Evidence map›Paper›PMID 31834931›Full record

ArticleThe Journal of experimental medicine2020

Functional interactions between Mi-2β and AP1 complexes control response and recovery from skin barrier disruption.

Sayaka Shibata, Mariko Kashiwagi, Bruce A Morgan, Katia Georgopoulos

Abstract read
In one paragraph

Article in The Journal of experimental medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

8 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Keratinocytes: pleiotropic orchestrators of cutaneous immunity and Inflammation - Emerging therapeutic paradigms in dermatological pathologies.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 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

4 authors.

Sayaka ShibataCutaneous Biology Research Center, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA.
Mariko KashiwagiCutaneous Biology Research Center, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA.
Bruce A MorganCutaneous Biology Research Center, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA.
Katia GeorgopoulosCutaneous Biology Research Center, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA.

Funding

Epigenetic regulation of proinflammatory responses in the skinR01AR069132 · NIAMS · MASSACHUSETTS GENERAL HOSPITAL · PI GEORGOPOULOS, KATIA · 2016 to 2020
$1.8M
Melanocortin receptor function in the dermal papilla of the hair follicleR21AR072976 · NIAMS · MASSACHUSETTS GENERAL HOSPITAL · PI MORGAN, BRUCE A · 2018 to 2019
$391k
NIAMS NIH HHS R01 AR069132NIAMS NIH HHS R21 AR072976
6 · The paper itself

Abstract

Keratinocytes respond to environmental signals by eliciting induction of genes that preserve skin's integrity. Here we show that the transcriptional response to stress signaling is supported by short-lived epigenetic changes. Comparison of chromatin accessibility and transcriptional changes induced by barrier disruption or by loss of the nucleosome remodeler Mi-2β identified their striking convergence in mouse and human keratinocytes. Mi-2β directly repressed genes induced by barrier disruption by restricting AP1-enriched promoter-distal sites, occupied by Mi-2β and JUNB at steady state and by c-JUN after Mi-2β depletion or stress signaling. Barrier disruption led to a modest reduction in Mi-2β expression and a further selective reduction of Mi-2β localization at stress response genes, possibly through competition with activated c-JUN. Consistent with a repressive role at stress response genes, genetic ablation of Mi-2β did not prevent reestablishment of barrier integrity but was required for return to homeostasis. Thus, a competition between Mi-2β-repressive and activating AP1 complexes may permit rapid transcriptional response to and resolution from stress signaling.

Indexed as

AnimalsCells, CulturedHomeostasisHumansKeratinocytesMi-2 Nucleosome Remodeling and Deacetylase ComplexMiceMice, Inbred C57BLMice, TransgenicPromoter Regions, GeneticSignal TransductionSkinTranscription Factor AP-1Transcription, GeneticCHD4 protein, humanMi-2 Nucleosome Remodeling and Deacetylase ComplexTranscription Factor AP-1

Identifiers

PMID31834931
PMCPMC7062528

What OpenQuestion holds

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LicenceCC BY-NC-SA
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.