Evidence map›Paper›PMID 30760778›Full record

ArticleScientific reports2019

DRUGPATH - a novel bioinformatic approach identifies DNA-damage pathway as a regulator of size maintenance in human ESCs and iPSCs.

Boris Kovacic, Margit Rosner, Karin Schlangen, Nina Kramer, Markus Hengstschläger

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

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.5field-weighted citation impact, top 36% 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

5 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Human Embryo Models and Drug Discovery.International journal of molecular sciences · 2021
    Review
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

5 authors at 1 institution in 1 country.

Boris KovacicInstitute of Medical Genetics, Center for Pathobiochemistry and Genetics, Medical University of Vienna (MUV), Vienna, Austria. boris.kovacic@meduniwien.ac.at.ORCID 0000-0002-1148-4149
Margit RosnerInstitute of Medical Genetics, Center for Pathobiochemistry and Genetics, Medical University of Vienna (MUV), Vienna, Austria.
Karin SchlangenSection for Biosimulation and Bioinformatics, Center for Medical Statistics, Informatics and Intelligent Systems, Medical University of Vienna (MUV), Vienna, Austria.
Nina KramerInstitute of Medical Genetics, Center for Pathobiochemistry and Genetics, Medical University of Vienna (MUV), Vienna, Austria.
Markus HengstschlägerInstitute of Medical Genetics, Center for Pathobiochemistry and Genetics, Medical University of Vienna (MUV), Vienna, Austria.
Medical University of Vienna · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Genetic and biochemical screening approaches often fail to identify functionally relevant pathway networks because many signaling proteins contribute to multiple gene ontology pathways. We developed a DRUGPATH-approach to predict pathway-interactomes from high-content drug screen data. DRUGPATH is based upon combining z-scores of effective inhibitors with their corresponding and validated targets. We test DRUGPATH by comparing homeostatic pathways in human embryonic stem cells (hESCs), human induced pluripotent stem cells (hiPSCs) and human amniotic fluid stem cells (hAFSCs). We show that hAFSCs utilize distinct interactomes compared to hESCs/hiPSCs and that pathways orchestrating cell cycle and apoptosis are strongly interconnected, while pathways regulating survival and size are not. Interestingly, hESCs/hiPSCs regulate their size by growing exact additional sizes during each cell cycle. Chemical and genetic perturbation studies show that this "adder-model" is dependent on the DNA-damage pathway. In the future, the DRUGPATH-approach may help to predict novel pathway interactomes from high-content drug screens.

Indexed as

DNA DamageApoptosisAtaxia Telangiectasia Mutated ProteinsCell Cycle CheckpointsCell SizeComputational BiologyDimethyl SulfoxideEnzyme InhibitorsHuman Embryonic Stem CellsHumansIndazolesInduced Pluripotent Stem CellsRNA InterferenceRNA, Small InterferingSulfonamides2-(1H-indazol-4-yl)-6-(4-methanesulfonylpiperazin-1-ylmethyl)-4-morpholin-4-ylthieno(3,2-d)pyrimidineAtaxia Telangiectasia Mutated ProteinsDimethyl SulfoxideEnzyme InhibitorsIndazolesRNA, Small InterferingSulfonamides

Identifiers

PMID30760778
PMCPMC6374489
OpenAlexW2914155742

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.