Evidence map›Paper›PMID 27440222›Full record

ArticleeLife2016

Calcium influx through CRAC channels controls actin organization and dynamics at the immune synapse.

Catherine A Hartzell, Katarzyna I Jankowska, Janis K Burkhardt, Richard S Lewis

Abstract read
In one paragraph

Article in eLife, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing 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.

3 · Its place in the literature

Who cites it

64 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Mechanobiological Dynamics-Inspired Mechanomodulatory Biomaterials.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Review
  6. Review
  7. Review
  8. Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Imaging actin organisation and dynamics in 3D.Journal of cell science · 2024
    Article
  14. Multifaceted control of T cell differentiation by STIM1.Trends in biochemical sciences · 2023
    Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. βCells · 2022
    Article

4 more citing papers are in PubMed but not listed here.

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

4 authors.

Catherine A HartzellImmunology Program, Stanford University, Stanford, United States.
Katarzyna I JankowskaDepartment of Pathology and Laboratory Medicine, Children's Hospital of Philadelphia Research Institute, Philadelphia, United States.
Janis K BurkhardtDepartment of Pathology and Laboratory Medicine, Children's Hospital of Philadelphia Research Institute, Philadelphia, United States.
Richard S LewisImmunology Program, Stanford University, Stanford, United States.ORCID 0000-0002-6010-7403

Funding

Ion Channels and Signaling Mechanisms in T LymphocytesR37GM045374 · NIGMS · STANFORD UNIVERSITY · PI LEWIS, RICHARD S · 2012 to 2021
$6.2M
Costimulatory ligand mobility effects on T cell activationR01GM104867 · NIGMS · CHILDREN'S HOSP OF PHILADELPHIA · PI BURKHARDT, JANIS K. · 2013 to 2016
$1.3M
NIGMS NIH HHS R01 GM104867NIGMS NIH HHS R37 GM045374
6 · The paper itself

Abstract

T cell receptor (TCR) engagement opens Ca(2+) release-activated Ca(2+) (CRAC) channels and triggers formation of an immune synapse between T cells and antigen-presenting cells. At the synapse, actin reorganizes into a concentric lamellipod and lamella with retrograde actin flow that helps regulate the intensity and duration of TCR signaling. We find that Ca(2+) influx is required to drive actin organization and dynamics at the synapse. Calcium acts by promoting actin depolymerization and localizing actin polymerization and the actin nucleation promotion factor WAVE2 to the periphery of the lamellipod while suppressing polymerization elsewhere. Ca(2+)-dependent retrograde actin flow corrals ER tubule extensions and STIM1/Orai1 complexes to the synapse center, creating a self-organizing process for CRAC channel localization. Our results demonstrate a new role for Ca(2+) as a critical regulator of actin organization and dynamics at the synapse, and reveal potential feedback loops through which Ca(2+) influx may modulate TCR signaling.

Indexed as

Cell AdhesionProtein MultimerizationActinsAntigen-Presenting CellsCalciumCalcium Release Activated Calcium ChannelsCells, CulturedHumansT-LymphocytesActinsCalciumCalcium Release Activated Calcium Channelsactin dynamicscalciumcalcium release-activated calcium (CRAC) channelscell biologyendoplasmic reticulumhumanimmunological synapseimmunologyT lymphocyte

Identifiers

PMID27440222
PMCPMC4956410

What OpenQuestion holds

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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.