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- W2479374966 abstract "T cell receptor (TCR) engagement opens Ca2+ release-activated Ca2+ (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 Ca2+ 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. Ca2+-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 Ca2+ as a critical regulator of actin organization and dynamics at the synapse, and reveal potential feedback loops through which Ca2+ influx may modulate TCR signaling." @default.
- W2479374966 created "2016-08-23" @default.
- W2479374966 creator A5038454800 @default.
- W2479374966 creator A5039653234 @default.
- W2479374966 creator A5074702377 @default.
- W2479374966 creator A5079895950 @default.
- W2479374966 date "2016-07-21" @default.
- W2479374966 modified "2023-10-08" @default.
- W2479374966 title "Calcium influx through CRAC channels controls actin organization and dynamics at the immune synapse" @default.
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- W2479374966 doi "https://doi.org/10.7554/elife.14850" @default.
- W2479374966 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4956410" @default.
- W2479374966 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/27440222" @default.
- W2479374966 hasPublicationYear "2016" @default.
- W2479374966 type Work @default.
- W2479374966 sameAs 2479374966 @default.