Evidence map›Paper›PMID 20463010›Full record

ArticleThe Journal of biological chemistry2010

Protein kinase D is implicated in the reversible commitment to differentiation in primary cultures of mouse keratinocytes.

Azadeh Jadali, Soosan Ghazizadeh

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
3.5field-weighted citation impact, top 9% 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

19 citing papers in PubMed, 35 citations in OpenAlex.

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  8. Protein kinase D signaling in cancer: A friend or foe?Biochimica et biophysica acta. Reviews on cancer · 2017
    Review
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  15. Emerging roles of protein kinase D1 in cancer.Molecular cancer research : MCR · 2011
    Review
  16. Ultraviolet activation of PKD: implications for skin cancer.Future oncology (London, England) · 2011
    Article
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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

2 authors at 1 institution in 2 countries.

Azadeh JadaliGraduate Program in Molecular and Cellular Biology, Stony Brook University, Stony Brook, New York 11794, USA.
Soosan Ghazizadeh
Stony Brook University · US

Funding

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 AR056013
6 · The paper itself

Abstract

Although commitment to epidermal differentiation is generally considered to be irreversible, differentiated keratinocytes (KCs) have been shown to maintain a regenerative potential and to reform skin epithelia when placed in a suitable environment. To obtain insights into the mechanism of reinitiation of this proliferative response in differentiated KCs, we examined the reversibility of commitment to Ca(2+)-induced differentiation. Lowering Ca(2+) concentration to micromolar levels triggered culture-wide morphological and biochemical changes, as indicated by derepression of cyclin D1, reinitiation of DNA synthesis, and acquisition of basal cell-like characteristics. These responses were inhibited by Goedecke 6976, an inhibitor of protein kinase D (PKD) and PKCalpha, but not with GF109203X, a general inhibitor of PKCs, suggesting PKD activation by a PKC-independent mechanism. PKD activation followed complex kinetics with a biphasic early transient phosphorylation within the first 6 h, followed by a sustained and progressive phosphorylation beginning at 24 h. The second phase of PKD activation was followed by prolonged ERK1/2 signaling and progression to DNA synthesis in response to the low Ca(2+) switch. Specific knockdown of PKD-1 by RNA interference or expression of a dominant negative form of PKD-1 did not have a significant effect on normal KC proliferation and differentiation but did inhibit Ca(2+)-mediated reinitiation of proliferation and reversion in differentiated cultures. The present study identifies PKD as a major regulator of a proliferative response in differentiated KCs, probably through sustained activation of the ERK-MAPK pathway, and provides new insights into the process of epidermal regeneration and wound healing.

Indexed as

Cell DifferentiationAnimalsCalciumCarbazolesCell CycleCell ProliferationCells, CulturedDose-Response Relationship, DrugEnzyme ActivationEpidermal CellsEpidermisExtracellular SpaceKeratinocytesKineticsMAP Kinase Signaling SystemMiceCalciumCarbazolesGo 6976Protein Kinase Cprotein kinase D

Identifiers

PMID20463010
PMCPMC2906330
OpenAlexW2095211227

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.