signaling, protein secretion, interleukin-6, interleukin-8, macrophage differentiation, glomerular podocytes, protein turnover
- MeSH terms
- Amino Acids, Animals, Autophagy, Cell Line, Cytoplasm, Golgi Apparatus, Humans, Lysosomes, Phagosomes, Phenotype, Proteins, Genes, ras, Protein Biosynthesis, Vacuoles, Nocodazole, Interleukin-6, Interleukin-8, Cellular Senescence, Endoplasmic Reticulum, Rough, HL-60 Cells, Monomeric GTP-Binding Proteins, trans-Golgi Network, Cytoplasmic Vesicles, Podocytes, Mice, TOR Serine-Threonine Kinases
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