Evidence map›Paper›PMID 26527382›Full record

ArticleStem cell reports2015

Atypical PKC-iota Controls Stem Cell Expansion via Regulation of the Notch Pathway.

In Kyoung Mah, Rachel Soloff, Stephen M Hedrick, Francesca V Mariani

Open access · goldAbstract read
In one paragraph

Article in Stem cell reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

11 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Review
  3. Transcriptional Control of Apical-Basal Polarity Regulators.International journal of molecular sciences · 2021
    Review
  4. Article
  5. Article
  6. Article
  7. 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

4 authors at 2 institutions in 1 country.

In Kyoung MahBroad CIRM Center for Regenerative Medicine and Stem Cell Research, Keck School of Medicine, University of Southern California, 1425 San Pablo St., Los Angeles, CA 90033, USA.
Rachel SoloffDepartment of Biological Sciences, University of California, San Diego, La Jolla, CA 92093, USA.
Stephen M HedrickDepartment of Biological Sciences, University of California, San Diego, La Jolla, CA 92093, USA.
Francesca V MarianiBroad CIRM Center for Regenerative Medicine and Stem Cell Research, Keck School of Medicine, University of Southern California, 1425 San Pablo St., Los Angeles, CA 90033, USA. Electronic address: fmariani@usc.edu.
University of California, San Diego · USUniversity of Southern California · US

Funding

USC/NORRIS COMPREHENSIVE CANCER CENTER (CORE) SUPPORTP30CA014089 · NCI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI Fumito Ito · 1985 to 2026
$181.4M
Genetic regulation of the cartilage callus during large-scale bone repairR01AR069700 · NIAMS · UNIVERSITY OF SOUTHERN CALIFORNIA · PI MARIANI, FRANCESCA V · 2016 to 2021
$2.4M
A molecular basis for control of T cell memoryR01AI103440 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI HEDRICK, STEPHEN M · 2013 to 2017
$2.3M
NCI NIH HHS P30 CA014089NCI NIH HHS P30CA014089NIAID NIH HHS R01 AI103440NIAMS NIH HHS R01 AR069700
6 · The paper itself

Abstract

The number of stem/progenitor cells available can profoundly impact tissue homeostasis and the response to injury or disease. Here, we propose that an atypical PKC, Prkci, is a key player in regulating the switch from an expansion to a differentiation/maintenance phase via regulation of Notch, thus linking the polarity pathway with the control of stem cell self-renewal. Prkci is known to influence symmetric cell division in invertebrates; however a definitive role in mammals has not yet emerged. Using a genetic approach, we find that loss of Prkci results in a marked increase in the number of various stem/progenitor cells. The mechanism used likely involves inactivation and symmetric localization of NUMB, leading to the activation of NOTCH1 and its downstream effectors. Inhibition of atypical PKCs may be useful for boosting the production of pluripotent stem cells, multipotent stem cells, or possibly even primordial germ cells by promoting the stem cell/progenitor fate.

Indexed as

Cell Self RenewalAnimalsCells, CulturedEmbryonic Stem CellsIsoenzymesMiceProtein Kinase CProtein Kinase C-lambdaReceptor, Notch1IsoenzymesNotch1 protein, mouseProtein Kinase CProtein Kinase C-lambdaReceptor, Notch1

Identifiers

PMID26527382
PMCPMC4649379
OpenAlexW1882422544

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.