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Deficiency of the 15-kDa selenoprotein led to cytoskeleton remodeling and non-apoptotic membrane blebbing through a RhoA/ROCK pathwayстатья
Информация о цитировании статьи получена из
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Web of Science
Статья опубликована в журнале из списка Web of Science и/или Scopus
Дата последнего поиска статьи во внешних источниках: 10 декабря 2018 г.
- Авторы: Bang Jeyoung, Jang Mihyun, Huh Jang Hoe, Ji-Woon Na, Shim Myoungsup, Carlson Bradley A., Tobe Ryuta, Tsuji Petra A., Gladyshev Vadim N., Hatfield Dolph L., Lee Byeong Jae
- Журнал: Biochemical and Biophysical Research Communications
- Том: 456
- Номер: 4
- Год издания: 2015
- Издательство: Academic Press
- Местоположение издательства: United States
- Первая страница: 884
- Последняя страница: 890
- DOI: 10.1016/j.bbrc.2014.12.059
- Аннотация: The 15-kDa selenoprotein (Sep15) has been implicated in etiology of some types of cancer. Herein, inducible RNAi cell lines were established and cell morphology and motility were analyzed. The majority of Sep15-deficient cells (>95%) formed membrane blebs in a dynamic manner. Blebbing cells transformed cell morphology from a normal flat spindle shape to a spherical morphology. In blebbing cells, actin fibers moved to the cell periphery, covering and obscuring visualization of α-tubulin. Bleb formation was suppressed by the inhibitors of Rho-associated protein kinase (ROCK), RhoA or myosin light chain (MLC), restoring blebbing cells to wild-type morphology. RhoA activation and phosphorylation of myosin phosphatase target subunit 1 was induced by Sep15 knockdown. Sep15-deficient cells were non-apoptotic, and displayed a distinct relative localization of F-actin and α-tubulin from typical apoptotic blebbing cells. Our data suggest that Sep15 in Chang liver cells regulates the pathway that antagonizes RhoA/ROCK/MLC-dependent non-apoptotic bleb formation.
- Добавил в систему: Гладышев Вадим Николаевич