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Example sentences for: caspases
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First, to determine whether a mutation in amino-terminal RING domain of BRCA1 preferentially targeted either the mitochondrial [ 25 ] or Fas/Fas ligand apoptotic pathway [ 24 ] , levels of the respective initiator caspases 9 and 8 were determined.
This leaves the possibility that conjugated bile acids may activate the apoptotic cascade through Fas receptor in this cell line, as glycine-conjugated bile acids do in hepatocytes [ 25 ] . However, the activation of caspases does not require a specific kind of bile acid transporter since TCA is not toxic to McArdle RH-7777 cells irrespective of whether these cells internalize bile acids via ntcp or asbt.
Fas contains a single transmembrane domain and belongs to the tumor necrosis factor (TNF)/nerve growth factor family [ 8 ] . FasL contains a single transmembrane domain and is also a member of the same TNF family [ 9 ] . A soluble form of FasL has been described, but appears to be less capable of inducing apoptosis, when compared with the bound form [ 10 11 ] . The binding of FasL with Fas initiates receptor oligomerization, which recruits Fas-associated death domain (FADD) [ 12 ] . FADD binds procaspase-8 and permits activation of caspase-8 through self-cleavage [ 13 ] . Caspase-8 activates the effector caspases, which commits the cell to the orderly process of apoptosis [ 14 15 ] . In addition, caspase-8 cleaves Bcl-2-interactive-death-agonist (Bid) [ 16 ] . Truncated Bid localizes to the mitochondria and promotes cytochrome c release; this process also serves as a major apoptotic-signaling pathway for Fas [ 16 17 18 ] . Depending upon the amount of caspase-8 that is activated, the predominant pathway can be either Bid cleavage with subsequent mitochondrial release of cytochrome c or activation of the effector caspase pathway [ 18 ] . Resident cells of the kidney express both Fas and FasL and Fas/FasL signaling is functional in these cells [ 19 20 21 22 23 24 ] . A recent review by Ortiz and associates [ 25 ] noted that the combined literature demonstrating participation of Fas/FasL pathway in renal injury essentially fulfilled Koch's postulates.
At present, it is not known how conjugated bile acids activate caspases in CHO.asbt.
The essential step in plasma membrane destabilization and MP-release very likely is a caspase-dependent sphingomyelin hydrolysis, which leads to the production of ceramide [ 28 29 30 ] . It is possible, however, that sphingomyelin hydrolysis and MP-release may be a consequence of the action of initiator caspases or other ZVAD sensitive proteases rather than only executioner caspases [ 15 31 32 ] . Our study was performed in HUVEC culture, which may have particular properties in respect of MP release when compared with endothelial cells from other organs.
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