Targeting the NFAT:AP-1 transcriptional complex on DNA with a small-molecule inhibitor.


Journal

Proceedings of the National Academy of Sciences of the United States of America
ISSN: 1091-6490
Titre abrégé: Proc Natl Acad Sci U S A
Pays: United States
ID NLM: 7505876

Informations de publication

Date de publication:
14 05 2019
Historique:
pubmed: 26 4 2019
medline: 31 3 2020
entrez: 26 4 2019
Statut: ppublish

Résumé

The transcription factor nuclear factor of activated T cells (NFAT) has a key role in both T cell activation and tolerance and has emerged as an important target of immune modulation. NFAT directs the effector arm of the immune response in the presence of activator protein-1 (AP-1), and T cell anergy/exhaustion in the absence of AP-1. Envisioning a strategy for selective modulation of the immune response, we designed a FRET-based high-throughput screen to identify compounds that disrupt the NFAT:AP-1:DNA complex. We screened ∼202,000 small organic compounds and identified 337 candidate inhibitors. We focus here on one compound,

Identifiants

pubmed: 31019078
pii: 1820604116
doi: 10.1073/pnas.1820604116
pmc: PMC6525529
doi:

Substances chimiques

Acetamides 0
Cytokines 0
NFATC Transcription Factors 0
Small Molecule Libraries 0
Transcription Factor AP-1 0
DNA 9007-49-2

Types de publication

Evaluation Study Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

9959-9968

Subventions

Organisme : NIH HHS
ID : S10 OD016262
Pays : United States
Organisme : NIAID NIH HHS
ID : R01 AI040127
Pays : United States
Organisme : NIAID NIH HHS
ID : R01 AI109842
Pays : United States
Organisme : NCRR NIH HHS
ID : S10 RR027366
Pays : United States
Organisme : NIAID NIH HHS
ID : R56 AI109842
Pays : United States
Organisme : NCI NIH HHS
ID : P30 CA016042
Pays : United States

Déclaration de conflit d'intérêts

Conflict of interest statement: A.R. and P.G.H. are founders of CalciMedica, Inc., and members of its scientific advisory board.

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Auteurs

Giuliana P Mognol (GP)

Division of Signaling and Gene Expression, La Jolla Institute for Immunology, La Jolla, CA 92037.

Edahí González-Avalos (E)

Division of Signaling and Gene Expression, La Jolla Institute for Immunology, La Jolla, CA 92037.
Bioinformatics and Systems Biology Graduate Program, University of California, San Diego, La Jolla, CA 92093.

Srimoyee Ghosh (S)

Immune Disease Institute, Boston Children's Hospital, Boston, MA 02115.
Program in Cellular and Molecular Medicine, Boston Children's Hospital, Boston, MA 02115.

Roberto Spreafico (R)

Signaling Systems Laboratory, University of California, Los Angeles, CA 90095.

Aparna Gudlur (A)

Division of Signaling and Gene Expression, La Jolla Institute for Immunology, La Jolla, CA 92037.

Anjana Rao (A)

Division of Signaling and Gene Expression, La Jolla Institute for Immunology, La Jolla, CA 92037.
Sanford Consortium for Regenerative Medicine, La Jolla, CA 92037.
Department of Pharmacology, University of California, San Diego, La Jolla, CA 92093.
Moores Cancer Center, University of California, San Diego, La Jolla, CA 92093.

Robert Damoiseaux (R)

Molecular Screening Shared Resource, California NanoSystems Institute, University of California, Los Angeles, CA 90095.

Patrick G Hogan (PG)

Division of Signaling and Gene Expression, La Jolla Institute for Immunology, La Jolla, CA 92037; phogan@lji.org.
Moores Cancer Center, University of California, San Diego, La Jolla, CA 92093.
Program in Immunology, University of California, San Diego, La Jolla, CA 92037.

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