Evidence map›Paper›PMID 20354143›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2010

The death effector domain protein PEA-15 negatively regulates T-cell receptor signaling.

Sandra Pastorino, Hemamalini Renganathan, Maisel J Caliva, Erin L Filbert, John Opoku-Ansah, Florian J Sulzmaier, Joanna E Gawecka, Guy Werlen, Andrey S Shaw, Joe W Ramos

Open access · greenAbstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.7field-weighted citation impact, top 31% 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

15 citing papers in PubMed, 22 citations in OpenAlex.

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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

10 authors at 6 institutions in 1 country.

Sandra PastorinoNatural Products and Cancer Biology Program, Cancer Research Center of Hawaii, University of Hawaii at Manoa, Honolulu, Hawaii 96813, USA.
Hemamalini Renganathan
Maisel J Caliva
Erin L Filbert
John Opoku-Ansah
Florian J Sulzmaier
Joanna E Gawecka
Guy Werlen
Andrey S Shaw
Joe W Ramos
University of Hawaiʻi at Mānoa · USUniversity of Hawaii System · USCancer Center of Hawaii · USHoward Hughes Medical Institute · USRutgers, The State University of New Jersey · USWashington University in St. Louis · US

Funding

WORLDWIDE EPIDEMIOLOGY &EPIZOOTIOLOGY OF HANTAVIRUSG12RR003061 · NCRR · UNIVERSITY OF HAWAII AT MANOA · PI OSTRANDER, GARY K · 1986 to 2011
$32.3M
UHI COBRE: P3: GROUP A STREPT IN RELATION TO ACUTE RHEUMATIC FEVER IN HAWAIIP20RR018727 · NCRR · UNIVERSITY OF HAWAII AT MANOA · PI HOANG, TUNG T · 2003 to 2011
$13.8M
Regulation of Cell Signaling and AdhesionR01CA093849 · NCI · UNIVERSITY OF HAWAII AT MANOA · PI RAMOS, JOE WILLIAM · 2002 to 2006
$1.2M
Howard Hughes Medical InstituteNCI NIH HHS CA03849NCI NIH HHS R01 CA093849NCRR NIH HHS G12 RR003061NCRR NIH HHS G12RR003061NCRR NIH HHS P20 RR018727NCRR NIH HHS P20RR018727
6 · The paper itself

Abstract

PEA-15 is a death effector domain-containing phosphoprotein that binds ERK and restricts it to the cytoplasm. PEA-15 also binds to FADD and thereby blocks apoptosis induced by death receptors. Abnormal expression of PEA-15 is associated with type II diabetes and some cancers; however, its physiological function remains unclear. To determine the function of PEA-15 in vivo, we used C57BL/6 mice in which the PEA-15 coding region was deleted. We thereby found that PEA-15 regulates T-cell proliferation. PEA-15-null mice did not have altered thymic or splenic lymphocyte cellularity or differentiation. However, PEA-15 deficient T cells had increased CD3/CD28-induced nuclear translocation of ERK and increased activation of IL-2 transcription and secretion in comparison to control wild-type littermates. Indeed, activation of the T-cell receptor in wild-type mice caused PEA-15 release of ERK. In contrast, overexpression of PEA-15 in Jurkat T cells blocked nuclear translocation of ERK and IL-2 transcription. Finally, PEA-15-null T cells showed increased IL-2 dependent proliferation on stimulation. No differences in T cell susceptibility to apoptosis were found. Thus, PEA-15 is a novel player in T-cell homeostasis. As such this work may have far reaching implications in understanding how the immune response is controlled.

Indexed as

Signal TransductionActive Transport, Cell NucleusAnimalsApoptosis Regulatory ProteinsCell ProliferationExtracellular Signal-Regulated MAP KinasesHumansInterleukin-2Jurkat CellsMiceMice, Inbred C57BLMice, KnockoutPhosphoproteinsReceptors, Antigen, T-CellT-LymphocytesApoptosis Regulatory ProteinsExtracellular Signal-Regulated MAP KinasesInterleukin-2Pea15 protein, mousePhosphoproteinsReceptors, Antigen, T-Cell

Identifiers

PMID20354143
PMCPMC2909277
OpenAlexW2012321301

What OpenQuestion holds

Textmetadata
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.