Evidence map›Paper›PMID 31123148›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2019

Coupling of COPII vesicle trafficking to nutrient availability by the IRE1α-XBP1s axis.

Lin Liu, Jie Cai, Huimin Wang, Xijun Liang, Qian Zhou, Chenyun Ding, Yuangang Zhu, Tingting Fu, Qiqi Guo, Zhisheng Xu and 12 more

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.8field-weighted citation impact, top 10% of its field
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.

3 · Its place in the literature

Who cites it

30 citing papers in PubMed, 59 citations in OpenAlex.

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  15. ER exit in physiology and disease.Frontiers in molecular biosciences · 2024
    Review
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  18. Cells · 2023
    Review
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4 · The record

Corrections and comments

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

22 authors at 6 institutions in 2 countries.

Lin LiuThe State Key Laboratory of Pharmaceutical Biotechnology-MOE Key Laboratory of Model Animals for Disease Study, Department of Spine Surgery, Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School, Model Animal Research Center of Nanjing University, Nanjing 210061, China.
Jie CaiHubei Key Laboratory of Cell Homeostasis, College of Life Sciences, Institute for Advanced Studies, Wuhan University, Wuhan 430072, China.
Huimin WangThe State Key Laboratory of Membrane Biology, Center for Life Sciences and Institute of Molecular Medicine, Peking University, Beijing 100101, China.
Xijun LiangThe State Key Laboratory of Pharmaceutical Biotechnology-MOE Key Laboratory of Model Animals for Disease Study, Department of Spine Surgery, Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School, Model Animal Research Center of Nanjing University, Nanjing 210061, China.
Qian ZhouThe State Key Laboratory of Pharmaceutical Biotechnology-MOE Key Laboratory of Model Animals for Disease Study, Department of Spine Surgery, Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School, Model Animal Research Center of Nanjing University, Nanjing 210061, China.
Chenyun DingThe State Key Laboratory of Pharmaceutical Biotechnology-MOE Key Laboratory of Model Animals for Disease Study, Department of Spine Surgery, Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School, Model Animal Research Center of Nanjing University, Nanjing 210061, China.
Yuangang ZhuThe State Key Laboratory of Membrane Biology, Center for Life Sciences and Institute of Molecular Medicine, Peking University, Beijing 100101, China.
Tingting FuThe State Key Laboratory of Pharmaceutical Biotechnology-MOE Key Laboratory of Model Animals for Disease Study, Department of Spine Surgery, Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School, Model Animal Research Center of Nanjing University, Nanjing 210061, China.
Qiqi GuoThe State Key Laboratory of Pharmaceutical Biotechnology-MOE Key Laboratory of Model Animals for Disease Study, Department of Spine Surgery, Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School, Model Animal Research Center of Nanjing University, Nanjing 210061, China.
Zhisheng XuThe State Key Laboratory of Pharmaceutical Biotechnology-MOE Key Laboratory of Model Animals for Disease Study, Department of Spine Surgery, Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School, Model Animal Research Center of Nanjing University, Nanjing 210061, China.
Liwei XiaoThe State Key Laboratory of Pharmaceutical Biotechnology-MOE Key Laboratory of Model Animals for Disease Study, Department of Spine Surgery, Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School, Model Animal Research Center of Nanjing University, Nanjing 210061, China.
Jing LiuThe State Key Laboratory of Pharmaceutical Biotechnology-MOE Key Laboratory of Model Animals for Disease Study, Department of Spine Surgery, Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School, Model Animal Research Center of Nanjing University, Nanjing 210061, China.
Yujing YinThe State Key Laboratory of Pharmaceutical Biotechnology-MOE Key Laboratory of Model Animals for Disease Study, Department of Spine Surgery, Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School, Model Animal Research Center of Nanjing University, Nanjing 210061, China.
