Open AccessMutations to Bid Cleavage Sites Protect Hepatocytes From Apoptosis After Ischemia/Reperfusion Injury
Author(s) -
Erica Riddle-Taylor,
Kazuhito Nagasaki,
Joseph Lopez,
Carlos O. Esquivel,
Olivia M. Martinez,
Sheri M. Krams
Publication year - 2007
Publication title -
transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.45
H-Index - 204
eISSN - 1534-6080
pISSN - 0041-1337
DOI - 10.1097/01.tp.0000281555.18782.2b
Subject(s) - apoptosis , reperfusion injury , cleavage (geology) , ischemia , microbiology and biotechnology , chemistry , medicine , biology , biochemistry , paleontology , fracture (geology)
Apoptosis of hepatocytes contributes to many forms of liver pathology and can compromise liver function. Hepatocytes have been shown to require mitochondrial disruption to execute apoptosis, a process that is controlled by members of the Bcl-2 family. Bid is a proapoptotic Bcl-2 family member that is cleaved to its active form, tBid, by caspase 8 and granzyme B. Studies in the Bid-deficient mouse have established that hepatocytes require Bid to undergo apoptosis.