Evidence map›Paper›PMID 33605979›Full record

ArticleThe Journal of cell biology2021

Phosphorylation of SNX27 by MAPK11/14 links cellular stress-signaling pathways with endocytic recycling.

Lejiao Mao, Chenyi Liao, Jiao Qin, Yanqiu Gong, Yifei Zhou, Shasha Li, Zhe Liu, Huaqing Deng, Wankun Deng, Qingxiang Sun and 6 more

Open access · greenAbstract read
In one paragraph

Article in The Journal of cell biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

29 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
  2. Review
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  8. Omic AI reveals new autophagy regulators from the Atg1 interactome inFrontiers in cell and developmental biology · 2025
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  15. FAM91A1-TBC1D23 complex structure reveals human genetic variations susceptible for PCH.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  16. Article
  17. Cryo-EM structure of the Mon1-Ccz1-RMC1 complex reveals molecular basis of metazoan RAB7A activation.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  18. Article
  19. SCGN deficiency is a risk factor for autism spectrum disorder.Signal transduction and targeted therapy · 2023
    Article
  20. Receptor Recycling by Retromer.Molecular and cellular biology · 2023
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

16 authors at 4 institutions in 2 countries.

Lejiao Mao *Key Laboratory of Birth Defects and Related Diseases of Women and Children, Department of Paediatrics, West China Second University Hospital, State Key Laboratory of Biotherapy, Sichuan University, Chengdu, China.
Chenyi Liao *Laboratory of Molecular Modeling and Design, State Key Laboratory of Molecular Reaction Dynamics, Dalian Institute of Chemical Physics, Chinese Academy of Sciences, Dalian, China.
Jiao QinKey Laboratory of Birth Defects and Related Diseases of Women and Children, Department of Paediatrics, West China Second University Hospital, State Key Laboratory of Biotherapy, Sichuan University, Chengdu, China.
Yanqiu GongState Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, China.
Yifei ZhouKey Laboratory of Birth Defects and Related Diseases of Women and Children, Department of Paediatrics, West China Second University Hospital, State Key Laboratory of Biotherapy, Sichuan University, Chengdu, China.
Shasha LiKey Laboratory of Birth Defects and Related Diseases of Women and Children, Department of Paediatrics, West China Second University Hospital, State Key Laboratory of Biotherapy, Sichuan University, Chengdu, China.
Zhe LiuKey Laboratory of Birth Defects and Related Diseases of Women and Children, Department of Paediatrics, West China Second University Hospital, State Key Laboratory of Biotherapy, Sichuan University, Chengdu, China.
Huaqing DengKey Laboratory of Birth Defects and Related Diseases of Women and Children, Department of Paediatrics, West China Second University Hospital, State Key Laboratory of Biotherapy, Sichuan University, Chengdu, China.
Wankun DengDepartment of Bioinformatics and Systems Biology, Key Laboratory of Molecular Biophysics of Ministry of Education, College of Life Science and Technology, Huazhong University of Science and Technology, Wuhan, China.
Qingxiang SunState Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, China.
Xianming MoState Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, China.
Yu XueDepartment of Bioinformatics and Systems Biology, Key Laboratory of Molecular Biophysics of Ministry of Education, College of Life Science and Technology, Huazhong University of Science and Technology, Wuhan, China.
Daniel D BilladeauDivision of Oncology Research and Schulze Center for Novel Therapeutics, Mayo Clinic, Rochester, MN.
Lunzhi DaiState Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, China.
Guohui LiLaboratory of Molecular Modeling and Design, State Key Laboratory of Molecular Reaction Dynamics, Dalian Institute of Chemical Physics, Chinese Academy of Sciences, Dalian, China.
Da JiaKey Laboratory of Birth Defects and Related Diseases of Women and Children, Department of Paediatrics, West China Second University Hospital, State Key Laboratory of Biotherapy, Sichuan University, Chengdu, China.
Sichuan University · CNDalian Institute of Chemical Physics · CNHuazhong University of Science and Technology · CNMayo Clinic · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endocytosed proteins can be delivered to lysosomes for degradation or recycled to either the trans-Golgi network or the plasma membrane. It remains poorly understood how the recycling versus degradation of cargoes is determined. Here, we show that multiple extracellular stimuli, including starvation, LPS, IL-6, and EGF treatment, can strongly inhibit endocytic recycling of multiple cargoes through the activation of MAPK11/14. The stress-induced kinases in turn directly phosphorylate SNX27, a key regulator of endocytic recycling, at serine 51 (Ser51). Phosphorylation of SNX27 at Ser51 alters the conformation of its cargo-binding pocket and decreases the interaction between SNX27 and cargo proteins, thereby inhibiting endocytic recycling. Our study indicates that endocytic recycling is highly dynamic and can crosstalk with cellular stress-signaling pathways. Suppression of endocytic recycling and enhancement of receptor lysosomal degradation serve as new mechanisms for cells to cope with stress and save energy.

Indexed as

EndocytosisMAP Kinase Signaling SystemProteolysisStress, PhysiologicalHeLa CellsHumansMitogen-Activated Protein Kinase 11Mitogen-Activated Protein Kinase 14PhosphorylationSorting NexinsMitogen-Activated Protein Kinase 11Mitogen-Activated Protein Kinase 14SNX27 protein, humanSorting Nexins

Identifiers

PMID33605979
PMCPMC7901142
OpenAlexW3130625796

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.