ArticleMolecular and cellular biology1991
Constitutively expressed c-myb abrogates the requirement for insulinlike growth factor 1 in 3T3 fibroblasts.
Article in Molecular and cellular biology, 1991. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 79 citations in OpenAlex.
- Molecular Signatures of the Insulin-like Growth Factor 1-mediated Epithelial-Mesenchymal Transition in Breast, Lung and Gastric Cancers.International journal of molecular sciences · 2018Review
- Tumor suppressors govern insulin-like growth factor signaling pathways: implications in metabolism and cancer.Oncogene · 2012Review
- HoxA9 induces insulin-like growth factor-1 receptor expression in B-lineage acute lymphoblastic leukemia.Leukemia · 2008Article
- Review
- Review
- Resistance to apoptosis in CTLL-2 cells constitutively expressing c-Myb is associated with induction of BCL-2 expression and Myb-dependent regulation of bcl-2 promoter activity.Proceedings of the National Academy of Sciences of the United States of America · 1997Article
- Activation of hepatic stellate cells by TGF alpha and collagen type I is mediated by oxidative stress through c-myb expression.The Journal of clinical investigation · 1995Article
- Constitutive expression of B-myb can bypass p53-induced Waf1/Cip1-mediated G1 arrest.Proceedings of the National Academy of Sciences of the United States of America · 1994Article
- A functional insulin-like growth factor I receptor is required for the mitogenic and transforming activities of the epidermal growth factor receptor.Molecular and cellular biology · 1994Article
- DNA and redox state induced conformational changes in the DNA-binding domain of the Myb oncoprotein.The EMBO journal · 1993Article
- Regulation of proliferation and cytokine expression of bone marrow fibroblasts: role of c-myb.The Journal of experimental medicine · 1993Article
- Mechanism of c-myc regulation by c-Myb in different cell lineages.Molecular and cellular biology · 1993Article
- The growth-stimulatory effect of simian virus 40 T antigen requires the interaction of insulinlike growth factor 1 with its receptor.Molecular and cellular biology · 1992Article
- Regulation of BALB/c 3T3 fibroblast proliferation by B-myb is accompanied by selective activation of cdc2 and cyclin D1 expression.Proceedings of the National Academy of Sciences of the United States of America · 1992Article
- Oncogenicity of AKR mink cell focus-inducing murine leukemia virus correlates with induction of chronic phosphatidylinositol signal transduction.Journal of virology · 1992Article
- Roles of insulinlike growth factor 1 (IGF-1) and the IGF-1 receptor in epidermal growth factor-stimulated growth of 3T3 cells.Molecular and cellular biology · 1992Article
- Altered chromosome 6 in immortal human fibroblasts.Molecular and cellular biology · 1992Article
- Positive autoregulation of c-myb expression via Myb binding sites in the 5' flanking region of the human c-myb gene.Molecular and cellular biology · 1991Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
The proto-oncogene c-myb, whose expression is usually limited to cells of the hematopoietic lineages, can be expressed in fibroblasts if placed under the control of a constitutive promoter, such as the simian virus SV40 early promoter. 3T3 cells carrying a constitutively expressed human c-myb were found to grow in 1% serum or in a serum-free, platelet-derived growth factor-supplemented medium, whereas the parent cell line, BALB/c 3T3, needed insulinlike growth factor 1 (IGF-1) in addition to platelet-derived growth factor for growth. myb-carrying cells, however, could not grow in platelet-poor plasma. In fibroblasts, therefore, a constitutively expressed c-myb can abrogate the requirement for platelet-poor plasma or IGF-1. When 3T3 cells constitutively expressed both c-myc and c-myb, they could grow in serum-free medium without added growth factors. The ability of c-myb to abrogate in fibroblasts the IGF-1 requirement seems to be due to its ability to induce overexpression of IGF-1, as indicated by an increase in steady-state levels of IGF-1 mRNA. These results have some important implications; for instance, they suggest a commonality of pathways for entry into S phase in different cell types and the possibility of a myb-like or myb-equivalent gene product of critical importance for entry of fibroblasts into S phase.
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