Article in Journal of immunology (Baltimore, Md. : 1950), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.2field-weighted citation impact, top 58% 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
1 citing paper in PubMed, 2 citations in OpenAlex.
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
8 authors at 2 institutions in 1 country.
Richard Virgen-SlaneLaboratory of Molecular Immunology, Infectious and Inflammatory Diseases Center, Sanford Burnham Prebys Medical Discovery Institute, La Jolla, CA 92037.ORCID 0000-0002-0011-3844
Ricardo G CorreaLaboratory of Molecular Immunology, Infectious and Inflammatory Diseases Center, Sanford Burnham Prebys Medical Discovery Institute, La Jolla, CA 92037.ORCID 0000-0001-6940-7034
Parham Ramezani-RadNational Cancer Institute-Designated Cancer Center, Sanford Burnham Prebys Medical Discovery Institute, La Jolla, CA 92037; and.
Seth Steen-FuentesLaboratory of Molecular Immunology, Infectious and Inflammatory Diseases Center, Sanford Burnham Prebys Medical Discovery Institute, La Jolla, CA 92037.ORCID 0000-0001-7984-5548
Thiago DetanicoLaboratory of Molecular Immunology, Infectious and Inflammatory Diseases Center, Sanford Burnham Prebys Medical Discovery Institute, La Jolla, CA 92037.
Michael J DiCandidoDepartment of Immunology and Respiratory Disease Research, Boehringer Ingelheim Pharmaceuticals, Inc., Ridgefield, CT 06877.
Jun LiDepartment of Immunology and Respiratory Disease Research, Boehringer Ingelheim Pharmaceuticals, Inc., Ridgefield, CT 06877.
Carl F WareLaboratory of Molecular Immunology, Infectious and Inflammatory Diseases Center, Sanford Burnham Prebys Medical Discovery Institute, La Jolla, CA 92037; cware@sbpdiscovery.org.ORCID 0000-0002-5006-418X
Sanford Burnham Prebys Medical Discovery Institute · USBoehringer Ingelheim (United States) · US
Funding
Tumor Microenvironment and Cancer ImmunologyP30CA030199 · NCI · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI ELENA B PASQUALE · 1985 to 2026
$107.2M
Virology CoreP01CA177322 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI WU, TING-TING · 2014 to 2018
$8.7M
HVEM-BTLA system in InflammationR01AI067890 · NIAID · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI WARE, CARL F · 2007 to 2016
$4.3M
Rheumatic Diseases Research Training GrantT32AR064194 · NIAMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI GARY S FIRESTEIN, Monica Guma · 2013 to 2026
$3.8M
HVEM-BTLA Pathway in LymphomaR01CA164679 · NCI · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI WARE, CARL F · 2012 to 2016
Lymphotoxin β receptor (LTβR) signaling is crucial for lymphoid tissue organogenesis and immune homeostasis. To identify novel regulatory mechanisms for signaling, we implemented a two-step screen that uses coexpression analysis of human fibroblasts undergoing LTβR stimulation and affinity-purification mass spectrometry for the LTβR signaling protein TNFR-associated factor 3 (TRAF3). We identify Ewing sarcoma (EWS) protein as a novel LTβR signaling component that associates with TRAF3 but not with TNFR-associated factor 2 (TRAF2). The EWS:TRAF3 complex forms under unligated conditions that are disrupted following activation of the LTβR. We conclude that EWS limits expression of proinflammatory molecules, GM-CSF, and ERK-2, promoting immune homeostasis.
Indexed as
Granulocyte-Macrophage Colony-Stimulating FactorHEK293 CellsHumansLymphotoxin beta ReceptorMAP Kinase Signaling SystemMitogen-Activated Protein Kinase 1Multiprotein ComplexesRNA-Binding Protein EWSTNF Receptor-Associated Factor 2TNF Receptor-Associated Factor 3EWSR1 protein, humanGranulocyte-Macrophage Colony-Stimulating FactorLTBR protein, humanLymphotoxin beta ReceptorMAPK1 protein, humanMitogen-Activated Protein Kinase 1Multiprotein ComplexesPSMD2 protein, humanRNA-Binding Protein EWSTNF Receptor-Associated Factor 2TNF Receptor-Associated Factor 3TRAF3 protein, human
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.
Cutting Edge: The RNA-Binding Protein Ewing Sarcoma Is a Novel Modulator of Lymphotoxin β Receptor Signaling. · full record | OpenQuestion