Evidence map›Paper›PMID 31817229›Full record

ArticleCells2019

RAC1B: A Guardian of the Epithelial Phenotype and Protector Against Epithelial-Mesenchymal Transition.

Rabea Zinn, Hannah Otterbein, Hendrik Lehnert, Hendrik Ungefroren

Open access · goldAbstract read
In one paragraph

Article in Cells, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.9field-weighted citation impact, top 13% 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

22 citing papers in PubMed, 29 citations in OpenAlex.

  1. Review
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  17. RAC1B Regulation ofCancers · 2020
    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 1 institution in 1 country.

Rabea ZinnFirst Department of Medicine, UKSH, Campus Lübeck, 23552 Lübeck, Germany.
Hannah OtterbeinFirst Department of Medicine, UKSH, Campus Lübeck, 23552 Lübeck, Germany.
Hendrik LehnertFirst Department of Medicine, UKSH, Campus Lübeck, 23552 Lübeck, Germany.
Hendrik UngefrorenFirst Department of Medicine, UKSH, Campus Lübeck, 23552 Lübeck, Germany.
Universitäres Kinderwunschzentrum Lübeck · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The small GTPase Ras-related C3 botulinum toxin substrate 1B (RAC1B) has been shown to potently inhibit transforming growth factor (TGF)-β1-induced cell migration and epithelial-mesenchymal transition (EMT) in pancreatic and breast epithelial cells, but the underlying mechanism has remained obscure. Using a panel of pancreatic ductal adenocarcinoma (PDAC)-derived cell lines of different differentiation stages, we show that RAC1B is more abundantly expressed in well differentiated as opposed to poorly differentiated cells. Interestingly, RNA interference-mediated knockdown of RAC1B decreased expression of the epithelial marker protein E-cadherin, encoded by

Indexed as

Epithelial-Mesenchymal TransitionAntigens, CDCadherinsCarcinomaCell Line, TumorCell MovementEpithelial CellsHumansMAP Kinase Signaling SystemMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Pancreatic NeoplasmsPhenotyperac1 GTP-Binding ProteinSnail Family Transcription FactorsTransforming Growth Factor betaAntigens, CDCadherinsCDH1 protein, humanMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3rac1 GTP-Binding ProteinRAC1 protein, humanSNAI1 protein, humanSnail Family Transcription FactorsTransforming Growth Factor betaVimentinepithelial-mesenchymal transitionextracellular signal-regulated kinasepancreatic ductal adenocarcinomaRAC1RAC1BRho GTPasesignalingtransforming growth factor-β

Identifiers

PMID31817229
PMCPMC6952788
OpenAlexW2992889814

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.