Lei FangThe State Key Laboratory of Pharmaceutical Biotechnology, Jiangsu Key Laboratory of Molecular Medicine and School of Medicine, Nanjing University, Nanjing 210093, China.
Bin XueThe State Key Laboratory of Pharmaceutical Biotechnology, Jiangsu Key Laboratory of Molecular Medicine and School of Medicine, Nanjing University, Nanjing 210093, China.
Yan WangHubei Key Laboratory of Cell Homeostasis, College of Life Sciences, Institute for Advanced Studies, Wuhan University, Wuhan 430072, China.
Zhuo-Xian MengDepartment of Pathology and Pathophysiology, Zhejiang University School of Medicine, Hangzhou 310058, Zhejiang, China.
Aibin HePeking Center for Life Sciences, Institute of Molecular Medicine, Peking University, Beijing 100871, China.ORCID 0000-0002-3489-2305
Jian-Liang LiIntegrative Bioinformatics, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709.ORCID 0000-0002-6487-081X
Yong LiuHubei Key Laboratory of Cell Homeostasis, College of Life Sciences, Institute for Advanced Studies, Wuhan University, Wuhan 430072, China.
Xiao-Wei ChenThe State Key Laboratory of Membrane Biology, Center for Life Sciences and Institute of Molecular Medicine, Peking University, Beijing 100101, China; xiaowei_chen@pku.edu.cn ganzj@nju.edu.cn.
Zhenji GanThe State Key Laboratory of Pharmaceutical Biotechnology-MOE Key Laboratory of Model Animals for Disease Study, Department of Spine Surgery, Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School, Model Animal Research Center of Nanjing University, Nanjing 210061, China; xiaowei_chen@pku.edu.cn ganzj@nju.edu.cn.
Nanjing Drum Tower Hospital · CNPeking University · CNWuhan University · CNState Key Laboratory of Pharmaceutical BiotechnologyNational Institute of Environmental Health Sciences · USZhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The cytoplasmic coat protein complex-II (COPII) is evolutionarily conserved machinery that is essential for efficient trafficking of protein and lipid cargos. How the COPII machinery is regulated to meet the metabolic demand in response to alterations of the nutritional state remains largely unexplored, however. Here, we show that dynamic changes of COPII vesicle trafficking parallel the activation of transcription factor X-box binding protein 1 (XBP1s), a critical transcription factor in handling cellular endoplasmic reticulum (ER) stress in both live cells and mouse livers upon physiological fluctuations of nutrient availability. Using live-cell imaging approaches, we demonstrate that XBP1s is sufficient to promote COPII-dependent trafficking, mediating the nutrient stimulatory effects. Chromatin immunoprecipitation (ChIP) coupled with high-throughput DNA sequencing (ChIP-seq) and RNA-sequencing analyses reveal that nutritional signals induce dynamic XBP1s occupancy of promoters of COPII traffic-related genes, thereby driving the COPII-mediated trafficking process. Liver-specific disruption of the inositol-requiring enzyme 1α (IRE1α)-XBP1s signaling branch results in diminished COPII vesicle trafficking. Reactivation of XBP1s in mice lacking hepatic IRE1α restores COPII-mediated lipoprotein secretion and reverses the fatty liver and hypolipidemia phenotypes. Thus, our results demonstrate a previously unappreciated mechanism in the metabolic control of liver protein and lipid trafficking: The IRE1α-XBP1s axis functions as a nutrient-sensing regulatory nexus that integrates nutritional states and the COPII vesicle trafficking.

Indexed as

AnimalsCell MovementChromatin ImmunoprecipitationCOP-Coated VesiclesEndoplasmic ReticulumEndoplasmic Reticulum StressEndoribonucleasesLipidsLiverMaleMiceMice, Inbred C57BLNutrientsPromoter Regions, GeneticProtein Serine-Threonine KinasesProtein TransportEndoribonucleasesErn1 protein, mouseLipidsNutrientsProtein Serine-Threonine KinasesX-Box Binding Protein 1Xbp1 protein, mouseCOPIIliver steatosismetabolic sensingnutrient availabilityXBP1s

Identifiers

PMID31123148
PMCPMC6575159
OpenAlexW2946237195

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.