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Article

Definition of functional domains in P135gag-myb-ets and p48v-myb proteins required to maintain the response of neuroretina cells to basic fibroblast growth factor.

Journal of virology - 1 Jan 1992

Garrido C, Leprince D, Lipsick J S, Stehelin D, Gospodarowicz D, Saule S

Abstract excerpt

The v-myb- and v-ets-containing E26 retrovirus induces the proliferation of chicken neuroretina (CNR) cells in minimal medium. Proliferation of E26 CNR cells is strongly stimulated by basic fibroblast growth factor (bFGF). The v-myb-containing avian myeloblastosis virus also induces the proliferation of infected CNR cells stimulated by bFGF. Both E26 CNR and avian myeloblastosis virus CNR cells are able to form...

Topics

Animals
Avian Myeloblastosis Virus
Base Sequence
Cell Division
Cell Line
Chick Embryo
DNA, Viral
Fibroblast Growth Factor 2
Gene Products, gag
Kinetics
Molecular Sequence Data

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Mutation

Oncogene Proteins v-myb

Retina

Retroviridae Proteins, Oncogenic

Source

Open in PubMed Open full text

Identifiers

PMID: 1727478
DOI: 10.1128/JVI.66.1.160-166.1992
PMCID: PMC238271

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 29 Aug 2026. Prepared record publication-1727478-2026-08-29.1. Manifest publication-graph-cohort-2026-08-29.1.

Source receipt: PubMed via Helena Literature Corpus, retrieved 29 Aug 2026.

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Definition of functional domains in P135gag-myb-ets and p48v-myb proteins required to maintain the response of neuroretina cells to basic fibroblast growth factor.PMID 1727478Read ↗

Back-mutation of the V-Ets to the C-Ets carboxy-terminal amino acids in the P135gag-myb-ets results in chicken neuroretina cells transformation and loss of basic fibroblast growth factor responsiveness.Semantic proximity Read ↗

Mutations in the DNA-binding and transcriptional activation domains of v-Myb cooperate in transformation.Semantic proximity Read ↗

Fos expression induces growth arrest in tumorigenic neuroretina cells.Semantic proximity Read ↗

Transformation by v-myb correlates with trans-activation of gene expression.Semantic proximity Read ↗

Avian myeloblastic cell lines transformed by two nuclear oncoproteins, P135gag-myb-ets and p61/63myc: a model of retinoic acid-induced differentiation not abrogated by v-erbA.Semantic proximity Read ↗

v-myb and v-ets transform chicken erythroid cells and cooperate both in trans and in cis to induce distinct differentiation phenotypes.Semantic proximity Read ↗

Analysis of the v-myb structural components important for transactivation of gene expression.Semantic proximity Read ↗

Transcriptional activation potential of normal and tumor-associated myb isoforms does not correlate with their ability to block GCSF-induced terminal differentiation of murine myeloid precursor cells.Semantic proximity Read ↗

Oncogenic mutations cause dramatic, qualitative changes in the transcriptional activity of c-Myb.Semantic proximity Read ↗

v-Myb DNA binding is required to block thrombocytic differentiation of Myb-Ets-transformed multipotent haematopoietic progenitors.Semantic proximity Read ↗

Myb-induced chromatin remodeling at a dual enhancer/promoter element involves non-coding rna transcription and is disrupted by oncogenic mutations of v-myb.Semantic proximity Read ↗

Mutational analysis of the role of the carboxy-terminal region of the v-erbB protein in erythroid cell transformation.Semantic proximity Read ↗

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