Matches in SemOpenAlex for { <https://semopenalex.org/work/W2289284908> ?p ?o ?g. }
- W2289284908 endingPage "704" @default.
- W2289284908 startingPage "695" @default.
- W2289284908 abstract "Apoptosis is a form of programmed cell death that is critical for basic human development and physiology. One of the more important surprises in cell biology in the last two decades is the extent to which mitochondria represent a physical point of convergence for many apoptosis-inducing signals in mammalian cells. Mitochondria not only adjudicate the decision of whether or not to commit to cell death, but also release toxic proteins culminating in widespread proteolysis, nucleolysis, and cell engulfment. Interactions among BCL-2 family proteins at the mitochondrial outer membrane control the release of these toxic proteins and, by extension, control cellular commitment to apoptosis. This pathway is particularly relevant to cancer treatment, as most cancer chemotherapies trigger mitochondrial-mediated apoptosis. In this Review, we discuss recent advances in the BCL-2 family interactions, their control by upstream factors, and how the mitochondria itself alters these interactions. We also highlight recent clinical insights into mitochondrial-mediated apoptosis and novel cancer therapies that exploit this pathway. Apoptosis is a form of programmed cell death that is critical for basic human development and physiology. One of the more important surprises in cell biology in the last two decades is the extent to which mitochondria represent a physical point of convergence for many apoptosis-inducing signals in mammalian cells. Mitochondria not only adjudicate the decision of whether or not to commit to cell death, but also release toxic proteins culminating in widespread proteolysis, nucleolysis, and cell engulfment. Interactions among BCL-2 family proteins at the mitochondrial outer membrane control the release of these toxic proteins and, by extension, control cellular commitment to apoptosis. This pathway is particularly relevant to cancer treatment, as most cancer chemotherapies trigger mitochondrial-mediated apoptosis. In this Review, we discuss recent advances in the BCL-2 family interactions, their control by upstream factors, and how the mitochondria itself alters these interactions. We also highlight recent clinical insights into mitochondrial-mediated apoptosis and novel cancer therapies that exploit this pathway." @default.
- W2289284908 created "2016-06-24" @default.
- W2289284908 creator A5018461011 @default.
- W2289284908 creator A5022857112 @default.
- W2289284908 date "2016-03-01" @default.
- W2289284908 modified "2023-10-16" @default.
- W2289284908 title "Mitochondria—Judges and Executioners of Cell Death Sentences" @default.
- W2289284908 cites W1480948328 @default.
- W2289284908 cites W1488648621 @default.
- W2289284908 cites W1560899257 @default.
- W2289284908 cites W1607777232 @default.
- W2289284908 cites W1624747819 @default.
- W2289284908 cites W1628370182 @default.
- W2289284908 cites W1809311761 @default.
- W2289284908 cites W1810630981 @default.
- W2289284908 cites W1913661233 @default.
- W2289284908 cites W1935831932 @default.
- W2289284908 cites W1965217295 @default.
- W2289284908 cites W1967354499 @default.
- W2289284908 cites W1968188734 @default.
- W2289284908 cites W1968505830 @default.
- W2289284908 cites W1969331809 @default.
- W2289284908 cites W1971234510 @default.
- W2289284908 cites W1973363947 @default.
- W2289284908 cites W1976720365 @default.
- W2289284908 cites W1977323318 @default.
- W2289284908 cites W1979471022 @default.
- W2289284908 cites W1984547206 @default.
- W2289284908 cites W1985563073 @default.
- W2289284908 cites W1986134476 @default.
- W2289284908 cites W1987821813 @default.
- W2289284908 cites W1988917342 @default.
- W2289284908 cites W1989428846 @default.
- W2289284908 cites W1989554731 @default.
- W2289284908 cites W1990218982 @default.
- W2289284908 cites W1990983360 @default.
- W2289284908 cites W1994068418 @default.
- W2289284908 cites W1994891218 @default.
- W2289284908 cites W1995354282 @default.
- W2289284908 cites W1995773170 @default.
- W2289284908 cites W1998574123 @default.
- W2289284908 cites W1999197294 @default.
- W2289284908 cites W2002439304 @default.
- W2289284908 cites W2004094291 @default.
- W2289284908 cites W2008376982 @default.
- W2289284908 cites W2008715871 @default.
- W2289284908 cites W2008841394 @default.
- W2289284908 cites W2009183764 @default.
- W2289284908 cites W2009183786 @default.
- W2289284908 cites W2009450633 @default.
- W2289284908 cites W2012076962 @default.
- W2289284908 cites W2012173926 @default.
- W2289284908 cites W2016575124 @default.
- W2289284908 cites W2018104469 @default.
- W2289284908 cites W2023153839 @default.
- W2289284908 cites W2024996523 @default.
- W2289284908 cites W2025897016 @default.
- W2289284908 cites W2026873116 @default.
- W2289284908 cites W2027069808 @default.
- W2289284908 cites W2029370718 @default.
- W2289284908 cites W2031100736 @default.
- W2289284908 cites W2033873142 @default.
- W2289284908 cites W2034269086 @default.
- W2289284908 cites W2034591877 @default.
- W2289284908 cites W2036411709 @default.
- W2289284908 cites W2041542870 @default.
- W2289284908 cites W2045855955 @default.
- W2289284908 cites W2047107948 @default.
- W2289284908 cites W2047115666 @default.
- W2289284908 cites W2047322721 @default.
- W2289284908 cites W2048870844 @default.
- W2289284908 cites W2049807952 @default.
- W2289284908 cites W2050866010 @default.
- W2289284908 cites W2052853635 @default.
- W2289284908 cites W2055516802 @default.
- W2289284908 cites W2057257609 @default.
- W2289284908 cites W2057257618 @default.
- W2289284908 cites W2057315090 @default.
- W2289284908 cites W2057713336 @default.
- W2289284908 cites W2059416155 @default.
- W2289284908 cites W2059958613 @default.
- W2289284908 cites W2062853648 @default.
- W2289284908 cites W2063176993 @default.
- W2289284908 cites W2063362926 @default.
- W2289284908 cites W2064560680 @default.
- W2289284908 cites W2064937772 @default.
- W2289284908 cites W2066171290 @default.
- W2289284908 cites W2068444709 @default.
- W2289284908 cites W2068606395 @default.
- W2289284908 cites W2068962767 @default.
- W2289284908 cites W2074800090 @default.
- W2289284908 cites W2078229640 @default.
- W2289284908 cites W2078949828 @default.
- W2289284908 cites W2079795230 @default.
- W2289284908 cites W2081883332 @default.
- W2289284908 cites W2082293892 @default.
- W2289284908 cites W2083086786 @default.
- W2289284908 cites W2083113305 @default.