Responsiveness to transforming growth factor-beta (TGF-beta) restored by genetic complementation between cells defective in TGF-beta receptors I and II.

摘要: Selection of mutant Mv1Lu mink lung epithelial cells resistant to growth inhibition by transforming factor-beta (TGF-beta) has led the isolation cell clones with distinct alterations in type I and II TGF-beta receptors. Certain present a decreased number or complete loss detectable receptor. Other show and/or altered electrophoretic mobility receptor, concomitant Using somatic hybridization analysis we demonstrate recessive nature these mutants respect wild-type phenotype define various complementation groups. Among these, hybrids between that express only receptor (R mutants) neither (DRa rescue expression Moreover, regain full responsiveness 1, as measured DNA synthesis well stimulation fibronectin plasminogen activator inhibitor-1 production. These results provide evidence for an interaction components that, cells, both types is required mediation biological responses 1.