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Fig. 6. Modelling a requirement for the cytoskeleton in prolactin signalling. (A) Our initial hypothesis suggested that the actin cytoskeleton is necessary for crosstalk between integrin-containing adhesion complexes and prolactin (P)-mediated signal transduction (magenta arrow), but the data in this paper suggest that this model is not correct. (B) Disruption of the microfilaments for up to 4 hours has no effect on prolactin signalling and activation of Stat5. This indicates that the signals downstream of PrlR are independent of the cortical actin network. Because Prl signalling is ECM dependent (Edwards et al., 1998), ligand-activated prolactin receptors might accumulate within multiprotein clusters of proteins localized to focal adhesions or, alternatively, that integrin-regulated adhesion complexes activate PrlR through long-range signals. (C) Disruption of the microfilaments for more than 4 hours leads to delayed restriction in Stat5 activation. Phosphorylation of PrlR, but not Stat5, can still be induced by ligand. Loss of microfilaments might lead to a delayed activation or synthesis of phosphatases or other inhibitors of cytokine signalling (green inhibitory arrow).
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