Evidence map›Paper›PMID 29302052›Full record

ArticleGenes and immunity2019

The Act1 D10N missense variant impairs CD40 signaling in human B-cells.

Ning Yu, Sylviane Lambert, Joshua Bornstein, Rajan P Nair, Charlotta Enerbäck, James T Elder

Open access · greenAbstract read
In one paragraph

Article in Genes and immunity, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.3field-weighted citation impact, top 46% 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

2 citing papers in PubMed, 5 citations in OpenAlex.

  1. N4BP1 acts as a potent negative regulator of IL-17 signaling by blocking the translation of Act1 mRNA.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Article
  2. Article
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

6 authors at 1 institution in 2 countries.

Ning YuDepartment of Dermatology, University of Michigan, Ann Arbor, MI, USA. ning_yu@vip.163.com.
Sylviane LambertDepartment of Dermatology, University of Michigan, Ann Arbor, MI, USA.
Joshua BornsteinDepartment of Dermatology, University of Michigan, Ann Arbor, MI, USA.
Rajan P NairDepartment of Dermatology, University of Michigan, Ann Arbor, MI, USA.
Charlotta EnerbäckDepartment of Dermatology, University of Michigan, Ann Arbor, MI, USA.
James T ElderDepartment of Dermatology, University of Michigan, Ann Arbor, MI, USA. jelder@umich.edu.
University of Michigan–Ann Arbor · US

Funding

Linkage analysis of familial psoriasis(Supplement)R01AR042742 · NIAMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI ELDER, JAMES TILFORD · 1994 to 2021
$10.1M
Genetic and Genomic Dissection of Psoriatic ArthritisR01AR063611 · NIAMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI ELDER, JAMES TILFORD, GLADMAN, DAFNA D · 2012 to 2023
$6.2M
Identification of Psoriatic Arthritis Genes in the MHCR01AR050511 · NIAMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI ELDER, JAMES TILFORD · 2004 to 2013
$4.2M
Combined Analysis of Gene Expression and DNA Variation in PsoriasisR01AR054966 · NIAMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI ELDER, JAMES TILFORD · 2007 to 2011
$3.2M
Functional Genomics of PsoriasisR01AR065183 · NIAMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI ELDER, JAMES TILFORD · 2013 to 2016
$1.7M
NIAMS NIH HHS R01 AR042742NIAMS NIH HHS R01 AR050511NIAMS NIH HHS R01 AR054966NIAMS NIH HHS R01 AR063611NIAMS NIH HHS R01 AR065183
6 · The paper itself

Abstract

The TRAF3IP2 gene resides within one of at least 63 psoriasis susceptibility loci and encodes Act1, an adapter protein involved in IL-17 receptor and CD40 signaling pathways. TRAF3IP2 is distinctive (among <10% of candidate susceptibility genes) in that a strongly disease-associated variant encodes a missense SNP predicted to be functionally relevant (SNP rs33980500 C/T encoding Act1 pD10N). As assessed by flow cytometry, Act1 protein was expressed at the highest levels in monocytes, with lower levels in T-cells and B-cells. However, monocytes, T-cells and B-cells failed to respond to IL-17A stimulation of PBMC, as measured by flow cytometric determination of NF-κB phospho-p65. As an alternative stimulus, we treated PBMCs with trimerized recombinant human CD40L and assessed p65, p38 and Erk phosphorylation in CD19

Indexed as

MAP Kinase Signaling SystemAdaptor Proteins, Signal TransducingAdultAgedAged, 80 and overB-LymphocytesCD40 AntigensCells, CulturedFemaleHumansMaleMiddle AgedMitogen-Activated Protein Kinase 3Mutation, Missensep38 Mitogen-Activated Protein KinasesPsoriasisAdaptor Proteins, Signal TransducingCD40 AntigensMitogen-Activated Protein Kinase 3p38 Mitogen-Activated Protein KinasesTRAF3IP2 protein, humanTranscription Factor RelATumor Necrosis Factor Receptor-Associated Peptides and Proteins

Identifiers

PMID29302052
PMCPMC6033699
OpenAlexW2781630806

What OpenQuestion 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 OpenQuestion graph.