Please use this identifier to cite or link to this item:
|Title:||A shift in the Bax/Bcl-2 balance may activate caspase-3 and modulate apoptosis in experimental glomerulonephritis.|
El Nahas AM
|Citation:||KIDNEY INT, 2002, 62 (4), pp. 1301-1313|
|Abstract:||Although apoptosis has been linked to the renal cell deletion and ensuing renal fibrosis, its regulating mechanisms remain obscure. Of the known regulators of apoptosis, the best characterized is the Bax to Bcl-2 ratio. However, its importance in controlling apoptosis in glomerulonephritis is unclear. Here, using the nephrotoxic nephritis (NTN) model, we evaluated Bax/Bcl-2 in relation to changes in the apoptosis co-ordination enzyme, caspase-3.|
|Appears in Collections:||Published Articles, Dept. of Infection, Immunity and Inflammation|
Files in This Item:
There are no files associated with this item.
Items in LRA are protected by copyright, with all rights reserved, unless otherwise indicated.