Article in The Journal of cell biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it
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.
2 · The registry
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.
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
5 · Who and what money
Authors and funding
21 authors.
Weijing Yao *Department of Biochemistry and Department of Hepatobiliary and Pancreatic Surgery of the First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.ORCID 0000-0003-0354-6511
Yingcong Chen *Department of Biochemistry and Department of Hepatobiliary and Pancreatic Surgery of the First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.ORCID 0000-0001-6505-3478
Yi Zhang *Department of Biochemistry and Department of Hepatobiliary and Pancreatic Surgery of the First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.ORCID 0000-0002-7000-5689
Shu Zhong *School of Life Sciences, Central China Normal University, Wuhan, China.ORCID 0009-0006-9909-049X
Miaojuan YeXinyuan Institute of Medicine and Biotechnology, School of Life Sciences and Medicine, Zhejiang Sci-Tech University, Hangzhou, China.ORCID 0009-0003-1217-8842
Yuting ChenDepartment of Biochemistry and Department of Hepatobiliary and Pancreatic Surgery of the First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.ORCID 0000-0002-0595-5717
Siyu FanDepartment of Biochemistry and Department of Hepatobiliary and Pancreatic Surgery of the First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.ORCID 0009-0006-8228-4060
Miao YeXinyuan Institute of Medicine and Biotechnology, School of Life Sciences and Medicine, Zhejiang Sci-Tech University, Hangzhou, China.ORCID 0009-0005-5535-6148
Huan YangDepartment of Biochemistry and Department of Hepatobiliary and Pancreatic Surgery of the First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.ORCID 0000-0001-6068-6874
Yixing LiDepartment of Biochemistry and Department of Hepatobiliary and Pancreatic Surgery of the First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.ORCID 0000-0003-3187-8919
Choufei WuKey Laboratory of Vector Biology and Pathogen Control of Zhejiang Province, School of Life Sciences, Huzhou University, Huzhou, China.ORCID 0009-0007-9961-8271
Mingzhu FanMass Spectrometry & Metabolomics Core Facility, Key Laboratory of Structural Biology of Zhejiang Province, Westlake University, Hangzhou, China.ORCID 0000-0002-9365-3574
Shan FengMass Spectrometry & Metabolomics Core Facility, Key Laboratory of Structural Biology of Zhejiang Province, Westlake University, Hangzhou, China.ORCID 0000-0001-6474-4429
Zhaoxiang HeDepartment of Biophysics and Department of Critical Care Medicine of Sir Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou, China.ORCID 0009-0005-9553-8106
Long ZhouDepartment of Biophysics and Department of Critical Care Medicine of Sir Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou, China.ORCID 0000-0002-1864-8951
Liqin ZhangKey Laboratory of Vector Biology and Pathogen Control of Zhejiang Province, School of Life Sciences, Huzhou University, Huzhou, China.ORCID 0000-0003-4812-6617
Yigang WangXinyuan Institute of Medicine and Biotechnology, School of Life Sciences and Medicine, Zhejiang Sci-Tech University, Hangzhou, China.ORCID 0000-0003-4546-8179
Wei LiuDepartment of Biochemistry and Department of Hepatobiliary and Pancreatic Surgery of the First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.ORCID 0000-0002-8033-4718
Jingjing TongSchool of Life Sciences, Central China Normal University, Wuhan, China.ORCID 0009-0008-7479-0654
Du FengGuangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Degradation, Affiliated Cancer Hospital and Institute of Guangzhou Medical University, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, China.ORCID 0000-0002-2489-4702
Cong YiDepartment of Biochemistry and Department of Hepatobiliary and Pancreatic Surgery of the First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.ORCID 0000-0001-6853-6563
Funding
National Key Research and Development Program of China 2021YFC2600104National Natural Science Foundation of China 32122028Zhejiang Provincial Natural Science Foundation LR21C070001
6 · The paper itself
Abstract
Autophagy is essential for maintaining glucose homeostasis. However, the mechanism by which cells sense and respond to glucose starvation to induce autophagy remains incomplete. Here, we show that calcium serves as a fundamental triggering signal that connects environmental sensing to the formation of the autophagy initiation complex during glucose starvation. Mechanistically, glucose starvation instigates the release of vacuolar calcium into the cytoplasm, thus triggering the activation of Rck2 kinase. In turn, Rck2-mediated Atg11 phosphorylation enhances Atg11 interactions with Bmh1/2 bound to the Snf1-Sip1-Snf4 complex, leading to recruitment of vacuolar membrane-localized Snf1 to the PAS and subsequent Atg1 activation, thereby initiating autophagy. We also identified Glc7, a protein phosphatase-1, as a critical regulator of the association between Bmh1/2 and the Snf1 complex. We thus propose that calcium-triggered Atg11-Bmh1/2-Snf1 complex assembly initiates autophagy by controlling Snf1-mediated Atg1 activation in response to glucose starvation.
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.
Ca2+-triggered Atg11-Bmh1/2-Snf1 complex assembly initiates autophagy upon glucose starvation. · full record | OpenQuestion