Bim regulation miRrors microRNA 17∼92 cluster expression in endothelial cells in vivo.

X W Meng, S H Kaufmann

Abstract readEditorialComment

In one paragraph

Article in Cell death and differentiation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it

0cells of the map it votes in

1citing papers in PubMed

–field-weighted citation impact

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

1 citing paper in PubMed.

Upregulation of microRNA-17-5p contributes to hypoxia-induced proliferation in human pulmonary artery smooth muscle cells through modulation of p21 and PTEN.Respiratory research · 2018
Article

4 · The record

Corrections and comments

Comment on
Pro-apoptotic BIM is an essential initiator of physiological endothelial cell death independent of regulation by FOXO3.2014

5 · Who and what money

Authors and funding

2 authors.

X W Meng1] Division of Oncology Research, Department of Oncology, Mayo Clinic, Rochester, MN 55905, USA [2] Department of Molecular Pharmacology and Experimental Therapeutics, Mayo Clinic, Rochester, MN 55905, USA.

S H Kaufmann1] Division of Oncology Research, Department of Oncology, Mayo Clinic, Rochester, MN 55905, USA [2] Department of Molecular Pharmacology and Experimental Therapeutics, Mayo Clinic, Rochester, MN 55905, USA.

Funding

Anticancer drug-induced BH3-only protein.Bak interactionsR01CA166741 · NCI · MAYO CLINIC ROCHESTER · PI KAUFMANN, SCOTT H · 2012 to 2016

$1.6M

NCI NIH HHS R01 CA166741

6 · The paper itself

Abstract

PubMed holds no abstract for this paper.

Indexed as

AnimalsApoptosisApoptosis Regulatory ProteinsBcl-2-Like Protein 11Endothelial CellsForkhead Box Protein O3Forkhead Transcription FactorsMembrane ProteinsProto-Oncogene ProteinsApoptosis Regulatory ProteinsBcl2l11 protein, mouseBcl-2-Like Protein 11Forkhead Box Protein O3Forkhead Transcription FactorsFoxO3 protein, mouseMembrane ProteinsProto-Oncogene Proteins

Identifiers

PMID25283596

DOI10.1038/cdd.2014.127

PMCPMC4211366

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.