| First Author | Karsan A | Year | 1996 |
| Journal | Blood | Volume | 87 |
| Issue | 8 | Pages | 3089-96 |
| PubMed ID | 8605321 | Mgi Jnum | J:32602 |
| Mgi Id | MGI:80096 | Doi | 10.1182/blood.v87.8.3089.bloodjournal8783089 |
| Citation | Karsan A, et al. (1996) Cloning of human Bcl-2 homologue: inflammatory cytokines induce human A1 in cultured endothelial cells. Blood 87(8):3089-96 |
| abstractText | Bcl-2 is an intracellular membrane-associated protein that functions to block programmed cell death. Despite recurrent exposure to cellular toxins from the circulation and tissue, endothelial cells are remarkably resistant to cell death. Because Bcl-2 protein levels are low or undetectable in endothelial cells, we postulated that other members of the growing Bcl-2 family would be present in endothelial cells to provide protection against apoptosis. Degenerate primers to two conserved regions of the Bcl-2 family were used to amplify potential homologues in endothelial cells. This strategy resulted in the isolation of a human Bcl-2 homologue related to murine Al, a recently identified member of this family. We show here that, in endothelial cells, human Al is rapidly inducible by phorbol ester and the inflammatory cytokines, tumor necrosis factor-alpha and interleukin-1beta, but not by the growth factors, basic fibroblast growth factor or vascular endothelial growth factor. Al is the only known Bcl-2 family member that is inducible by inflammatory cytokines, suggesting that it may play a protective role during inflammation. Additionally, vascular smooth muscle cells and various nonhematopoietic tissues express human Al, indicating that human Al is a widely expressed Bcl-2 homologue. |
