.... While the therapeutic importance of VRK2 family proteins is known, the specific roles of VRK2A and its interplay with apoptotic regulator Bcl-xL (B-cell lymphoma-extra Large) remain elusive. Bcl-xL regulates cell death by interacting with BAX (B-cell lymphoma-2 Associated X-protein), controlling its...

... of a second VDAC1 molecule. When the N-terminal region α-helix structure was perturbed, intra-molecular cross-linking was abolished and dimerization was enhanced. This mutant also displays reduced voltage-gating and reduced binding to hexokinase, but not to the anti-apoptotic proteins Bcl-2 and Bcl-xL...

... embryonic fibroblasts), we found that the endogenous anti-apoptotic Bcl-2 protein Bcl-xL prevented apoptosis initiated by H 2 O 2 . The BH3 (Bcl-2 homology 3)-only Bcl-2 protein Noxa was required for H 2 O 2 -induced cell death and was the single BH3-only Bcl-2 protein whose pro-apoptotic activity...

... identified in the protein, thus making it a potential new member of the BH3-only protein family. In the present study, we provide NMR, SPR (surface plasmon resonance) and crystallographic evidence that a peptide spanning residues 147–172 in SOUL interacts with the anti-apoptotic protein Bcl-xL. We have...

..., Bad, Bak or Bid. However, bound HK2 (hexokinase 2) and Bcl-xL were decreased in end-ischaemic mitochondria. We conclude that cytochrome c loss during ischaemia, caused by outer membrane permeabilization, is a major determinant of H 2 O 2 production by mitochondria under pathophysiological conditions...

... in the absence of growth factors. However, apoptosis was inhibited by overexpressed antiapoptotic protein Bcl-xL. Moreover, we found that SARS-CoV E protein interacted with Bcl-xL in vitro and endogenous Bcl-xL in vivo and that Bcl-xL interaction with SARS-CoV E protein was mediated by BH3 (Bcl-2 homology domain...

... in yeast. Using this sys- tem, we have focused on the action of the anti-apoptotic family member Bcl-xL, and have defined the quantitative relationships that underlie the antagonistic action of this protein on the lethal consequences of expression of the pro-apoptotic family member Bax. This system has...

... of action of NSAIDs is inhibition of cyclo-oxygenase 2 (COX-2) and thereby also inhibition of the production of the main COX-2 product prosta- glandin E # [8]. COX-2 was suggested as a possible link between Abbreviations used: Bad, Bcl-2/Bcl-XL-antagonist, causing cell death ; COX-2, cyclo-oxygenase 2; Int...

... are expressed as mean fluorescence units S.E.M. (n fl 3). *, Significantly less than basal activity (P ! 0.05). (a) 26 S proteasome activity (units) Treatment Control cells bcl-xL cells Chymotrypsin-like substrate (LLVY-NH-Mec) 85.9 4.3 58.3 3.8 Trypsin-like substrate (LSTR-NH-Mec) 11.6 0.1 11.8 0.9...

..., for FLAP than MK886. When tested to determine its ability to induce apoptosis, MK591 was less effective than MK886. At 8 h after treating FL5.12 cells with either 10 lM MK886 or 10 lM MK591, 27.0 Figure 1 FLAP (A) and bcl-xL (B) expression in various haematopoietic cell lines Cells were lysed...