Dibutyryl cyclic AMP mimics ovariectomy: nuclear protein phosphorylation in mammary tumor regression.
Growth of mammary carcinoma induced by 7,12-dimethyl-benz(a) anthracene is arrested by either ovariectomy or treatment with N6,O2-dibutyryl cyclic adenosine 3',5'-monophosphate (dibutyryl cyclic AMP). When this occurs, a new nonhistone protein species becomes the predominant endogenous substrate of cyclic AMP-dependent protein kinase in the tumor nuclei. Phosphorylation of this regression-associated protein ceases when resumption of tumor growth is induced by either the injection of 17 beta-estradiol or cessation of dibutyryl cyclic AMP treatment. Thus phosphorylation of regression-associated protein may play a role in the regression of hormone-dependent mammary tumors.
D000818:Animals; D003994:Bucladesine / Q000627:therapeutic use*; D002369:Castration; D002467:Cell Nucleus / Q000378:metabolism; D002868:Chromosomal Proteins, Non-Histone / Q000378:metabolism*; D004958:Estradiol / Q000494:pharmacology; D005260:Female; D006657:Histones / Q000378:metabolism; D008325:Mammary Neoplasms, Experimental / Q000188:drug therapy / Q000378:metabolism / Q000628:therapy* / Q000648:ultrastructure; D011494:Protein Kinases / Q000378:metabolism*; D051381:Rats
D002868:Chromosomal Proteins, Non-Histone; D006657:Histones; D004958:Estradiol; D003994:Bucladesine; D011494:Protein Kinases