Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.2.1.31 (beta-glucuronidase)
 7,680 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have investigated the effect of alpha-amanitin treatment of mouse blastocysts on their further development. Twenty-four-hour treatments with alpha-amanitin at 1 microg/ml do not interfere with embryo survival or gross morphological development over the next few days although the rate of synthesis of polyA-containing RNA is dramatically reduced during exposure to the antimetabolite. Effects upon rates of protein synthesis are not observed initially, but incorporation of (35S)methionine into acid-insoluble material is ultimately inhibited by approximately 50% in all the treated samples. Developmental markers do not all respond in the same way to the alpha-amanitin treatments used. Whereas levels of beta-glucuronidase and plasminogen activator are virtually unaffected by the antimetabolite, alpha-amanitin treatment interferes with delta5,3beta-hydroxysteroid dehydrogenase activity in trophoblast cells and formation of a bilayered inner cell mass. The effects upon the latter markers differ quantitatively with the various exposure periods to alpha-amanitin. On the basis of these observations, we propose that mRNAs for at least some developmental markers in mouse blastocysts are synthesized long before they are translated.
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PMID:Effects of alpha-amanitin on programming of mouse blastocyst development. 2073 71