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Proceedings of the National Academy of Sciences of the United States of America logoLink to Proceedings of the National Academy of Sciences of the United States of America
. 1981 Feb;78(2):1189–1193. doi: 10.1073/pnas.78.2.1189

Specific receptors for phorbol esters in lymphoid cell populations: role in enhanced production of T-cell growth factor.

J J Sando, M L Hilfiker, D S Salomon, J J Farrar
PMCID: PMC319973  PMID: 6972041

Abstract

Phorbol ester tumor promoters act synergistically with concanavalin A to cause production of T-cell growth factor by normal human peripheral blood lymphocytes. A specific, saturable, binding component which may mediate the phorbol ester effect has been identified by using [20-3H]phorbol 12,13-dibutyrate in a whole-cell binding assay. Specific binding is maximal with 5 min at 37 or 23 degrees C but the level of bound ligand rapidly decreases to about 50% within 1 hr. At 4 degrees C, 2 hr are required to reach maximal binding, and the binding is stable for at least 20 hr. Binding is reversible at 37 and 4 degrees C with time courses similar to those for initial binding at the respective temperatures. Saturation of the specific binding occurs at a concentration (approximately 30 nM) consistent with that producing maximal T-cell growth factor activity. Scatchard analysis of the binding after 30 min at 37 degrees C demonstrates a lower Kd (9 nM) than that determined after 2 hr at 4 degrees C (22 nM). The median number of sites per cell for six donors was 2 X 10(5) (range, 1.3-4 X 10(5). Other tumor-promoting phorbol esters compete for [20-3H]phorbol 12,13-dibutyrate binding in approximate proportion to their activity in stimulating T-cell growth factor production. Phorbol, 4-alpha-phorbol didecanoate, dexamethasone, retinoic acid, butyric acid, and dimethyl sulfoxide do not compete for specific binding.

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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

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