Цитологія і генетика 2023, том 57, № 4, 3-10
Cytology and Genetics 2023, том 57, № 4, 291–297, doi: https://www.doi.org/https://doi.org/10.3103/S0095452723040023

Роль білків BCR і FNBP1 у фагоцитозі як модель мембранних перебудов при хронічній мієлоїдній лейкемії

Антоненко С.В., Гур’янов Д.С., Кравчук І.В., Дибков М.В., Швачко Л.П., Телегєєв Г.Д.

  • Інститут молекулярної біології і генетики НАН України, Україна, 03143, Київ, вул. Акад. Заболотного, 150

Хронічна мієлоїдна лейкемія – це мієлопроліферативне новоутворення, що виникає внаслідок появи аномальних гемопоетичних стовбурових клітин, які несуть онкобілок Bcr-Abl, як результат реципрокної транслокації між 9 та 22 хромосомою. Основні елементи патогенезу захворювання обумовлені як підвищеною тирозинкіназною активністю білка Abl, так і роллю Bcr частини гібридного білка. Наявність РН домену в Bcr обумовлює його взаємодію з PI(3)P фагосомальної мембрани. Нами продемонстровано, що ця взаємодія супроводжується колокалізацією Bcr з білком FNBPI у фагосомах клітин макрофагів J774. Представлена модель впливу онкопротеїну Bcr-Abl на утворення надлишку АФК при ХМЛ за рахунок неконтрольованої експресії фагосомальної НАДФ-оксидази.

Ключові слова: хронічна мієлоїдна лейкемія, Bcr-Abl, FNBP1, фагосома, НАДФ-оксидаза

Цитологія і генетика
2023, том 57, № 4, 3-10

Current Issue
Cytology and Genetics
2023, том 57, № 4, 291–297,
doi: https://doi.org/10.3103/S0095452723040023

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