Expression of receptor protein-tyrosine phosphatase alpha mRNA and protein during mouse embryogenesis.

Receptor protein-tyrosine phosphatase alpha (RPTP alpha) is a transmembrane member of the family of protein-tyrosine phosphatases (PTPs) that has been implicated in neuronal differentiation in vitro. Here we demonstrate that RPTP alpha is differentially expressed during mouse embryogenesis in a spatio-temporal manner. RPTP alpha expression was detectable in 6 days post coitum (dpc) embryos, but not in 7.

Truncated activin type II receptors inhibit bioactivity by the formation of heteromeric complexes with activin type I. receptors.

Truncated activin type II receptors have been reported to inhibit activin receptor signaling in Xenopus embryos, although the mechanism of action for this effect has not been fully understood. In the present study we demonstrate that in P19 embryonal carcinoma cells both the induction of the activin responsive 3TP-lux reporter construct and the inhibition of retinoic acid-induced neuronal differentiation by activin are blocked by expression of a truncated activin receptor. To reveal the mechanism of action of truncated activin receptors, the interaction between different activin receptors has been investigated upon coexpression in COS cells followed by cross-linking of 125I-activin A and subsequent immunoprecipitation.

Retinoic acid resistance of the variant embryonal carcinoma cell line RAC65 is caused by expression of a truncated RAR alpha.

P19 embryonal carcinoma (EC) cells differentiate when treated with retinoic acid (RA). The P19 EC-derived mutant cell line RAC65 is resistant to the differentiation-inducing activity of RA. We show that these cells express a truncated retinoic acid receptor alpha(mRAR alpha-RAC65), probably due to the integration of a transposon-like element in the RAR alpha gene.

Stimulation of TPA-responsive element activity by a cooperative action of insulin and estrogen in human breast cancer cells.

Approximately one third of the human breast tumors are estradiol (E2)-dependent in the initial stages of the disease. E2 is thought to stimulate growth indirectly, through induced production of autocrine polypeptide growth factors. In this hypothesis constitutive production of such growth factors would lead to the loss of E2 dependence, as associated with progression of the disease.