Biopolym. Cell. 2004; 20(3):193-206.
http://dx.doi.org/10.7124/bc.0006A6
Огляди
До проблеми множинної лікарської стійкости: гіпермутабільність як механізм захисту метаболічних мішеней бактеріальної клітини від цитотоксичних ксенобіотиків
1Черепенко О. Й., 1Говорун Д. М.
  1. Інститут молекулярної біології і генетики НАН України
    Вул. Академіка Заболотного, 150, Київ, Україна, 03680

Abstract

Множинну стійкість до ліків (МСЛ) вивчають переважно з позицій функціонування множинних експортерів та переван­таження клітини білками. Проте в багатьох випадках ця проблема не знаходить свого вирішення. У представленому огляді на тлі основних досягнень вивчення МЛС стисло подаються власні результати виявлення МЛС за рахунок тісно зчеплених генів, що утворюють касети, в яких мутації виникають одночасно. Касети (на відміну від інших генів-доместосом) мають, на нашу думку, спеціальне розташування (енвіронсоми), шр забезпечує їхній контакт із внутрішньо­клітинним простором та головним внутрішньоклітинним потоком речовин. Геном містить ~100 енвіронсом і стійкість виникає, якщо хоч би в одній з них з'явилася мутація. Коли мутаген опиняється у внутрішньоклітинному потоці, касета енвіронсоми першою сприймає мутагенний удар. Якщо вона кодує білки з притаманною їм природною неструктурованістю, а мутація може спричинити перехід у молекулі білка від гнучкості до жорсткості, то це може викликати зміни геометрії внутрішньоклітинного простору. Внаслідок цих змін ліганди не зможуть потрапляти до мішеней, що призведе до фенотипу множинної стійкості до ліків.
Повний текст: (PDF, російською)

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