Stimulation of glucose uptake by transforming growth factor beta: evidence for the requirement of epidermal growth factor-receptor activation.
Transforming growth factor beta ( TGF-beta), derived from human platelets, stimulates the uptake of 2-deoxy-glucose by cultured cell monolayers 2- to 4-fold. Stimulation can be detected as early as 30 min with as little as 0.1 ng of TGF-beta per ml and maximal effects can be obtained at 2 hr with 1 ng of the growth factor per ml. TGF-beta- induced stimulation of sugar uptake is enhanced by the co-addition of platelet-derived growth factor (10 ng/ml) or epidermal growth factor ( EGF, 1 ng/ml). The NR-6 variant of mouse 3T3 cells, which lack EGF receptors, is not stimulated by TGF-beta. Antisera to EGF receptors that block 125I- labeled EGF binding also inhibit TGF-beta stimulation of 2-deoxyglucose uptake, although 125I-labeled TGF-beta binding remains unimpaired. In contrast, anti-sera to the EGF receptor, which do not block EGF binding, have no measurable effect on the TGF-beta-stimulated uptake of 2-deoxyglucose. We confirm that the receptor for TGF-beta is distinct from the receptor for EGF and we conclude that TGF-beta stimulation of 2-deoxyglucose uptake requires the co-activation of the EGF receptor kinase system.[1]References
- Stimulation of glucose uptake by transforming growth factor beta: evidence for the requirement of epidermal growth factor-receptor activation. Inman, W.H., Colowick, S.P. Proc. Natl. Acad. Sci. U.S.A. (1985) [Pubmed]
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