期刊
BIOORGANIC & MEDICINAL CHEMISTRY LETTERS
卷 17, 期 6, 页码 1667-1670出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.bmcl.2006.12.102
关键词
apoptosis; mitochondria; drug
资金
- NIAID NIH HHS [AI 47450] Funding Source: Medline
Although PK11195 binds to the peripheral benzodiazepine receptor with nanomolar affinity, significant data exist which suggest that it has another cellular target distinct from the PBR. Here we demonstrate that PK11195 inhibits F1F0-ATPase activity in an OSCP-dependent manner, similar to the pro-apoptotic benzodiazepine Bz-423. Importantly, our data indicate that cellular responses observed with micromolar concentrations of PK11195, which are commonly attributed to modulation of the PBR, are likely a direct result of mitochondrial F1F0-ATPase inhibition. (c) 2007 Elsevier Ltd. All rights reserved.
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