Warning: Undefined variable $zfal in C:\Inetpub\vhosts\kidney.de\httpdocs\mlpefetch.php on line 525
Deprecated: str_replace(): Passing null to parameter #3 ($subject) of type array|string is deprecated in C:\Inetpub\vhosts\kidney.de\httpdocs\mlpefetch.php on line 525
Warning: Undefined variable $sterm in C:\Inetpub\vhosts\kidney.de\httpdocs\mlpefetch.php on line 530
free
Warning: Undefined variable $sterm in C:\Inetpub\vhosts\kidney.de\httpdocs\mlpefetch.php on line 531
free free
English Wikipedia
Nephropedia Template TP (
Twit Text
DeepDyve Pubget Overpricing |
lüll Mitochondrial signaling in cell death via the Bcl-2 family Leibowitz B; Yu JCancer Biol Ther 2010[Mar]; 9 (6): 417-22Apoptosis is a critical process for the maintenance of tissue homeostasis and prevention of tumorigenesis. The members of the Bcl-2 family of proteins are the central regulators of the intrinsic apoptotic pathway. Within the Bcl-2 family, the BH3-only subfamily of proteins is tasked with sensing a broad range of apoptotic stimuli and transmitting this signal to other Bcl-2 proteins to initiate programmed cell death. This family of proteins is highly regulated at both transcriptional and post-translational levels, as well as by prominent protein-protein interactions among the family members. Bcl-2 family proteins are often deregulated in cancer, with overexpression of antiapoptotic members, as well as mutations or defects in proapoptotic members. These proteins have been the subject of intensive study for many years and the complex relationships between their regulation and tumorigenesis have spawned a new thinking about cancer treatment. New generations of small molecule Bcl-2 family inhibitors and BH3 and SMAC mimetics have brought new optimism to the pursuit of more individualized and effective cancer therapies.|*Genes, bcl-2[MESH]|Animals[MESH]|Apoptosis/drug effects/*physiology[MESH]|Cell Death[MESH]|Humans[MESH]|Mitochondria/metabolism/*physiology[MESH]|Proteins/metabolism/pharmacology[MESH]|Signal Transduction[MESH] |