Evidence map›Paper›PMID 20495997›Full record

ReviewCellular and molecular life sciences : CMLS2010

Post-transcriptional control during chronic inflammation and cancer: a focus on AU-rich elements.

Khalid S A Khabar

Open access · hybridAbstract readReview
In one paragraph

Review in Cellular and molecular life sciences : CMLS, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 papers.

0numbers the graph read from it
0cells of the map it votes in
95citing papers in PubMed
7.8field-weighted citation impact, top 2% 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

95 citing papers in PubMed, 156 citations in OpenAlex.

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35 more citing papers are in PubMed but not listed here.

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

1 author at 1 institution in 1 country.

Khalid S A KhabarProgram in BioMolecular Research, King Faisal Specialist Hospital and Research Center, Riyadh, 11211, Saudi Arabia. khabar@kfshrc.edu.sa
King Faisal Specialist Hospital & Research Centre · SA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A considerable number of genes that code for AU-rich mRNAs including cytokines, growth factors, transcriptional factors, and certain receptors are involved in both chronic inflammation and cancer. Overexpression of these genes is affected by aberrations or by prolonged activation of several signaling pathways. AU-rich elements (ARE) are important cis-acting short sequences in the 3'UTR that mediate recognition of an array of RNA-binding proteins and affect mRNA stability and translation. This review addresses the cellular and molecular mechanisms that are common between inflammation and cancer and that also govern ARE-mediated post-transcriptional control. The first part examines the role of the ARE-genes in inflammation and cancer and sequence characteristics of AU-rich elements. The second part addresses the common signaling pathways in inflammation and cancer that regulate the ARE-mediated pathways and how their deregulations affect ARE-gene regulation and disease outcome.

Indexed as

3' Untranslated RegionsAlternative SplicingBase CompositionCyclooxygenase 2Gene Expression RegulationHumansInflammationMitogen-Activated Protein KinasesModels, BiologicalNeoplasmsPhosphatidylinositol 3-KinasesRNA, MessengerSignal TransductionTumor Necrosis Factor-alphaVascular Endothelial Growth Factor A3' Untranslated RegionsCyclooxygenase 2Mitogen-Activated Protein KinasesPhosphatidylinositol 3-KinasesPTGS2 protein, humanRNA, MessengerTumor Necrosis Factor-alphaVascular Endothelial Growth Factor A

Identifiers

PMID20495997
PMCPMC2921490
OpenAlexW2032598909

What OpenQuestion holds

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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.