Evidence map›Paper›PMID 31235500›Full record

ArticleJournal of cell science2019

NKG2D-DAP10 signaling recruits EVL to the cytotoxic synapse to generate F-actin and promote NK cell cytotoxicity.

Katelynn M Wilton, Brittany L Overlee, Daniel D Billadeau

Open access · bronzeAbstract read
In one paragraph

Article in Journal of cell science, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
0.7field-weighted citation impact, top 31% 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

17 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
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  13. Review
  14. NK Cells in aFrontiers in immunology · 2021
    Review
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  17. 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

3 authors at 1 institution in 1 country.

Katelynn M WiltonDepartment of Immunology, Schulze Center for Novel Therapeutics, College of Medicine, Mayo Clinic, Rochester, MN 55905, USA.
Brittany L OverleeDivision of Oncology, Schulze Center for Novel Therapeutics, College of Medicine, Mayo Clinic, Rochester, MN 55905, USA.
Daniel D BilladeauDepartment of Immunology, Schulze Center for Novel Therapeutics, College of Medicine, Mayo Clinic, Rochester, MN 55905, USA billadeau.daniel@mayo.edu.ORCID 0000-0002-2296-9547
Mayo Clinic · US

Funding

Medical Scientist Traning Program at Mayo ClinicT32GM065841 · NIGMS · MAYO CLINIC ROCHESTER · PI KAUFMANN, SCOTT H, SCHIMMENTI, LISA A · 2003 to 2022
$5.8M
MECHANISMS OF NATURAL KILLER CELL ACTIVATIONR01CA047752 · NCI · MAYO CLINIC ROCHESTER · PI BILLADEAU, DANIEL D · 1990 to 2012
$3.8M
Mechanisms Regulating Human NK Cell CytotoxicityR01AI120949 · NIAID · MAYO CLINIC ROCHESTER · PI BILLADEAU, DANIEL D · 2016 to 2020
$2.0M
NCI NIH HHS R01 CA047752NIAID NIH HHS R01 AI120949NIGMS NIH HHS T32 GM065841
6 · The paper itself

Abstract

Natural killer (NK) cells eliminate abnormal cells through the release of cytolytic granule contents. In this process, NK cells must adhere to target cells through integrin-mediated adhesion, which is highly dependent on the generation of F-actin. Ena/VASP-like (EVL) is an actin regulatory protein previously shown to regulate integrin-mediated adhesion in other cell types, but its role in NK cell biology is not known. Herein, we show that EVL is recruited to the NK cell cytotoxic synapse and is required for NK cell cytotoxicity. Significantly, EVL is involved in the generation of F-actin at the cytotoxic synapse, antibody-stimulated spreading, and NK cell-target cell adhesion. EVL interacts with WASP (also known as WAS) and VASP and is required for localization of both proteins to the synapse. Recruitment of EVL to points of cellular activation occurs through the receptor NKG2D-DAP10 (also known as KLRK1 and HCST, respectively) via a binding site previously implicated in VAV1 and Grb2 recruitment. Taken together, this study implicates DAP10-mediated Grb2 and VAV1 signaling in the recruitment of an EVL-containing actin regulatory complex to the cytotoxic synapse where it can promote F-actin nucleation leading to NK cell-mediated killing.

Indexed as

Actin CytoskeletonActinsCell Adhesion MoleculesCell Line, TumorCytotoxicity, ImmunologicGRB2 Adaptor ProteinHumansKiller Cells, NaturalLymphocyte ActivationNK Cell Lectin-Like Receptor Subfamily KProtein BindingProto-Oncogene Proteins c-vavReceptors, ImmunologicSignal TransductionActinsCell Adhesion MoleculesGRB2 Adaptor ProteinGRB2 protein, humanHCST protein, humanKLRK1 protein, humanNK Cell Lectin-Like Receptor Subfamily KProto-Oncogene Proteins c-vavReceptors, ImmunologicVAV1 protein, humanActin polymerizationCytotoxicityEVLNK cell

Identifiers

PMID31235500
PMCPMC7055393
OpenAlexW2953903189

What OpenQuestion holds

Textmetadata
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.