Asset Details
Do you wish to reserve the book?
Caspases 3 and 7: Key Mediators of Mitochondrial Events of Apoptosis
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
Caspases 3 and 7: Key Mediators of Mitochondrial Events of Apoptosis
Do you wish to request the book?
Caspases 3 and 7: Key Mediators of Mitochondrial Events of Apoptosis
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
Caspases 3 and 7: Key Mediators of Mitochondrial Events of Apoptosis
2006
Overview
The current model of apoptosis holds that upstream signals lead to activation of downstream effector caspases. We generated mice deficient in the two effectors, caspase 3 and caspase 7, which died immediately after birth with defects in cardiac development. Fibroblasts lacking both enzymes were highly resistant to both mitochondrial and death receptor-mediated apoptosis, displayed preservation of mitochondrial membrane potential, and had defective nuclear translocation of apoptosis-inducing factor (AIF). Furthermore, the early apoptotic events of Bax translocation and cytochrome c release were also delayed. We conclude that caspases 3 and 7 are critical mediators of mitochondrial events of apoptosis.
Publisher
American Association for the Advancement of Science,The American Association for the Advancement of Science
Subject
/ Animals
/ Apoptosis Inducing Factor - metabolism
/ bcl-2-Associated X Protein - metabolism
/ Biological and medical sciences
/ Cell structures and functions
/ death
/ Enzymes
/ Female
/ Fundamental and applied biological sciences. Psychology
/ Heart Defects, Congenital - etiology
/ Male
/ Mice
/ Mitochondrial Membranes - physiology
/ Molecular and cellular biology
/ Rodents
