Life, death and kidneys
- 1 January 1998
- journal article
- review article
- Published by Wolters Kluwer Health in Current Opinion in Nephrology and Hypertension
- Vol. 7 (1) , 5-12
- https://doi.org/10.1097/00041552-199801000-00002
Abstract
Apoptosis plays an integral role during nephrogenesis and is tightly regulated by bcl-2. Transgenic mice manifesting a loss of bcl-2 expression demonstrate fulminant apoptosis of the metanephric blastema during kidney formation leading to renal hypoplasia at birth and multicystic renal disease later in life. In adult kidneys, the rate of apoptosis and level of bcl-2 expression are relatively low. Renal disease can alter the rate of apoptosis and/or elevate bcl-2 expression. The implications of such alterations are discussed.Keywords
This publication has 41 references indexed in Scilit:
- Inhibition of Bax Channel-Forming Activity by Bcl-2Science, 1997
- Controlling Cell DeathScience, 1997
- Expression of bcl‐2 oncoprotein in renal cell tumoursThe Journal of Pathology, 1995
- Modulation of apoptosis by the widely distributed Bcl-2 homologue BakNature, 1995
- Bad, a heterodimeric partner for Bcl-xL and Bcl-2, displaces bax and promotes cell deathCell, 1995
- Towards a genetic basis for kidney developmentMechanisms of Development, 1994
- Disruption of epithelial cell-matrix interactions induces apoptosisThe Journal of cell biology, 1994
- Bcl-2 heterodimerizes in vivo with a conserved homolog, Bax, that accelerates programed cell deathCell, 1993
- bcl-x, a bcl-2-related gene that functions as a dominant regulator of apoptotic cell deathCell, 1993
- Cloning and structural analysis of cDNAs for bcl-2 and a hybrid bcl-2/immunoglobulin transcript resulting from the t(14;18) translocationCell, 1986