Evidence map›Paper›PMID 9032278›Full record

ArticleMolecular and cellular biology1997

E2a-Pbx1 induces aberrant expression of tissue-specific and developmentally regulated genes when expressed in NIH 3T3 fibroblasts.

X Fu, M P Kamps

Open access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

27 citing papers in PubMed, 100 citations in OpenAlex.

  1. Review
  2. FXYD5: Na(+)/K(+)-ATPase Regulator in Health and Disease.Frontiers in cell and developmental biology · 2016
    Review
  3. Article
  4. Detection of E2A-PBX1 fusion transcripts in human non-small-cell lung cancer.Journal of experimental & clinical cancer research : CR · 2013
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Function of FXYD proteins, regulators of Na, K-ATPase.Journal of bioenergetics and biomembranes · 2005
    Review
  15. Article
  16. Identification of a purine-rich intronic enhancer element in the mouse eosinophil-associated ribonuclease 2 (mEar 2) gene.Mammalian genome : official journal of the International Mammalian Genome Society · 2004
    Article
  17. Article
  18. Phospholemman (FXYD1) associates with Na,K-ATPase and regulates its transport properties.Proceedings of the National Academy of Sciences of the United States of America · 2002
    Article
  19. Article
  20. Dysadherin, a cancer-associated cell membrane glycoprotein, down-regulates E-cadherin and promotes metastasis.Proceedings of the National Academy of Sciences of the United States of America · 2002
    Article
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.

X FuDepartment of Pathology, University of California, San Diego, School of Medicine, La Jolla 92093, USA.
M P Kamps
University of San Diego · US

Funding

TRANSFERRING MECHANISMS AND BIOCHEMICAL REGULATION OF E2A-PBX1P01CA050528 · NCI · UNIVERSITY OF CALIFORNIA SAN DIEGO · PI FERAMISCO, JAMES R · 1989 to 1997
–
NCI NIH HHS 2 PO1 CA 50528-04
6 · The paper itself

Abstract

The E2a-Pbx1 oncoprotein contains the transactivation domain of E2a joined to the DNA-binding homeodomain (HD) of Pbx1. In mice, E2a-Pbx1 transforms T lymphoblasts and fibroblasts and blocks myeloblast differentiation. Pbx1 and E2a-Pbx1 bind DNA as heterodimers with other HD proteins whose expression is tissue specific. While the transactivation domain of E2a is required for all forms of transformation, DNA binding by the Pbx1 HD is essential for blocking myeloblast differentiation but dispensable for fibroblast or T-lymphoblast transformation. These properties suggest (i) that E2a-Pbx1 causes cellular transformation by activating gene transcription, (ii) that transcription of E2a-Pbx1 target genes is normally regulated by ubiquitous Pbx proteins and tissue-specific partners, and (iii) that DNA-binding mutants of E2a-Pbx1 activate a subset of all gene targets. To test these predictions, genes induced in NIH 3T3 fibroblasts by E2a-Pbx1 were identified and examined for tissue- and stage-specific expression and their differential abilities to be upregulated by E2a-Pbx1 in NIH 3T3 fibroblasts and myeloblasts and by a DNA-binding mutant of E2a-Pbx1 in NIH 3T3 cells. Of 12 RNAs induced by E2a-Pbx1, 4 encoded known proteins (a J-C region of the immunoglobulin kappa light chain, natriuretic peptide receptor C, mitochondrial fumarase, and the 3',5'-cyclic nucleotide phosphodiesterase, PDE1A) and 5 encoded new proteins related to angiogenin, ion channels, villin, epidermal growth factor repeat proteins, and the human 2.19 gene product. Expression of many of these genes was tissue specific or developmentally regulated, and most were not expressed in fibroblasts, indicating that E2a-Pbx1 can induce ectopic expression of genes associated with lineage-specific differentiation.

Indexed as

Cell Transformation, Neoplastic3T3 CellsAmino Acid SequenceAnimalsBase SequenceBone Marrow CellsCell Line, TransformedGene Expression Regulation, DevelopmentalHomeodomain ProteinsHumansMiceMolecular Sequence DataOncogene Proteins, FusionRNA, MessengerTranscriptional ActivationE2A-Pbx1 fusion proteinHomeodomain ProteinsOncogene Proteins, FusionRNA, Messenger

Identifiers

PMID9032278
PMCPMC231876
OpenAlexW2124809439

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.