Ciklin-zavisimaya transkripcionnaya kinaza CDK8 i ee menee izuchennyj paralog CDK19 reguliruyut ekspressiyu zavisimyh genov posredstvom neskol'kih mekhanizmov. CDK8/19 mogut napryamuyu fosforilirovat' nekotorye transkripcionnye faktory (ICN, STAT1), no v to zhe vremya v sostave mediatornogo kompleksa eti kinazy reguliruyut transkripciyu za schet vzaimodejstviya s hromatinom v oblasti promotorov i enhanserov sootvetstvuyushchih genov. V poslednee vremya poyavlyayutsya raboty, demonstriruyushchie putem sravneniya effektov geneticheskoj inaktivacii i himicheskogo ingibirovaniya kinaznoj aktivnosti nalichie u CDK8/19 kinaza-nezavisimyh mekhanizmov dejstviya. Cel'yu raboty bylo poluchit' transgennyh myshej, sposobnyh k induciruemoj i tkanespecifichnoj ekspressii kinaznonegativnoj (lishennoj fosforiliruyushchej aktivnosti) formy CDK8 — CDK8(D173A), kotoryh vposledstvii mozhno budet ispol'zovat' dlya izucheniya kinaza-nezavisimyh mekhanizmov dejstviya CDK8 in vivo. Metodom sluchajnogo transgeneza v rezul'tate mikroin"ekcij linejnoj DNK v pronukleus nami polucheny chetyre transgennyh osobi F0, dve iz kotoryh stali rodonachal'nikami otdel'nyh linij. Dlya vsekh F0 i poluchennyh linij izmerena kopijnost' integrirovavshejsya konstrukcii. Dannaya model' mozhet byt' ispol'zovana dlya izucheniya kinaza-nezavisimyh svojstv belkov CDK8/19.
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