Overexpression of the Bcl-2 Protein Increases the Half-life of p21Bax

Abstract

Bax protein can be post-translationally regulated by Bcl-2, probably in a tissue-specific fashion, and suggest the existence of a feedback mechanism that may help to maintain the ratio of Bcl-2 to Bax protein in physiologically appropriate ranges.

Chemosensitivity of B cell chronic lymphocytic leukemia and correlated expression of proteins regulating apoptosis, cell cycle and DNA repair

“…Lack of this correlation in normal B cells supports the interpretation that this phenomenon may not occur under physiological conditions. In fact, data of Miyashita et al 23 demonstrate that abnormally high expression of Bcl-2 can lead to increased half life of Bax by a putative post-translational modulation. It seems possible, therefore, that the correlated expression of Bcl-2 and Bax in B-CLL cells may evolve during the aberrant overexpression of Bcl-2 in the leukemic cells.…”

Channels formed by subnanomolar concentrations of the toxin aerolysin trigger apoptosis of T lymphomas

“…LD À is a B-lymphoblastoid cell line with a previously characterized PIGA mutation derived from a patient with paroxysmal nocturnal haemoglobinuria (Brodsky et al, 1997). The CEM bcl2 line is a T-lineage acute lymphoblastic leukaemia cell line induced to overexpress bcl-2 (Miyashita et al, 1995). LD and CEM cell lines were maintained in RPMI with 1640 medium (Gibco) and 10% heat-inactivated fetal calf serum (FCS).…”

P53 and radiation responses

“…The second group of genes encodes proteins that localize to the cytoplasm, including PIDD and PIGs Lin et al, 2000). The third group of genes encodes proteins that localize to the mitochondria (e.g., BAX, NOXA, PUMA, P53 Aip1 , BID) (Miyashita et al, 1995;Oda et al, 2000a, b;Sax et al, 2002). Among all of the above genes, the disappointment is that none of them appears to be a principal mediator of the P53 apoptotic signal.…”