Evidence map›Paper›PMID 26831087›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2016

Tle1 tumor suppressor negatively regulates inflammation in vivo and modulates NF-κB inflammatory pathway.

Selvi Ramasamy, Borja Saez, Subhankar Mukhopadhyay, Daching Ding, Alwiya M Ahmed, Xi Chen, Ferdinando Pucci, Rae'e Yamin, Jianfeng Wang, Mikael J Pittet and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed, 1 pooled it
3.1field-weighted citation impact, top 9% 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

50 citing papers in PubMed, 1 synthesis or guideline pooled it, 71 citations in OpenAlex.

  1. Pooled it
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  5. Uncovering cancer dependencies in peptide-interacting protein pockets.bioRxiv : the preprint server for biology · 2026
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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

13 authors at 5 institutions in 2 countries.

Selvi RamasamyDepartment of Pediatrics, Divisions of Medical Genetics and Pediatric Hematology/Oncology, MassGeneral Hospital for Children, Center for Human Genetics Research and MGH Cancer Center, Massachusetts General Hospital, Boston, MA 02114; dsweetser@mgh.harvard.edu sramasamy2@partners.org.
Borja SaezCenter for Regenerative Medicine, Massachusetts General Hospital, Boston, MA 02114; Department of Stem Cell and Regenerative Biology, Harvard University, Cambridge, MA 02138; Harvard Stem Cell Institute, Cambridge, MA 02138;
Subhankar MukhopadhyayMicrobial Pathogenesis Group, Wellcome Trust Sanger Institute, Hinxton, Cambridge CB10 1SA, United Kingdom;
Daching DingDepartment of Pediatrics, Divisions of Medical Genetics and Pediatric Hematology/Oncology, MassGeneral Hospital for Children, Center for Human Genetics Research and MGH Cancer Center, Massachusetts General Hospital, Boston, MA 02114;
Alwiya M AhmedDepartment of Pediatric Surgery, MassGeneral Hospital for Children, Massachusetts General Hospital, Boston, MA 02114;
Xi ChenDepartment of Pediatrics, Divisions of Medical Genetics and Pediatric Hematology/Oncology, MassGeneral Hospital for Children, Center for Human Genetics Research and MGH Cancer Center, Massachusetts General Hospital, Boston, MA 02114;
Ferdinando PucciCenter for Systems Biology, Massachusetts General Hospital, Boston, MA 02114.
Rae'e YaminDepartment of Pediatrics, Divisions of Medical Genetics and Pediatric Hematology/Oncology, MassGeneral Hospital for Children, Center for Human Genetics Research and MGH Cancer Center, Massachusetts General Hospital, Boston, MA 02114;
Jianfeng WangDepartment of Pediatrics, Divisions of Medical Genetics and Pediatric Hematology/Oncology, MassGeneral Hospital for Children, Center for Human Genetics Research and MGH Cancer Center, Massachusetts General Hospital, Boston, MA 02114;
Mikael J PittetCenter for Systems Biology, Massachusetts General Hospital, Boston, MA 02114.
Cassandra M KelleherDepartment of Pediatric Surgery, MassGeneral Hospital for Children, Massachusetts General Hospital, Boston, MA 02114;
David T ScaddenCenter for Regenerative Medicine, Massachusetts General Hospital, Boston, MA 02114; Department of Stem Cell and Regenerative Biology, Harvard University, Cambridge, MA 02138; Harvard Stem Cell Institute, Cambridge, MA 02138;
David A SweetserDepartment of Pediatrics, Divisions of Medical Genetics and Pediatric Hematology/Oncology, MassGeneral Hospital for Children, Center for Human Genetics Research and MGH Cancer Center, Massachusetts General Hospital, Boston, MA 02114; dsweetser@mgh.harvard.edu sramasamy2@partners.org.
Massachusetts General Hospital · USCenter for Human Genetics · USCenter for Systems Biology · USHarvard Stem Cell Institute · USWellcome Sanger Institute · GB

Funding

Molecular Analysis of Del(9q) Acute Myeloid LeukemiaR01CA115772 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI SWEETSER, DAVID A · 2006 to 2010
$2.0M
NCI NIH HHS R01 CA115772
6 · The paper itself

Abstract

Tle1 (transducin-like enhancer of split 1) is a corepressor that interacts with a variety of DNA-binding transcription factors and has been implicated in many cellular functions; however, physiological studies are limited. Tle1-deficient (Tle1(Δ/Δ)) mice, although grossly normal at birth, exhibit skin defects, lung hypoplasia, severe runting, poor body condition, and early mortality. Tle1(Δ/Δ) mice display a chronic inflammatory phenotype with increased expression of inflammatory cytokines and chemokines in the skin, lung, and intestine and increased circulatory IL-6 and G-CSF, along with a hematopoietic shift toward granulocyte macrophage progenitor and myeloid cells. Tle1(Δ/Δ) macrophages produce increased inflammatory cytokines in response to Toll-like receptor (TLR) agonists and lipopolysaccharides (LPS), and Tle1(Δ/Δ) mice display an enhanced inflammatory response to ear skin 12-O-tetradecanoylphorbol-13-acetate treatment. Loss of Tle1 not only results in increased phosphorylation and activation of proinflammatory NF-κB but also results in decreased Hes1 (hairy and enhancer of split-1), a negative regulator of inflammation in macrophages. Furthermore, Tle1(Δ/Δ) mice exhibit accelerated growth of B6-F10 melanoma xenografts. Our work provides the first in vivo evidence, to our knowledge, that TLE1 is a major counterregulator of inflammation with potential roles in a variety of inflammatory diseases and in cancer progression.

Indexed as

Genes, Tumor SuppressorAnimalsCo-Repressor ProteinsInflammationMiceMice, TransgenicNF-kappa BCo-Repressor ProteinsNF-kappa BTle1 protein, mouseHES1inflammationNF-κBTLE1tumor suppressor

Identifiers

PMID26831087
PMCPMC4763742
OpenAlexW2255106017

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.