Evidence map›Paper›PMID 31018906›Full record

ArticleJournal of autoimmunity2019

Tmem178 negatively regulates store-operated calcium entry in myeloid cells via association with STIM1.

Zhengfeng Yang, Hui Yan, Wentao Dai, Ji Jing, Yihu Yang, Sahil Mahajan, Yubin Zhou, Weikai Li, Claudia Macaubas, Elizabeth D Mellins and 3 more

Abstract read
In one paragraph

Article in Journal of autoimmunity, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.4field-weighted citation impact, top 24% 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

13 citing papers in PubMed, 18 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Proteins Interacting with STIM1 and Store-Operated CaProgress in molecular and subcellular biology · 2021
    Review
  9. Article
  10. Article
  11. Article
  12. The role of Stim1 in the progression of lupus nephritis in mice.International journal of clinical and experimental pathology · 2020
    Article
  13. Review
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

13 authors at 5 institutions in 2 countries.

Zhengfeng YangDepartment of Orthopaedics, Washington University School of Medicine, St. Louis, MO, 63110, USA.
Hui YanDepartment of Orthopaedics, Washington University School of Medicine, St. Louis, MO, 63110, USA.
Wentao DaiShanghai Center for Bioinformation Technology & Shanghai Engineering Research Center of Pharmaceutical Translation, Shanghai Industrial Technology Institute, 1278 Keyuan Road, Shanghai, 201203, China.
Ji JingInstitute of Biosciences and Technology, Texas A&M University College of Medicine, Houston, TX 77030, USA.
Yihu YangDepartment of Biochemistry and Molecular Biophysics, Washington University School of Medicine, St. Louis, MO, USA.
Sahil MahajanDepartment of Orthopaedics, Washington University School of Medicine, St. Louis, MO, 63110, USA.
Yubin ZhouInstitute of Biosciences and Technology, Texas A&M University College of Medicine, Houston, TX 77030, USA.
Weikai LiDepartment of Biochemistry and Molecular Biophysics, Washington University School of Medicine, St. Louis, MO, USA.
Claudia MacaubasDepartment of Pediatrics, Program in Immunology, Stanford University, Stanford, CA 94305, USA.
Elizabeth D MellinsDepartment of Pediatrics, Program in Immunology, Stanford University, Stanford, CA 94305, USA.
Chien-Cheng ShihWashington University Center for Cellular Imaging, Washington University School of Medicine, St. Louis, MO, 63110, USA.
James A J FitzpatrickWashington University Center for Cellular Imaging, Washington University School of Medicine, St. Louis, MO, 63110, USA; Department of Cell Biology & Physiology, Washington University School of Medicine, St. Louis, MO, USA; Department of Neuroscience, Washington University School of Medicine, St. Louis, MO, USA; Department of Biomedical Engineering, Washington University, St. Louis, MO, USA.
Roberta FaccioDepartment of Orthopaedics, Washington University School of Medicine, St. Louis, MO, 63110, USA; Shriners Hospitals for Children, St. Louis MO, USA. Electronic address: faccior@wustl.edu.
Washington University in St. Louis · USStanford University · USTexas A&M University · USShanghai Industrial Technology Institute · CNShriners Hospitals for Children - St. Louis · US

Funding

Regulatory Pathways in Osteoclasts and Immune Cells during Inflammatory ArthritisR01AR053628 · NIAMS · WASHINGTON UNIVERSITY · PI FACCIO, ROBERTA · 2006 to 2015
$3.2M
MOLECULAR CONTROL OF CALCIUM INFLUX AT THE ER-PLASMA MEMBRANE JUNCTIONSR01GM112003 · NIGMS · TEXAS A&M UNIVERSITY HEALTH SCIENCE CTR · PI ZHOU, YUBIN · 2014 to 2022
$2.7M
Novel Regulators of Inflammatory Arthritis and Bone ErosionR01AR066551 · NIAMS · WASHINGTON UNIVERSITY · PI FACCIO, ROBERTA · 2015 to 2020
$2.0M
Optogenetic toolkit for remote control of voltage-gated calcium channelsR21GM126532 · NIGMS · TEXAS A&M UNIVERSITY HEALTH SCIENCE CTR · PI HAN, GANG, ZHOU, YUBIN · 2018 to 2019
$443k
NIAMS NIH HHS R01 AR053628NIAMS NIH HHS R01 AR066551NIGMS NIH HHS R01 GM112003NIGMS NIH HHS R21 GM126532
6 · The paper itself

Abstract

Store-operated calcium entry (SOCE) modulates cytosolic calcium in multiple cells. Endoplasmic reticulum (ER)-localized STIM1 and plasma membrane (PM)-localized ORAI1 are two main components of SOCE. STIM1:ORAI1 association requires STIM1 oligomerization, its re-distribution to ER-PM junctions, and puncta formation. However, little is known about the negative regulation of these steps to prevent calcium overload. Here, we identified Tmem178 as a negative modulator of STIM1 puncta formation in myeloid cells. Using site-directed mutagenesis, co-immunoprecipitation assays and FRET imaging, we determined that Tmem178:STIM1 association occurs via their transmembrane motifs. Mutants that increase Tmem178:STIM1 association reduce STIM1 puncta formation, SOCE activation, impair inflammatory cytokine production in macrophages and osteoclastogenesis. Mutants that reduce Tmem178:STIM1 association reverse these effects. Furthermore, exposure to plasma from arthritic patients decreases Tmem178 expression, enhances SOCE activation and cytoplasmic calcium. In conclusion, Tmem178 modulates the rate-limiting step of STIM1 puncta formation and therefore controls SOCE in inflammatory conditions.

Indexed as

AnimalsCalciumEndoplasmic ReticulumFemaleGene Expression RegulationHEK293 CellsHumansIntracellular Calcium-Sensing ProteinsMacrophage ActivationMacrophagesMaleMembrane ProteinsMiceMyeloid CellsNeoplasm ProteinsOsteogenesisCalciumIntracellular Calcium-Sensing ProteinsMembrane ProteinsNeoplasm ProteinsSARAF protein, humanSTIM1 protein, humanStromal Interaction Molecule 1transmembrane protein 178, humanMacrophage activationOsteoclastogenesisSOCESTIM1Tmem178

Identifiers

PMID31018906
PMCPMC7102427
OpenAlexW2940961266

What OpenQuestion holds

Textmetadata
LicenceTDM
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.