ArticleMolecular and cellular biology1989
Possible involvement of normal p21 H-ras in the insulin/insulinlike growth factor 1 signal transduction pathway.
Article in Molecular and cellular biology, 1989. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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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.
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Who cites it
11 citing papers in PubMed, 52 citations in OpenAlex.
- Article
- Insulin resistance and hyperinsulinaemia in the development and progression of cancer.Clinical science (London, England : 1979) · 2009Review
- Epidermal growth factor induces phosphorylation of extracellular signal-regulated kinase 2 via multiple pathways.Molecular and cellular biology · 1993Article
- cAMP antagonizes p21ras-directed activation of extracellular signal-regulated kinase 2 and phosphorylation of mSos nucleotide exchange factor.The EMBO journal · 1993Article
- The ras signaling pathway mimics insulin action on glucose transporter translocation.Proceedings of the National Academy of Sciences of the United States of America · 1993Article
- Common elements in interleukin 4 and insulin signaling pathways in factor-dependent hematopoietic cells.Proceedings of the National Academy of Sciences of the United States of America · 1993Article
- Ras activation by insulin and epidermal growth factor through enhanced exchange of guanine nucleotides on p21ras.Molecular and cellular biology · 1993Article
- The biochemistry of ras p21.The Biochemical journal · 1991Review
- Alteration of homeobox gene expression by N-ras transformation of PA-1 human teratocarcinoma cells.Molecular and cellular biology · 1991Article
- Insulin stimulation of gene expression mediated by p21ras activation.The EMBO journal · 1991Article
- Platelet-derived growth factor stimulates formation of active p21ras.GTP complex in Swiss mouse 3T3 cells.Proceedings of the National Academy of Sciences of the United States of America · 1990Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Expression of a mutant H-ras gene confers a transformed phenotype to rat-1 fibroblasts which is basically independent of exogenous growth factors (GFs). Rat-1 cells induced to express high levels of the normal H-ras gene were also found to display a transformed phenotype. In contrast to cells expressing mutant H-ras, these cells were dependent on GFs. We used this difference in GF dependence to analyze a possible involvement of exogenous GFs in H-ras function. Compared with untransformed rat-1 cells, cells overexpressing normal H-ras displayed an elevated response toward insulinlike growth factor 1 (IGF-1), insulin, and bombesin and an increased sensitivity toward phosphatidic acids. It was found that 8-bromo-cyclic AMP inhibited the responses to all GFs in rat-1 cells but had no effect on mutant-H-ras-transformed cells. In cells overexpressing normal H-ras, 8-bromo-cyclic AMP inhibited the responses to all GFs except those to insulin and IGF-1. This implies that overexpression of normal H-ras in the presence of insulin/IGF-1 is functionally similar to the expression of mutant H-ras, since mutant H-ras can circumvent this block by itself. These and other results strongly suggest a functional linkage between insulin/IGF-1 and normal p21 H-ras.
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