Evidence map›Paper›PMID 22701667›Full record

ArticlePloS one2012

MiR-34a represses Numbl in murine neural progenitor cells and antagonizes neuronal differentiation.

Sarah K Fineberg, Poppy Datta, Colleen S Stein, Beverly L Davidson

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

31 citing papers in PubMed, 50 citations in OpenAlex.

  1. MicroRNA-34a: the bad guy in age-related vascular diseases.Cellular and molecular life sciences : CMLS · 2021
    Review
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  9. Ablation of the microRNA-17-92 cluster in neural stem cells diminishes adult hippocampal neurogenesis and cognitive function.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
    Article
  10. miR-34a in Neurophysiology and Neuropathology.Journal of molecular neuroscience : MN · 2019
    Review
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
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  19. Convergent microRNA actions coordinate neocortical development.Cellular and molecular life sciences : CMLS · 2014
    Review
  20. Stochastic simulation of notch signaling reveals novel factors that mediate the differentiation of neural stem cells.Journal of computational biology : a journal of computational molecular cell biology · 2014
    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

4 authors at 1 institution in 1 country.

Sarah K FinebergDepartment of Internal Medicine, University of Iowa, Iowa City, Iowa, United States of America.
Poppy Datta
Colleen S Stein
Beverly L Davidson
University of Iowa · US

Funding

MEDICAL SCIENTIST TRAINING PROGRAMT32GM007337 · NIGMS · UNIVERSITY OF IOWA · PI GEYER, PAMELA K., LENTZ, STEVEN R · 1985 to 2020
$15.9M
miRNA-MEDIATED MODULATION OF NEURAL PROGENITOR CELL FATER21DA025132 · NIDA · UNIVERSITY OF IOWA · PI DAVIDSON, BEVERLY L. · 2008 to 2009
$300k
NIDA NIH HHS DA025132NIDA NIH HHS R21 DA025132NIGMS NIH HHS T32 GM007337
6 · The paper itself

Abstract

MicroRNA (miRNA) function is required for normal animal development, in particular in differentiation pathways from stem cell and precursor populations. In neurogenesis, it is becoming increasingly appreciated that miRNAs act at many stages to ensure proper progression. In this study we examined the role of miR-34a in neural progenitor cells (NPC) derived from murine embryonic cortex. We found that over-expression of miR-34a in NPC significantly reduced the neuron yield upon in vitro induction of differentiation. MiR-34a has several predicted targets in the Notch pathway, which operates to balance progenitor self-renewal and differentiation during cortical neurogenesis. We tested several Notch pathway players for regulation by miR-34a in undifferentiated NPC, and found that mRNA and protein levels of Numbl, a negative regulator of Notch signaling, as well as two downstream pro-neural genes usually blocked by Notch signaling, NeuroD1 and Mash1, were diminished, while Notch1 and Cbf1 transcripts were enhanced by miR-34a over-expression. Using a luciferase reporter assay, we verified the Numbl 3'-UTR as a direct miR-34a target. Correspondingly, knock-down of endogenous miR-34a resulted in increased Numbl, NeuroD1 and Mash1, and reduced Notch1 transcript levels. Together these results implicate Numbl as a physiologically relevant target of miR-34a in NPC, allowing for enhanced Notch signaling and inhibition of neuronal differentiation. This work extends our understanding of miR-34a-mediated control of cell differentiation from cancer to mammalian nervous system development.

Indexed as

AnimalsBlotting, WesternBromodeoxyuridineCell DifferentiationCloning, MolecularDNA PrimersFlow CytometryFluorescent Antibody TechniqueGene Expression Regulation, DevelopmentalGenetic VectorsHEK293 CellsHumansIntracellular Signaling Peptides and ProteinsLuciferasesMiceMice, Inbred C57BLBromodeoxyuridineDNA PrimersIntracellular Signaling Peptides and ProteinsLuciferasesMicroRNAsMIRN34a microRNA, mouseNerve Tissue ProteinsNumbl protein, mouseReceptors, Notch

Identifiers

PMID22701667
PMCPMC3372529
OpenAlexW2085516803

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.