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新着情報 |
○Bri3BPと薬物誘導アポトーシス (2007. 9)
Augmentation
of drug-induced cell death by ER protein BRI3BP
Tetsuo Yamazaki, Nozomi Sasaki, Miyuki Nishi, Daiju Yamazaki,
Atsushi Ikeda,
Yasushi Okuno, Shinji Komazaki and Hiroshi Takeshima
Biochem. Biophys. Res. Commun. 362,
971-975, 2007. |
Abstract
To determine the contribution of the endoplasmic reticulum
(ER) to cell fate decision, we focused on BRI3-binding
protein (BRI3BP) residing in this organelle. BRI3BP,
when overexpressed, augmented the apoptosis of human
embryonic kidney 293T cells challenged with drugs including
the anti-cancer agent etoposide. In contrast, the knockdown
of BRI3BP reduced the drug-triggered apoptosis. BRI3BP
overexpression enhanced both mitochondrial cytochrome
c release and caspases-3 activity in etoposide-treated
cells. In response to etoposide, the ER reorganized into
irregularly shaped lamellae in mock-transfected cells,
whereas in BRI3BP-overexpressing cells, such reorganization
was not observed. These observations suggest that BRI3BP
is involved in the structural dynamics of the ER and
affects mitochondrial viability. Taken together, BRI3BP,
widely expressed in animal cell types, seems to possess
a pro-apoptotic property and can potentiate drug-induced
apoptosis.
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