Evidence map›Paper›PMID 25695604›Full record

ArticleCell death & disease2015

APP intracellular domain acts as a transcriptional regulator of miR-663 suppressing neuronal differentiation.

R Shu, W Wong, Q H Ma, Z Z Yang, H Zhu, F J Liu, P Wang, J Ma, S Yan, J M Polo and 4 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell death & disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
2.6field-weighted citation impact, top 11% 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

39 citing papers in PubMed, 81 citations in OpenAlex.

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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

14 authors at 8 institutions in 4 countries.

R Shu1] Shunxi-Monash Immune Regeneration and Neuroscience Laboratories, Department of Anatomy and Developmental Biology, Monash University, Clayton, Victoria 3800, Australia [2] The Key Laboratory of Stem Cell and Regenerative Medicine, Institute of Molecular and Clinical Medicine, Kunming Medical College, Kunming 650031, China [3] Australian Regenerative Medicine Institute, Monash University, Clayton, Victoria 3800, Australia.
W Wong1] Department of Pharmacology, Yong Loo Lin School of Medicine, National University Health System, National University of Singapore, Singapore 119077, Singapore [2] Neurobiology and Ageing Programme, Life Sciences Institute, National University of Singapore, Singapore 119077, Singapore [3] Singapore Institute for Neurotechnology (SINAPSE), Singapore 117456, Singapore.
Q H MaInstitute of Neuroscience, Soochow University, Suzhou 215123, China.
Z Z Yang1] Shunxi-Monash Immune Regeneration and Neuroscience Laboratories, Department of Anatomy and Developmental Biology, Monash University, Clayton, Victoria 3800, Australia [2] The Key Laboratory of Stem Cell and Regenerative Medicine, Institute of Molecular and Clinical Medicine, Kunming Medical College, Kunming 650031, China.
H Zhu1] Shunxi-Monash Immune Regeneration and Neuroscience Laboratories, Department of Anatomy and Developmental Biology, Monash University, Clayton, Victoria 3800, Australia [2] The Key Laboratory of Stem Cell and Regenerative Medicine, Institute of Molecular and Clinical Medicine, Kunming Medical College, Kunming 650031, China.
F J Liu1] Australian Regenerative Medicine Institute, Monash University, Clayton, Victoria 3800, Australia [2] College of Animal Science and Technology, Henan University of Science and Technology, Luoyang 471000, China.
P WangDepartment of Pediatrics, Duke University School of Medicine, Durham, NC 27710, USA.
J MaShunxi-Monash Immune Regeneration and Neuroscience Laboratories, Department of Anatomy and Developmental Biology, Monash University, Clayton, Victoria 3800, Australia.
S YanThe Key Laboratory of Stem Cell and Regenerative Medicine, Institute of Molecular and Clinical Medicine, Kunming Medical College, Kunming 650031, China.
J M Polo1] Shunxi-Monash Immune Regeneration and Neuroscience Laboratories, Department of Anatomy and Developmental Biology, Monash University, Clayton, Victoria 3800, Australia [2] Australian Regenerative Medicine Institute, Monash University, Clayton, Victoria 3800, Australia.
C C A BernardAustralian Regenerative Medicine Institute, Monash University, Clayton, Victoria 3800, Australia.
L W StantonStem Cell and Developmental Biology Group, Genome Institute of Singapore, Singapore 138672, Singapore.
G S Dawe1] Department of Pharmacology, Yong Loo Lin School of Medicine, National University Health System, National University of Singapore, Singapore 119077, Singapore [2] Neurobiology and Ageing Programme, Life Sciences Institute, National University of Singapore, Singapore 119077, Singapore [3] Singapore Institute for Neurotechnology (SINAPSE), Singapore 117456, Singapore.
Z C Xiao1] Shunxi-Monash Immune Regeneration and Neuroscience Laboratories, Department of Anatomy and Developmental Biology, Monash University, Clayton, Victoria 3800, Australia [2] The Key Laboratory of Stem Cell and Regenerative Medicine, Institute of Molecular and Clinical Medicine, Kunming Medical College, Kunming 650031, China.
Monash University · AUSecond Affiliated Hospital of Kunming Medical College · CNAustralian Regenerative Medicine Institute · AUDuke University · USGenome Institute of Singapore · SGNational University Health System · SGNational University of Singapore · SGSoochow University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Amyloid precursor protein (APP) is best known for its involvement in the pathogenesis of Alzheimer's disease. We have previously demonstrated that APP intracellular domain (AICD) regulates neurogenesis; however, the mechanisms underlying AICD-mediated regulation of neuronal differentiation are not yet fully characterized. Using genome-wide chromatin immunoprecipitation approaches, we found that AICD is specifically recruited to the regulatory regions of several microRNA genes, and acts as a transcriptional regulator for miR-663, miR-3648 and miR-3687 in human neural stem cells. Functional assays show that AICD negatively modulates neuronal differentiation through miR-663, a primate-specific microRNA. Microarray data further demonstrate that miR-663 suppresses the expression of multiple genes implicated in neurogenesis, including FBXL18 and CDK6. Our results indicate that AICD has a novel role in suppression of neuronal differentiation via transcriptional regulation of miR-663 in human neural stem cells.

Indexed as

Amyloid beta-Protein PrecursorCell DifferentiationCell LineChromatin ImmunoprecipitationDNA-Binding ProteinsGene Expression RegulationHumansMicroRNAsNeuronsProtein BindingAmyloid beta-Protein PrecursorDNA-Binding ProteinsMicroRNAsMIRN663 microRNA, human

Identifiers

PMID25695604
PMCPMC4669786
OpenAlexW2076453500

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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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.