Bax-induced apoptotic cell death

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Bax-induced apoptotic cell death.

A is an ordered cascade of enzymatic events that culminates in cell death and the cleavage of DNA into characteristic nucleosomal fragments. It is operative during embryonic development and, during adult life, plays a key role in various physiological processes, such as tissue remodeling and execution and regulation of the immune response. The consequences of inappropriate apoptotic responses a...

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Apoptosis, a form of programmed cell death, is a process in multicellular organisms responsible for normal tissue development and homeostasis. The intrinsic pathway of apoptosis is principally regulated by protein-protein interactions within the BCL-2 family of proteins, which can prevent or promote mitochondrial dysfunction. There are over twenty BCL-2 family proteins grouped together based on...

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Two roads to death – Bax targets mitochondria by distinct routes before or during apoptotic cell death

Recent studies have revolutionized our understanding of how the crucial apoptosis effectors Bax and Bak target mitochondria to kill cells. We recently reported that an important determinant of the localization, oligomerization, and apoptotic function of Bax is an interaction with either mitochondrial voltage-dependent anion channel 2 (VDAC2) (in healthy cells) or Bak (in apoptotic cells).(1).

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Iron Overload Induced Apoptotic Cell Death in Isolated Rat Hepatocytes Mediated by Reactive Oxygen Species

Isolated rat hepatocytes in culture were incubated with different concentrations of iron-sorbitol (50, 100, 150, and 200 µM) to assess the changes in reactive oxygen species (ROS) and lipid peroxidation leading to apoptotic hepatocyte cell death. The viability of hepatocytes was declined depending on the iron concentration. One hour incubation of the cells with 100 µM iron resulted in decreased...

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Iron Overload Induced Apoptotic Cell Death in Isolated Rat Hepatocytes Mediated by Reactive Oxygen Species

Isolated rat hepatocytes in culture were incubated with different concentrations of iron-sorbitol (50, 100, 150, and 200 µM) to assess the changes in reactive oxygen species (ROS) and lipid peroxidation leading to apoptotic hepatocyte cell death. The viability of hepatocytes was declined depending on the iron concentration. One hour incubation of the cells with 100 µM iron resulted in decreased...

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ژورنال

عنوان ژورنال: Proceedings of the National Academy of Sciences

سال: 2000

ISSN: 0027-8424,1091-6490

DOI: 10.1073/pnas.97.2.529