These tumors use estradiol produced primarily via the sulfatase pathway in order to optimally grow and proliferate. Estrone sulfatase is active in the conversion of estrone sulfate in the blood to estrone that can enter the tumor cells. No buffer system for preparative IEF has been able to completely separate estrone sulfatase from other proteins in the solution. In addition, inhibitor studies have been conducted on estrone sulfatase. Inhibitors have been nucleophilic compounds that could react with a proposed FGly in the enzyme active site to prevent further substrate turnover.
Inactivation is a fast, reversible process.
Alternative splicing is regulated by three cis-elements. SE1, SE2, and ESS, located between the two splice sites. Proteins that bind to these sequences can enhance or repress spliceosome formation at each of the alternative splice sites. These studies attempt to develop an affinity chromatography approach to detect proteins binding specifically to these RNA sequences. RNAs can be covalently linked to a stationary phase before binding and eluting proteins from HeLa nuclear extract.