ArticleBMC biology2016
Autophagy-independent function of Atg1 for apoptosis-induced compensatory proliferation.
Article in BMC biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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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.
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.
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Who cites it
10 citing papers in PubMed, 24 citations in OpenAlex.
- Targeting secretory autophagy in solid cancers: mechanisms, immune regulation and clinical insights.Experimental hematology & oncology · 2025Review
- The nonautophagic functions of autophagy-related proteins.Autophagy · 2024Review
- Ghost messages: cell death signals spread.Cell communication and signaling : CCS · 2023Review
- Actin remodeling mediates ROS production and JNK activation to drive apoptosis-induced proliferation.PLoS genetics · 2022Article
- Resveratrol inhibits LPS-induced apoptosis in VSC4.1 motoneurons through enhancing SIRT1-mediated autophagy.Iranian journal of basic medical sciences · 2021Article
- Inhibiting ULK1 kinase decreases autophagy and cell viability in high-grade serous ovarian cancer spheroids.American journal of cancer research · 2020Article
- Review
- Autophagy suppresses Ras-driven epithelial tumourigenesis by limiting the accumulation of reactive oxygen species.Oncogene · 2017Article
- Killers creating new life: caspases drive apoptosis-induced proliferation in tissue repair and disease.Cell death and differentiation · 2017Review
- Nrf2 promotes progression of non-small cell lung cancer through activating autophagy.Cell cycle (Georgetown, Tex.) · 2017Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundATG1 belongs to the Uncoordinated-51-like kinase protein family. Members of this family are best characterized for roles in macroautophagy and neuronal development. Apoptosis-induced proliferation (AiP) is a caspase-directed and JNK-dependent process which is involved in tissue repair and regeneration after massive stress-induced apoptotic cell loss. Under certain conditions, AiP can cause tissue overgrowth with implications for cancer.
resultsHere, we show that Atg1 in Drosophila (dAtg1) has a previously unrecognized function for both regenerative and overgrowth-promoting AiP in eye and wing imaginal discs. dAtg1 acts genetically downstream of and is transcriptionally induced by JNK activity, and it is required for JNK-dependent production of mitogens such as Wingless for AiP. Interestingly, this function of dAtg1 in AiP is independent of its roles in autophagy and in neuronal development.
conclusionIn addition to a role of dAtg1 in autophagy and neuronal development, we report a third function of dAtg1 for AiP.
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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.