Evidence map›Paper›PMID 23153826›Full record

ReviewBiochimica et biophysica acta

Dysregulation of RNA polymerase I transcription during disease.

K M Hannan, E Sanij, L I Rothblum, R D Hannan, R B Pearson

Open access · greenAbstract readReview
In one paragraph

Review in Biochimica et biophysica acta. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed
4.7field-weighted citation impact, top 4% 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

75 citing papers in PubMed, 140 citations in OpenAlex.

  1. Article
  2. Article
  3. Fibrillarin: bridging ribosome biogenesis and apoptosis in cellular stress and disease.Apoptosis : an international journal on programmed cell death · 2026
    Review
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15 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

5 authors at 2 institutions in 2 countries.

K M HannanOncogenic Signalling and Growth Control Program, Peter MacCallum Cancer Centre, Locked Bag 1, A'Beckett St, Melbourne, Victoria 8006, Australia.
E Sanij
L I Rothblum
R D Hannan
R B Pearson
Peter MacCallum Cancer Centre · AUUniversity of Oklahoma Health Sciences Center · US

Funding

Ribosome Biogenesis: A Molecular Checkpoint for Cardiac HypertrophyR01HL077814 · NHLBI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI ROTHBLUM, LAWRENCE I · 2006 to 2009
$1.4M
Protein interactions and initiation by RNA polymerase IR01GM069841 · NIGMS · WEIS CENTER FOR RESEARCH-GEISINGER CLINC · PI ROTHBLUM, LAWRENCE I · 2005 to 2008
$874k
NHLBI NIH HHS R01 HL077814NIGMS NIH HHS R01 GM069841PHS HHS R01
6 · The paper itself

Abstract

Transcription of the ribosomal RNA genes by the dedicated RNA polymerase I enzyme and subsequent processing of the ribosomal RNA are fundamental control steps in the synthesis of functional ribosomes. Dysregulation of Pol I transcription and ribosome biogenesis is linked to the etiology of a broad range of human diseases. Diseases caused by loss of function mutations in the molecular constituents of the ribosome, or factors intimately associated with RNA polymerase I transcription and processing are collectively termed ribosomopathies. Ribosomopathies are generally rare and treatment options are extremely limited tending to be more palliative than curative. Other more common diseases are associated with profound changes in cellular growth such as cardiac hypertrophy, atrophy or cancer. In contrast to ribosomopathies, altered RNA polymerase I transcriptional activity in these diseases largely results from dysregulated upstream oncogenic pathways or by direct modulation by oncogenes or tumor suppressors at the level of the RNA polymerase I transcription apparatus itself. Ribosomopathies associated with mutations in ribosomal proteins and ribosomal RNA processing or assembly factors have been covered by recent excellent reviews. In contrast, here we review our current knowledge of human diseases specifically associated with dysregulation of RNA polymerase I transcription and its associated regulatory apparatus, including some cases where this dysregulation is directly causative in disease. We will also provide insight into and discussion of possible therapeutic approaches to treat patients with dysregulated RNA polymerase I transcription. This article is part of a Special Issue entitled: Transcription by Odd Pols.

Indexed as

Gene Expression RegulationTranscription, GeneticAnimalsGenetic Diseases, InbornHumansRibosomal ProteinsRNA Polymerase IRNA, RibosomalTranscription Factors, TFIIIRibosomal ProteinsRNA Polymerase IRNA, RibosomalTranscription Factors, TFIII

Identifiers

PMID23153826
PMCPMC3594452
OpenAlexW1979170620

What OpenQuestion holds

Textmetadata
LicenceTDM
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.