Evidence map›Paper›PMID 33762306›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2021

A role for keratin 17 during DNA damage response and tumor initiation.

Raji R Nair, Joshua Hsu, Justin T Jacob, Christopher M Pineda, Ryan P Hobbs, Pierre A Coulombe

Open access · greenAbstract readVideo-Audio Media
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
3.8field-weighted citation impact, top 6% 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

29 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  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

6 authors at 2 institutions in 1 country.

Raji R NairDepartment of Cell and Developmental Biology, University of Michigan Medical School, Ann Arbor, MI 48109.ORCID 0000-0001-5086-469X
Joshua HsuDepartment of Biochemistry and Molecular Biology, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, MD 21205.
Justin T JacobDepartment of Biochemistry and Molecular Biology, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, MD 21205.ORCID 0000-0001-6978-1640
Christopher M PinedaDepartment of Cell and Developmental Biology, University of Michigan Medical School, Ann Arbor, MI 48109.ORCID 0000-0002-6114-1689
Ryan P HobbsDepartment of Biochemistry and Molecular Biology, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, MD 21205; rhobbs@pennstatehealth.psu.edu coulombe@umich.edu.ORCID 0000-0002-2827-1828
Pierre A CoulombeDepartment of Cell and Developmental Biology, University of Michigan Medical School, Ann Arbor, MI 48109; rhobbs@pennstatehealth.psu.edu coulombe@umich.edu.ORCID 0000-0003-0680-2373
Johns Hopkins University · USUniversity of Michigan · US

Funding

TRAINING IN AREAS FUNDAMENTAL TO CANCER RESEARCHT32CA009110 · NCI · JOHNS HOPKINS UNIVERSITY · PI MATUNIS, MICHAEL J., WEERARATNA, ASHANI T · 1985 to 2025
$13.1M
Non-Canonical Functions of Keratin Proteins in SkinR01AR044232 · NIAMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI COULOMBE, PIERRE · 1996 to 2020
$8.6M
Keratins as novel determinants of tumor biologyR01CA160255 · NCI · JOHNS HOPKINS UNIVERSITY · PI COULOMBE, PIERRE · 2011 to 2017
$1.9M
NCI NIH HHS R01 CA160255NCI NIH HHS T32 CA009110NIAMS NIH HHS R01 AR044232
6 · The paper itself

Abstract

High levels of the intermediate filament protein keratin 17 (K17) are associated with poor prognoses for several human carcinomas. Studies in mouse models have shown that K17 expression is positively associated with growth, survival, and inflammation in skin and that lack of K17 delays onset of tumorigenesis. K17 occurs in the nucleus of human and mouse tumor keratinocytes where it impacts chromatin architecture, gene expression, and cell proliferation. We report here that K17 is induced following DNA damage and promotes keratinocyte survival. The presence of nuclear K17 is required at an early stage of the double-stranded break (DSB) arm of the DNA damage and repair (DDR) cascade, consistent with its ability to associate with key DDR effectors, including γ-H2A.X, 53BP1, and DNA-PKcs. Mice lacking K17 or with attenuated K17 nuclear import showed curtailed initiation in a two-step skin carcinogenesis paradigm. The impact of nuclear-localized K17 on DDR and cell survival provides a basis for the link between K17 induction and poor clinical outcomes for several human carcinomas.

Indexed as

DNA Repair9,10-Dimethyl-1,2-benzanthraceneActive Transport, Cell NucleusAnimalsCarcinogenesisCarcinomaCell NucleusCell SurvivalDNA Breaks, Double-StrandedFemaleGene Knockout TechniquesHeLa CellsHumansIntravital MicroscopyKeratin-17Keratinocytes9,10-Dimethyl-1,2-benzanthraceneKeratin-17KeratinsKRT17 protein, humanKrt17 protein, mouseDNA damageintermediate filamentkeratinskintumor

Identifiers

PMID33762306
PMCPMC8020757
OpenAlexW3139446757

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.