Background: Bax and Bcl-2 are the major members of Bcl-2 family whose play a key role in tumor progression or inhibition of intrinsic apoptotic pathway triggered by mitochondrial dysfunction. Therefore, the balance between pro- and anti-apoptotic members of this family can determine the cellular fate. Methods: In this study, the relative level of mRNA expression of Bax and Bcl-2 genes was deter...

The Bcl-2 family member Bax translocates from the cytosol to mitochondria, where it oligomerizes and permeabilizes the mitochondrial outer membrane to promote apoptosis. Bax activity is counteracted by prosurvival Bcl-2 proteins, but how they inhibit Bax remains controversial because they neither colocalize nor form stable complexes with Bax. We constrained Bax in its native cytosolic conformat...

The pro-apoptotic Bcl-2 protein Bax can permeabilize the outer mitochondrial membrane and therefore commit human cells to apoptosis. Bax is regulated by constant translocation to the mitochondria and retrotranslocation back into the cytosol. Bax retrotranslocation depends on pro-survival Bcl-2 proteins and stabilizes inactive Bax. Here we show that Bax retrotranslocation shuttles membrane-assoc...

Purpose: To determine the effect of melatonin in combination with capecitabine on proliferation and induction apoptosis MCF-7 SK-BR-3 breast cancer cell lines.Methods: The MTT assay (3- (4,5-dimethylthiazol-2-yl) -2,5-diphenyltetrazolium bromide) was performed to investigate lines half-maximal concentration (IC50) index. Expression apoptotic markers, Bax, Bcl-2, caspase-3 were measured by polym...

The dual functionality of the tumor suppressor BAX is implied by the nonapoptotic functions of other members of the BCL-2 family. To explore this, mitochondrial metabolism was examined in BAX-deficient HCT-116 cells as well as primary hepatocytes from BAX-deficient mice. Although mitochondrial density and mitochondrial DNA content were the same in BAX-containing and BAX-deficient cells, MitoTra...

Tumor necrosis factor alpha (TNF-alpha)-mediated death signaling causes the recruitment of monomeric pro- apoptotic Bax into a 500-kDa protein complex. The adenovirus Bcl-2 homologue, E1B 19K, inhibits TNF-alpha-mediated apoptosis, interacts with Bax, and blocked the formation of the 500-kDa Bax complex. TNF-alpha and truncated Bid induced Bax-Bax cross-linking, indicative of oligomerization, a...

Bax is cleaved by calpain at aspartate 33 (Asp33) to yield p18 Bax during stress-induced apoptosis. To assess the role of p18 Bax in apoptosis, an ecdysone-inducible expression system was generated. Similar levels of wild-type (WT) and noncleavable Asp33Ala (Asp-->Ala) Bax are induced in 293 cells while expression of N-terminal-deleted p18 (Delta1-33) Bax remains low (20% of full-length p21 Bax...

background: bcl-2 is the most important anti-apoptotic regulator and bax is a pro-apoptotic protein. the status of these parameters or the ration of bcl-2 to bax is important in malignant cell fate as well as normal cells. methods: sixty-two all patients and 62 healthy sex-and age-matched controls were studied. after genotyping, the promoter region of the bax and bcl-2 genes by rflp-pcr method ...