Evidence map›Paper›PMID 37566514›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2023

Cutting Edge: Induced Loss of Rasgrp1 in Peripheral CD4+ T Cells of Conditional Rasgrp1-Deficient Mice Reveals an Essential Role for Rasgrp1 in TCR/CD28-Induced Ras-MAPK Signaling.

Yating Chang, Praveen Manivannan, Abbas Doosti, Philip E Lapinski, Di Chen, Jeroen P Roose, Philip D King

Open access · greenAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.8field-weighted citation impact, top 25% 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

3 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
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

7 authors at 2 institutions in 1 country.

Yating ChangDepartment of Microbiology and Immunology, University of Michigan Medical School, Ann Arbor, MI.
Praveen ManivannanDepartment of Microbiology and Immunology, University of Michigan Medical School, Ann Arbor, MI.ORCID 0000-0002-2679-8626
Abbas DoostiDepartment of Microbiology and Immunology, University of Michigan Medical School, Ann Arbor, MI.ORCID 0000-0001-8052-5963
Philip E LapinskiDepartment of Microbiology and Immunology, University of Michigan Medical School, Ann Arbor, MI.
Di ChenDepartment of Microbiology and Immunology, University of Michigan Medical School, Ann Arbor, MI.ORCID 0000-0001-9509-2814
Jeroen P RooseDepartment of Anatomy, University of California, San Francisco, San Francisco, CA.ORCID 0000-0003-4746-2811
Philip D KingDepartment of Microbiology and Immunology, University of Michigan Medical School, Ann Arbor, MI.ORCID 0000-0002-5598-2748
University of Michigan · USUniversity of California, San Francisco · US

Funding

Understand the metabolic fitness of naïve T cellsP01AI091580 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI ARTHUR WEISS · 2011 to 2026
$31.1M
Roles of Macropinocytosis in HIV-1 infection of CD4+ T CellsR01AI165381 · NIAID · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI KING, PHILIP D, ONO, AKIRA · 2022 to 2025
$2.6M
NIAID NIH HHS P01 AI091580NIAID NIH HHS R01 AI165381
6 · The paper itself

Abstract

Ras guanine nucleotide-releasing protein 1 (Rasgrp1) is a Ras guanine nucleotide exchange factor that participates in the activation of the Ras-ERK signaling pathway in developing T cells and is required for efficient thymic T cell positive selection. However, the role of Rasgrp1 in mature peripheral T cells has not been definitively addressed, in part because peripheral T cells from constitutive Rasgrp1-deficient mice show an abnormal activated phenotype. In this study, we generated an inducible Rasgrp1-deficient mouse model to allow acute disruption of Rasgrp1 in peripheral CD4+ T cells in the context of normal T cell development. TCR/CD28-mediated activation of Ras-ERK signaling was blocked in Rasgrp1-deficient peripheral CD4+ T cells. Furthermore, Rasgrp1-deficient CD4+ T cells were unable to synthesize IL-2 and the high-affinity IL-2R and were unable to proliferate in response to TCR/CD28 stimulation. These findings highlight an essential function for Rasgrp1 for TCR/CD28-induced Ras-ERK activation in peripheral CD4+ T cells.

Indexed as

CD28 AntigensCD4-Positive T-LymphocytesAnimalsGuanine Nucleotide Exchange FactorsMiceMice, KnockoutReceptors, Antigen, T-CellCD28 AntigensGuanine Nucleotide Exchange FactorsRasgrp1 protein, mouseReceptors, Antigen, T-Cell

Identifiers

PMID37566514
PMCPMC10529702
OpenAlexW4385761183

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.