Suppression of v-sis-dependent transformation by the transcription factor, Egr-1.

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Back to search

Article

Suppression of v-sis-dependent transformation by the transcription factor, Egr-1.

Oncogene - 1 May 1994

Huang R P, Darland T, Okamura D, Mercola D, Adamson E D

Abstract excerpt

The transcription factor Egr-1, stimulates the activity of a number of genes and inhibits other genes, by binding to the sequence GCGGGGGCG in 5' enhancer regions. However, the functions of Egr-1 are obscure in spite of its rather ubiquitous expression. Egr-1 may play a role in proliferation in mitogen-stimulated cells but its expression is also correlated with the differentiated state in teratocarcinoma cells....

Topics

3T3 Cells
Animals
Base Sequence
Cell Adhesion
Cell Division
Cell Transformation, Neoplastic
DNA-Binding Proteins
Early Growth Response Protein 1
Immediate-Early Proteins
Mice
Mice, Inbred BALB C

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Mice, Nude

Molecular Sequence Data

Mutation

Neoplasm Transplantation

Oncogene Proteins v-sis

RNA, Antisense

Retroviridae Proteins, Oncogenic

Source

Open in PubMed

Identifiers

PMID: 8152797

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 29 Aug 2026. Prepared record publication-8152797-2026-08-29.1. Manifest publication-graph-cohort-2026-08-29.1.

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

Community interpretation

Discuss the evidence

Ask a question, add context or challenge an interpretation. Community activity is separate from scientific evidence strength.

discussions

replies

Citations encouraged

Claims remain attributable.

No discussion yet

Be the first to add a careful, cited interpretation.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Suppression of v-sis-dependent transformation by the transcription factor, Egr-1.PMID 8152797Read ↗

Transcription factor EGR-1 suppresses the growth and transformation of human HT-1080 fibrosarcoma cells by induction of transforming growth factor beta 1.Semantic proximity Read ↗

Decreased Egr-1 expression in human, mouse and rat mammary cells and tissues correlates with tumor formationSemantic proximity Read ↗

Loss of transcription factor IRF-1 affects tumor susceptibility in mice carrying the Ha-ras transgene or nullizygosity for p53.Semantic proximity Read ↗

Role of the WT1 tumor suppressor in murine hematopoiesisSemantic proximity Read ↗

IRF-1 reverts the transformed phenotype of oncogenically transformed cells in vitro and in vivo.Semantic proximity Read ↗

Interaction of ZPR1 with translation elongation factor-1alpha in proliferating cells.Semantic proximity Read ↗

Induction of apoptosis in Mv1Lu cells by expression of competitive RB1 mutants.Semantic proximity Read ↗

Transformation of rodent fibroblasts by herpes simplex virus: presence of morphological transforming region 1 (MTR 1) is not required for the maintenance of the transformed state.Semantic proximity Read ↗

Cellular commitment to oncogene-induced transformation or apoptosis is dependent on the transcription factor IRF-1.Semantic proximity Read ↗

Reversible transformation by v-sis: a model cell line for analysis of transformation by antisense methods.Semantic proximity Read ↗

Expression of the RB gene under the control of MuLV-LTR suppresses tumorigenicity of WERI-Rb-27 retinoblastoma cells in immunodefective mice.Semantic proximity Read ↗

UXT interacts with the transcriptional repressor protein EVI1 and suppresses cell transformation.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.