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Example sentences for: fasl
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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.
FasL, Fas antigen ligand (or CD95L and APO-1L)
The pronounced increases in Fas and FasL expression and activation of this pathway by the third week of study also correlated with previous evidence that documented irreversibility of the renal injury if the hypertension was not corrected by this time [ 5 ] . These data supported the view that the Fas/FasL pathway promoted nephrosclerosis in this model.
Activation of the Fas/FasL pathway may also serve as a mechanism of tubular epithelial cell loss and interstitial fibrosis, which are also prominent renal features of hypertension.
No difference was detected in the levels of caspase 9 or caspase 8 among the BRCA1+ or BRCA1wt cells, suggesting that the reduced cell survival in BRCA1+ cells was not associated with a difference in initiation of either the mitochondrial or the Fas/FasL apoptotic pathways.
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