Evidence map›Paper›PMID 18688029›Full record

ArticleThe American journal of pathology2008

Hedgehog signaling, keratin 6 induction, and sebaceous gland morphogenesis: implications for pachyonychia congenita and related conditions.

Li-Hong Gu, Pierre A Coulombe

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2008. 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
0.8field-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

23 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
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  3. Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Genetically modified laboratory mice with sebaceous glands abnormalities.Cellular and molecular life sciences : CMLS · 2016
    Review
  14. Beyond acne: Current aspects of sebaceous gland biology and function.Reviews in endocrine & metabolic disorders · 2016
    Review
  15. Article
  16. [Testosterone reduces the expression of keratinization-promoting genes in murine Meibomian glands].Der Ophthalmologe : Zeitschrift der Deutschen Ophthalmologischen Gesellschaft · 2013
    Article
  17. Article
  18. Pachyonychia congenita-associated alopecia.Case reports in pathology · 2012
    Article
  19. Article
  20. Article
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

2 authors at 1 institution in 1 country.

Li-Hong GuDepartment of Biological Chemistry, Johns Hopkins University School of Medicine, 725 N. Wolfe St., Baltimore, MD 21205, USA.
Pierre A Coulombe
Johns Hopkins University · US

Funding

TYPE II KERATIN GENES /PROTEINS IN COMPLEX EPITHELIAR01AR042047 · NIAMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI COULOMBE, PIERRE · 1995 to 2018
$7.1M
Keratin proteins and non-melanoma skin tumorsR21CA123530 · NCI · JOHNS HOPKINS UNIVERSITY · PI COULOMBE, PIERRE · 2007 to 2008
$361k
NCI NIH HHS R21 CA123530NIAMS NIH HHS R01 AR042047
6 · The paper itself

Abstract

Keratins 6a and b (K6a, K6b) belong to a subset of keratin genes with constitutive expression in epithelial appendages, and inducible expression in additional epithelia, when subjected to environmental challenges or disease. Mutations in K6a or K6b cause a broad spectrum of epithelial lesions that differentially affect nail, hair, and glands in humans. Some lesions reflect a loss of the structural support function shared by K6, other keratins, and intermediate filament proteins. The formation of sebaceous gland-derived epithelial cysts does not fit this paradigm, raising the question of the unique functions of different K6 isoforms in this setting. Here, we exploit a mouse model of constitutively expressed Gli2, a Hedgehog (Hh) signal effector, to show that K6a expression correlates with duct fate in sebaceous glands (SGs). Whether in the setting of Gli2 transgenic mice skin, which develops a prominent SG duct and additional pairs of highly branched SGs, or in wild-type mouse skin, K6a expression consistently coincides with Hh signaling in ductal tissue. Gli2 expression modestly transactivates a K6a promoter-driven reporter in heterologous systems. Our findings thus identify K6 as a marker of duct fate in SGs, partly in response to Hh signaling, with implications for the pathological expansion of SGs that arises in the context of certain keratin-based diseases and related disorders.

Indexed as

AnimalsFluorescent Antibody TechniqueGene ExpressionHedgehog ProteinsHumansImmunohistochemistryIn Situ HybridizationKeratin-6Kruppel-Like Transcription FactorsMaleMiceMice, TransgenicPachyonychia CongenitaPromoter Regions, GeneticReverse Transcriptase Polymerase Chain ReactionSebaceous GlandsGli2 protein, mouseHedgehog ProteinsKeratin-6Krt6a protein, mouseKruppel-Like Transcription FactorsZinc Finger Protein Gli2

Identifiers

PMID18688029
PMCPMC2527074
OpenAlexW55681898

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.