Evidence map›Paper›PMID 25973715›Full record

ArticleEuropean journal of immunology2015

Absence of both Sos-1 and Sos-2 in peripheral CD4(+) T cells leads to PI3K pathway activation and defects in migration.

Geoffrey Guittard, Robert L Kortum, Lakshmi Balagopalan, Nicolas Çuburu, Phan Nguyen, Connie L Sommers, Lawrence E Samelson

Open access · hybridAbstract read
In one paragraph

Article in European journal of immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.4field-weighted citation impact, top 17% 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

19 citing papers in PubMed, 25 citations in OpenAlex.

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  7. Ras GEF Mouse Models for the Analysis of Ras Biology and Signaling.Methods in molecular biology (Clifton, N.J.) · 2021
    Article
  8. Article
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  10. LRCH1 suppresses migration of CD4International journal of medical sciences · 2020
    Article
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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.

Geoffrey GuittardLaboratory of Cellular and Molecular Biology, Center for Cancer Research, National Cancer Institute, Bethesda, MD, USA.
Robert L KortumLaboratory of Cellular and Molecular Biology, Center for Cancer Research, National Cancer Institute, Bethesda, MD, USA.
Lakshmi BalagopalanLaboratory of Cellular and Molecular Biology, Center for Cancer Research, National Cancer Institute, Bethesda, MD, USA.
Nicolas ÇuburuLaboratory of Cellular Oncology, Center for Cancer Research, National Cancer Institute, Bethesda, MD, USA.
Phan NguyenLaboratory of Cellular and Molecular Biology, Center for Cancer Research, National Cancer Institute, Bethesda, MD, USA.
Connie L SommersLaboratory of Cellular and Molecular Biology, Center for Cancer Research, National Cancer Institute, Bethesda, MD, USA.
Lawrence E SamelsonLaboratory of Cellular and Molecular Biology, Center for Cancer Research, National Cancer Institute, Bethesda, MD, USA.
Center for Cancer Research · USNational Cancer Institute · US

Funding

Biochemical Basis of T Cell ActivationZIABC010304 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI SAMELSON, LAWRENCE · 2009 to 2025
$36.3M
BIOCHEMICAL BASIS OF T CELL ACTIVATIONZ01BC010304 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI SAMELSON, LAWRENCE E · 1999 to 2008
$2.6M
Intramural NIH HHS Z01 BC010304
6 · The paper itself

Abstract

Sos-1 and Sos-2 are ubiquitously expressed Ras-guanine exchange factors involved in Erk-MAP kinase pathway activation. Using mice lacking genes encoding Sos-1 and Sos-2, we evaluated the role of these proteins in peripheral T-cell signaling and function. Our results confirmed that TCR-mediated Erk activation in peripheral CD4(+) T cells does not depend on Sos-1 and Sos-2, although IL-2-mediated Erk activation does. Unexpectedly, however, we show an increase in AKT phosphorylation in Sos-1/2dKO CD4(+) T cells upon TCR and IL-2 stimulation. Activation of AKT was likely a consequence of increased recruitment of PI3K to Grb2 upon TCR and/or IL-2 stimulation in Sos-1/2dKO CD4(+) T cells. The increased activity of the PI3K/AKT pathway led to downregulation of the surface receptor CD62L in Sos-1/2dKO T cells and a subsequent impairment in T-cell migration.

Indexed as

AnimalsCD4-Positive T-LymphocytesCell MovementEnzyme ActivationGRB2 Adaptor ProteinInterleukin-2L-SelectinMiceMice, KnockoutPhosphatidylinositol 3-KinasesPhosphorylationProto-Oncogene Proteins c-aktReceptors, Antigen, T-CellSignal TransductionSon of Sevenless ProteinsSOS1 ProteinGRB2 Adaptor ProteinGrb2 protein, mouseInterleukin-2L-SelectinPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReceptors, Antigen, T-CellSon of Sevenless ProteinsSOS1 ProteinSos2 protein, mouseCD62LErkGrb2PI3K/AKTSignalingSosT cell

Identifiers

PMID25973715
PMCPMC4536155
OpenAlexW1921086417

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.