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Noncanonical binding of Lck to CD3ε promotes TCR signaling and CAR function

Authors
  • Hartl, Frederike A.1, 2, 3
  • Beck-Garcìa, Esmeralda1
  • Woessner, Nadine M.1, 2, 4
  • Flachsmann, Lea J.1
  • Cárdenas, Rubí M.-H. Velasco1, 2
  • Brandl, Simon M.1, 2, 4
  • Taromi, Sanaz5, 6
  • Fiala, Gina J.1, 2
  • Morath, Anna1, 2, 4
  • Mishra, Pankaj1
  • Yousefi, O. Sascha1, 2, 4
  • Zimmermann, Julia1
  • Hoefflin, Nico1, 2
  • Köhn, Maja1, 2
  • Wöhrl, Birgitta M.7
  • Zeiser, Robert2, 5
  • Schweimer, Kristian7
  • Günther, Stefan1
  • Schamel, Wolfgang W.1, 2, 3
  • Minguet, Susana1, 2, 3
  • 1 Albert-Ludwigs-University of Freiburg, Freiburg, Germany , Freiburg (Germany)
  • 2 Signalling Research Centres BIOSS and CIBSS, University of Freiburg, Freiburg, Germany , Freiburg (Germany)
  • 3 University Clinics and Medical Faculty, Freiburg, Germany , Freiburg (Germany)
  • 4 Albert-Ludwigs-University Freiburg, Freiburg, Germany , Freiburg (Germany)
  • 5 Medical Center, University of Freiburg, Faculty of Medicine, University of Freiburg, Freiburg, Germany , Freiburg (Germany)
  • 6 Furtwangen University, Campus VS-Schwenningen, Furtwangen, Germany , Furtwangen (Germany)
  • 7 University of Bayreuth, Bayreuth, Germany , Bayreuth (Germany)
Type
Published Article
Journal
Nature Immunology
Publisher
Springer Nature
Publication Date
Jul 20, 2020
Volume
21
Issue
8
Pages
902–913
Identifiers
DOI: 10.1038/s41590-020-0732-3
Source
Springer Nature
License
Yellow

Abstract

How Lck is recruited to the TCR to initiate signaling is not well known. Here Minguet and colleagues report a previously unknown binding motif in the CD3ε cytoplasmic tail that interacts in a noncanonical mode with the Lck SH3 domain that may help to improve TCR activation and the antitumor activity of a clinically approved CAR.

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