Evidence map›Paper›PMID 18195038›Full record

ArticleMolecular and cellular biology2008

Alternative RNA splicing produces multiple forms of c-Myb with unique transcriptional activities.

John P O'Rourke, Scott A Ness

Open access · greenAbstract readComparative Study
In one paragraph

Article in Molecular and cellular biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.0field-weighted citation impact, top 12% 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

30 citing papers in PubMed, 57 citations in OpenAlex.

  1. Article
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  8. Article
  9. c-MYB and DMTF1 in Cancer.Cancer investigation · 2019
    Review
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  11. 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

2 authors at 1 institution in 1 country.

John P O'RourkeDepartment of Molecular Genetics & Microbiology, MSC08 4660, 1 University of New Mexico, Albuquerque, NM 87131-0001, USA. jorourkejr@salud.unm.edu
Scott A Ness
University of New Mexico · US

Funding

WOMEN'S CANCERS RESEARCH PROGRAMP30CA118100 · NCI · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI Yolanda Sanchez · 2005 to 2026
$57.1M
CORE--VECTOR PRODUCTIONP30DK056465 · NIDDK · FRED HUTCHINSON CANCER RESEARCH CENTER · PI HEIMFELD, SHELLY · 1999 to 2014
$14.9M
TRANSFORMING FUNCTIONS OF THE V-MYB ONCOGENE PRODUCTR01CA058443 · NCI · UNIVERSITY OF NEW MEXICO · PI NESS, SCOTT A. · 1995 to 2010
$2.6M
Myb protein specificity in human hematopoietic cellsR01CA105257 · NCI · UNIVERSITY OF NEW MEXICO · PI NESS, SCOTT A. · 2005 to 2009
$1.3M
NCI NIH HHS CA058443NCI NIH HHS CA105257NCI NIH HHS P30 CA118100NCI NIH HHS R01 CA058443NCI NIH HHS R01 CA105257NIDDK NIH HHS DK56465NIDDK NIH HHS P30 DK056465
6 · The paper itself

Abstract

The c-Myb transcription factor regulates the proliferation and differentiation of hematopoietic cells, and activated alleles of c-myb induce leukemias and lymphomas in animals. Relatively minor changes in the structure of c-Myb protein change the genes that it regulates and can unleash its latent transforming activities. Here, quantitative assays were used to analyze the alternative splicing of human c-myb transcripts. We identified an array of variant transcripts, expressed in highly regulated, lineage-specific patterns, that were formed through the use of alternate exons 8A, 9A, 9B, 10A, 13A, and 14A. Expression levels of the different splice variant transcripts were regulated independently of one another during human hematopoietic cell differentiation, and the alternative splicing of c-myb mRNAs was increased in primary leukemia samples. The alternatively spliced c-myb transcripts were associated with polysomes and encoded a series of c-Myb proteins with identical DNA binding domains but unique C-terminal domains. In several types of assays, the variant c-Myb proteins exhibited quantitative and qualitative differences in transcriptional activities and specificities. The results suggest that the human c-myb gene encodes a family of related proteins with different transcriptional activities. Enhanced alternative splicing may be a mechanism for unmasking the transforming activity of c-myb in human leukemias.

Indexed as

Alternative SplicingGenes, mybAcute DiseaseAdenocarcinomaAdultBinding SitesBreast NeoplasmsCell Line, TumorChildExonsFemaleHematopoietic Stem CellsHumansJurkat CellsK562 CellsLeukemiaNeoplasm ProteinsProtein IsoformsProto-Oncogene Proteins c-mybRecombinant Fusion Proteins

Identifiers

PMID18195038
PMCPMC2268396
OpenAlexW2126846935

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.