Evidence map›Paper›PMID 24213370›Full record

ArticleThe Journal of investigative dermatology2014

Protein kinase D1 has a key role in wound healing and skin carcinogenesis.

Mohammad Rashel, Ninche Alston, Soosan Ghazizadeh

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of investigative dermatology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

14 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Potential role for protein kinase D inhibitors in prostate cancer.Journal of molecular medicine (Berlin, Germany) · 2023
    Review
  5. Review
  6. Review
  7. Review
  8. An Oxidative Stress-Related Gene Pair (Frontiers in immunology · 2021
    Article
  9. Review
  10. Article
  11. Protein kinase D signaling in cancer: A friend or foe?Biochimica et biophysica acta. Reviews on cancer · 2017
    Review
  12. Review
  13. Article
  14. 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

3 authors at 2 institutions in 1 country.

Mohammad RashelDepartment of Oral Biology and Pathology, Stony Brook University, Stony Brook, New York, USA.
Ninche AlstonDepartment of Oral Biology and Pathology, Stony Brook University, Stony Brook, New York, USA.
Soosan GhazizadehDepartment of Oral Biology and Pathology, Stony Brook University, Stony Brook, New York, USA. Electronic address: soosan.ghazizadeh@stonybrook.edu.
Stony Brook University · USStony Brook School · US

Funding

Role of Protein Kinase D in Skin EpitheliaR21AR061058 · NIAMS · STATE UNIVERSITY NEW YORK STONY BROOK · PI GHAZIZADEH, SOOSAN · 2011 to 2012
$396k
Skin regeneration by terminally differentiated keratinocytesR21AR056013 · NIAMS · STATE UNIVERSITY NEW YORK STONY BROOK · PI GHAZIZADEH, SOOSAN · 2008 to 2009
$372k
NIAMS NIH HHS AR056013NIAMS NIH HHS R21 AR056013NIAMS NIH HHS R21 AR061058
6 · The paper itself

Abstract

Protein kinase D (PKD) is a family of stress-responsive serine/threonine kinases implicated in the regulation of diverse cellular functions including cell growth, differentiation, apoptosis, and cell motility. Although all three isoforms are expressed in keratinocytes, their role in skin biology and pathology is poorly understood. We recently identified a critical role for PKD1 during reversal of keratinocyte differentiation in culture, suggesting a potential proproliferative role in epidermal adaptive responses. Here, we generated mice with targeted deletion of PKD1 in the epidermis to evaluate the significance of PKD1 in normal and hyperplastic conditions. These mice displayed a normal skin phenotype, indicating that PKD1 is dispensable for skin development and homeostasis. Upon wounding, however, PKD1-deficient mice exhibited delayed wound re-epithelialization correlated with a reduced proliferation and migration of keratinocytes at the wound edge. In addition, the hyperplastic and inflammatory responses to topical phorbol ester were significantly suppressed, suggesting involvement of PKD1 in tumor promotion. Consistently, when subjected to the two-stage chemical skin carcinogenesis protocol, PKD1-deficient mice were resistant to papilloma formation when compared with control littermates. These results revealed a critical proproliferative role for PKD1 in epidermal adaptive responses, suggesting a potential therapeutic target in skin wound and cancer treatment.

Indexed as

Gene Expression Regulation, NeoplasticWound HealingAnimalsCarcinogenesisCell DifferentiationCell MovementCell ProliferationEpidermisFemaleGene DeletionHomeostasisInflammationKeratinocytesMaleMiceMice, KnockoutProtein Kinase Cprotein kinase D

Identifiers

PMID24213370
PMCPMC3961536
OpenAlexW2162010184

What OpenQuestion holds

Textmetadata
LicenceTDM
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.