Evidence map›Paper›PMID 29237129›Full record

ReviewAnnual review of immunology2018

ZAP-70 in Signaling, Biology, and Disease.

Byron B Au-Yeung, Neel H Shah, Lin Shen, Arthur Weiss

Abstract readReview
In one paragraph

Review in Annual review of immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers.

0numbers the graph read from it
0cells of the map it votes in
88citing 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

88 citing papers in PubMed.

  1. Review
  2. Article
  3. Review
  4. Article
  5. T cell engagers in autoimmune diseases.Nature reviews. Immunology · 2026
    Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article

28 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.

Byron B Au-YeungDepartment of Medicine, Emory University School of Medicine, Atlanta, Georgia 30322, USA; email: byron.au-yeung@emory.edu.
Neel H ShahDepartment of Molecular and Cell Biology, University of California, Berkeley, California 94720, USA; email: neelshah@berkeley.edu.
Lin ShenDivision of Rheumatology, Rosalind Russell and Ephraim P. Engleman Rheumatology Research Center, University of California, San Francisco, California 94143, USA; email: lin.shen@ucsf.edu , art.weiss@ucsf.edu.
Arthur WeissDivision of Rheumatology, Rosalind Russell and Ephraim P. Engleman Rheumatology Research Center, University of California, San Francisco, California 94143, USA; email: lin.shen@ucsf.edu , art.weiss@ucsf.edu.

Funding

Understand the metabolic fitness of naïve T cellsP01AI091580 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI JEROEN ROOSE · 2011 to 2026
$31.1M
The cell and molecular mechanisms underlying CD28 costimulationR37AI114575 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI WEISS, ARTHUR · 2016 to 2023
$3.2M
Inhibition of ZAP-70 to selectively attenuate autoimmune disease-inducing T cellsK01AR065481 · NIAMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI AU-YEUNG, BYRON BENTON · 2014 to 2016
$385k
NIAID NIH HHS P01 AI091580NIAID NIH HHS R37 AI114575NIAMS NIH HHS K01 AR065481
6 · The paper itself

Abstract

T cells possess an array of functional capabilities important for host defense against pathogens and tumors. T cell effector functions require the T cell antigen receptor (TCR). The TCR has no intrinsic enzymatic activity, and thus signal transduction from the receptor relies on additional signaling molecules. One such molecule is the cytoplasmic tyrosine kinase ZAP-70, which associates with the TCR complex and is required for initiating the canonical biochemical signal pathways downstream of the TCR. In this article, we describe recent structure-based insights into the regulation and substrate specificity of ZAP-70, and then we review novel methods for determining the role of ZAP-70 catalytic activity-dependent and -independent signals in developing and mature T cells. Lastly, we discuss the disease states in mouse models and humans, which range from immunodeficiency to autoimmunity, that are caused by mutations in ZAP-70.

Indexed as

Disease SusceptibilitySignal TransductionAnimalsAutoimmunityBiomarkersCatalysisCell DifferentiationGene Expression RegulationHumansImmunityLymphocyte ActivationPhosphorylationProtein TransportStructure-Activity RelationshipSubstrate SpecificityT-LymphocytesBiomarkersZAP70 protein, humanZAP-70 Protein-Tyrosine Kinaseautoimmunityautoinhibitionimmune deficiencykinase regulationstructureT cell activationtyrosine phosphorylation

Identifiers

PMID29237129
PMCPMC13317156

What Socratic 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 Socratic graph.