Conclusions

ERa but not ERP directly interacts with CaM through the hinge region.

Substitutions (K302.303G), (K303R), or (K303A) but not (K299A, R300G,

K302A) ofERa render a mutant whose transcriptional activity becomes insensitive to inhibition by CaM antagonists. ERa K303R is hypersensitive to E2 as homodimer but also as heterodimer with wt ERa. Contrary to wt ERa, ERa

K303R-mediated transactivation at API promoters is inhibited by E2 and OH-TAM.

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