Evidence map›Paper›PMID 24424521›Full record

ArticleMucosal immunology2014

Mouse and human Notch-1 regulate mucosal immune responses.

D R Mathern, L E Laitman, Z Hovhannisyan, D Dunkin, S Farsio, T J Malik, G Roda, A Chitre, A C Iuga, G Yeretssian and 2 more

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Mucosal immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

23 citing papers in PubMed, 51 citations in OpenAlex.

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  12. Co-Expression Analysis Reveals Mechanisms Underlying the Varied Roles of NOTCH1 in NSCLC.Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer · 2019
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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

12 authors at 3 institutions in 1 country.

D R MathernImmunology Institute, Icahn School of Medicine at Mount Sinai, New York, New York, USA.
L E LaitmanImmunology Institute, Icahn School of Medicine at Mount Sinai, New York, New York, USA.
Z HovhannisyanImmunology Institute, Icahn School of Medicine at Mount Sinai, New York, New York, USA.
D DunkinDivision of Pediatric Gastroenterology, Icahn School of Medicine at Mount Sinai, New York, New York, USA.
S FarsioImmunology Institute, Icahn School of Medicine at Mount Sinai, New York, New York, USA.
T J MalikImmunology Institute, Icahn School of Medicine at Mount Sinai, New York, New York, USA.
G RodaImmunology Institute, Icahn School of Medicine at Mount Sinai, New York, New York, USA.
A Chitre1] Immunology Institute, Icahn School of Medicine at Mount Sinai, New York, New York, USA [2] Division of Experimental Medicine, San Francisco General Hospital, University of California, San Francisco, San Francisco, California, USA.
A C Iuga1] Immunology Institute, Icahn School of Medicine at Mount Sinai, New York, New York, USA [2] Department of Pathology and Cell Biology, Columbia University Medical Center, New York, New York, USA.
G YeretssianImmunology Institute, Icahn School of Medicine at Mount Sinai, New York, New York, USA.
M C BerinDivision of Pediatric Allergy and Immunology, Icahn School of Medicine at Mount Sinai, New York, New York, USA.
S DahanImmunology Institute, Icahn School of Medicine at Mount Sinai, New York, New York, USA.
Icahn School of Medicine at Mount Sinai · USColumbia University Irving Medical Center · USSan Francisco General Hospital · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The Notch-1 signaling pathway is responsible for homeostatic tight junction expression in vitro, and promotes barrier function in vivo in the RAG1-adoptive transfer model of colitis. In this study, we sought to determine the role of colonic Notch-1 in the lymphoepithelial crosstalk in health and disease. We utilized in vivo and in vitro knockdown to target the expression of Notch-1. We identified that epithelial Notch-1 is required for appropriate activation of intestinal epithelial cells at steady state and upon inflammatory stimulus. Notch-1 expression modulates mucosal chemokine and cytokine secretion, and FoxP3 and effector T-cell responses. We showed that epithelial Notch-1 controls the immune function of the epithelium through crosstalk with the nuclear factor-κB (NF-κB)/mitogen-activated protein kinase (MAPK) pathways that, in turn, elicits T-cell responses. Overall, epithelial Notch-1 bridges innate and adaptive immunity in the gut. Our findings highlight an indispensable role for Notch-1-mediated signaling in the intricate epithelial-immune crosstalk, and validate that epithelial Notch-1 is necessary and sufficient to support protective epithelial proinflammatory responses.

Indexed as

AnimalsCell LineChemokinesColitisColonCytokinesDisease Models, AnimalGene Expression RegulationGene Knockdown TechniquesHumansImmunity, MucosalInflammation MediatorsMiceMucous MembraneReceptor, Notch1Severity of Illness IndexChemokinesCytokinesInflammation MediatorsReceptor, Notch1Tight Junction Proteins

Identifiers

PMID24424521
OpenAlexW2083344417

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.