Evidence map›Paper›PMID 28821013›Full record

ArticlePLoS biology2017

Rictor positively regulates B cell receptor signaling by modulating actin reorganization via ezrin.

Lu Huang, Yongjie Zhang, Chenguang Xu, Xiaomei Gu, Linlin Niu, Jinzhi Wang, Xiaoyu Sun, Xiaoming Bai, Xingtian Xuan, Qubei Li and 9 more

Open access · goldAbstract read
In one paragraph

Article in PLoS biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

20 citing papers in PubMed, 33 citations in OpenAlex.

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  15. AKT2 deficiency impairs formation of the BCR signalosome.Cell communication and signaling : CCS · 2020
    Article
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  19. The "other" mTOR complex: New insights into mTORC2 immunobiology and their implications.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2019
    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

19 authors at 7 institutions in 3 countries.

Lu HuangChongqing Key Laboratory of Child Infection and Immunity, Children's Hospital of Chongqing Medical University, Chongqing, China.
Yongjie ZhangChongqing Key Laboratory of Child Infection and Immunity, Children's Hospital of Chongqing Medical University, Chongqing, China.
Chenguang XuMOE Key Laboratory of Protein Sciences, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, School of Life Sciences, Institute for Immunology, Tsinghua University, Beijing, China.
Xiaomei GuMOE Key Laboratory of Protein Sciences, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, School of Life Sciences, Institute for Immunology, Tsinghua University, Beijing, China.
Linlin NiuChongqing Key Laboratory of Child Infection and Immunity, Children's Hospital of Chongqing Medical University, Chongqing, China.
Jinzhi WangChongqing Key Laboratory of Child Infection and Immunity, Children's Hospital of Chongqing Medical University, Chongqing, China.
Xiaoyu SunChongqing Key Laboratory of Child Infection and Immunity, Children's Hospital of Chongqing Medical University, Chongqing, China.
Xiaoming BaiChongqing Key Laboratory of Child Infection and Immunity, Children's Hospital of Chongqing Medical University, Chongqing, China.
Xingtian XuanChongqing Key Laboratory of Child Infection and Immunity, Children's Hospital of Chongqing Medical University, Chongqing, China.
Qubei LiChildren's Hospital Respiratory Center of Chongqing Medical University, Chongqing, China.
Chunwei ShiDepartment of Pathogen Biology, School of Basic Medicine, Huazhong University of Science and Technology, Wuhan, China.
Bing YuDepartment of Pathogen Biology, School of Basic Medicine, Huazhong University of Science and Technology, Wuhan, China.
Heather MillerDepartment of Intracellular Pathogens, National Institute of Allergy and Infectious Diseases, Hamilton, Montana, United States of America.
Gangyi YangDepartment of Endocrinology, the Second Affiliated Hospital, Chongqing Medical University, Chongqing, China.
Lisa S WesterbergDepartment of Microbiology Tumor and Cell Biology, Karolinska Institutet, Stockholm, Sweden.
Wanli LiuMOE Key Laboratory of Protein Sciences, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, School of Life Sciences, Institute for Immunology, Tsinghua University, Beijing, China.
Wenxia SongDepartment of Cell Biology and Molecular Genetics, University of Maryland, College Park, Maryland, United States of America.
Xiaodong ZhaoChongqing Key Laboratory of Child Infection and Immunity, Children's Hospital of Chongqing Medical University, Chongqing, China.
Chaohong LiuDepartment of Pathogen Biology, School of Basic Medicine, Huazhong University of Science and Technology, Wuhan, China.ORCID http://orcid.org/0000-0003-0517-3835
Children's Hospital of Chongqing Medical University · CNHuazhong University of Science and Technology · CNTsinghua University · CNDalian Medical University · CNKarolinska Institutet · SENational Institute of Allergy and Infectious Diseases · USUniversity of Maryland, College Park · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

As the central hub of the metabolism machinery, the mammalian target of rapamycin complex 2 (mTORC2) has been well studied in lymphocytes. As an obligatory component of mTORC2, the role of Rictor in T cells is well established. However, the role of Rictor in B cells still remains elusive. Rictor is involved in B cell development, especially the peripheral development. However, the role of Rictor on B cell receptor (BCR) signaling as well as the underlying cellular and molecular mechanism is still unknown. This study used B cell-specfic Rictor knockout (KO) mice to investigate how Rictor regulates BCR signaling. We found that the key positive and negative BCR signaling molecules, phosphorylated Brutons tyrosine kinase (pBtk) and phosphorylated SH2-containing inositol phosphatase (pSHIP), are reduced and enhanced, respectively, in Rictor KO B cells. This suggests that Rictor positively regulates the early events of BCR signaling. We found that the cellular filamentous actin (F-actin) is drastically increased in Rictor KO B cells after BCR stimulation through dysregulating the dephosphorylation of ezrin. The high actin-ezrin intensity area restricts the lateral movement of BCRs upon stimulation, consequently reducing BCR clustering and BCR signaling. The reduction in the initiation of BCR signaling caused by actin alteration is associated with a decreased humoral immune response in Rictor KO mice. The inhibition of actin polymerization with latrunculin in Rictor KO B cells rescues the defects of BCR signaling and B cell differentiation. Overall, our study provides a new pathway linking cell metablism to BCR activation, in which Rictor regulates BCR signaling via actin reorganization.

Indexed as

ActinsAgammaglobulinaemia Tyrosine KinaseAnimalsB-LymphocytesBridged Bicyclo Compounds, HeterocyclicCarrier ProteinsCell MembraneCytoskeletal ProteinsEzrinImmunity, HumoralMaleMice, Inbred C57BLMice, KnockoutPhosphatidylinositol-3,4,5-Trisphosphate 5-PhosphatasesPolymerizationProtein-Tyrosine KinasesActinsAgammaglobulinaemia Tyrosine KinaseBridged Bicyclo Compounds, HeterocyclicCarrier ProteinsCytoskeletal ProteinsEzrinInpp5d protein, mouselatrunculin BPhosphatidylinositol-3,4,5-Trisphosphate 5-PhosphatasesProtein-Tyrosine KinasesRapamycin-Insensitive Companion of mTOR Proteinrictor protein, mouseThiazolidines

Identifiers

PMID28821013
PMCPMC5562439
OpenAlexW2745812047

What OpenQuestion holds

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LicenceCC BY
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.