Evidence map›Paper›PMID 24218583›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2013

Keratin 16 regulates innate immunity in response to epidermal barrier breach.

Juliane C Lessard, Sylvia Piña-Paz, Jeremy D Rotty, Robyn P Hickerson, Roger L Kaspar, Allan Balmain, Pierre A Coulombe

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 113 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
113citing papers in PubMed, 3 pooled it
6.4field-weighted citation impact, top 3% 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

113 citing papers in PubMed, 3 syntheses or guidelines pooled it, 201 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Trial
  5. Article
  6. Keratinocytes: A key player in skin immunity and their emerging roles in secondary lymphedema.JID innovations : skin science from molecules to population health · 2026
    Review
  7. Review
  8. Squamous-state excursions activate APOBEC3A in cancer.bioRxiv : the preprint server for biology · 2026
    Article
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  11. Article
  12. Review
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  20. Observational

53 more citing papers are in PubMed but not listed here.

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 3 institutions in 1 country.

Juliane C LessardDepartment of Biochemistry and Molecular Biology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD 21205.
Sylvia Piña-Paz
Jeremy D Rotty
Robyn P Hickerson
Roger L Kaspar
Allan Balmain
Pierre A Coulombe
Johns Hopkins University · USStanford University · USUCSF Helen Diller Family Comprehensive Cancer Center · US

Funding

Non-Canonical Functions of Keratin Proteins in SkinR01AR044232 · NIAMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI COULOMBE, PIERRE · 1996 to 2020
$8.6M
NIAMS NIH HHS AR44232NIAMS NIH HHS R01 AR044232
6 · The paper itself

Abstract

Mutations in the type I keratin 16 (Krt16) and its partner type II keratin 6 (Krt6a, Krt6b) cause pachyonychia congenita (PC), a disorder typified by dystrophic nails, painful hyperkeratotic calluses in glabrous skin, and lesions involving other epithelial appendages. The pathophysiology of these symptoms and its relationship to settings in which Krt16 and Krt6 are induced in response to epidermal barrier stress are poorly understood. We report that hyperkeratotic calluses arising in the glabrous skin of individuals with PC and Krt16 null mice share a gene expression signature enriched in genes involved in inflammation and innate immunity, in particular damage-associated molecular patterns. Transcriptional hyper-activation of damage-associated molecular pattern genes occurs following de novo chemical or mechanical irritation to ear skin and in spontaneously arising skin lesions in Krt16 null mice. Genome-wide expression analysis of normal mouse tail skin and benign proliferative lesions reveals a tight, context-dependent coregulation of Krt16 and Krt6 with genes involved in skin barrier maintenance and innate immunity. Our results uncover a role for Krt16 in regulating epithelial inflammation that is relevant to genodermatoses, psoriasis, and cancer and suggest a avenue for the therapeutic management of PC and related disorders.

Indexed as

AnimalsBlotting, WesternDNA PrimersGene Expression ProfilingGene Regulatory NetworksHumansImmunity, InnateKeratin-16Keratin-6MiceMicroarray AnalysisMicroscopy, Electron, TransmissionPachyonychia CongenitaReal-Time Polymerase Chain ReactionDNA PrimersKeratin-16Keratin-6epidermisintermediate filament

Identifiers

PMID24218583
PMCPMC3845144
OpenAlexW2045302710

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.