Defining the active site of Bax

July 31, 2007

In the August 1st issue of G&D, scientists from the University of Nebraska Medical Center, led by Dr. Xu Luo, have identified the long-sought-after homo-oligomerization domain of Bax.

The researchers demonstrate that the homo-oligomerization domain is, in fact, responsible for Bax's apoptotic activity. Structural analysis revealed that a three-helix unit - consisting of helix 2 from the BH3 domain, and helices 4 and 5 from the BH1 domain - together form the homo-oligomerization domain. Dr. Luo and colleagues went on to show that this is the minimal domain required for the permeabilization of the mitochondrial membrane and the corresponding induction of apoptosis.

"How activated Bax (or Bak) causes mitochondrial damage remains one of the most fascinating and important questions in apoptosis research. Establishing the causal relationship between homo-oligomerization and apoptotic activity of Bax and the identification of the Bax homo-oligomerization domain represent one step forward towards answering that question," explains Dr. Luo.
-end-


Cold Spring Harbor Laboratory

Related Apoptosis Articles from Brightsurf:

Thymoquinone induces apoptosis & DNA damage in 5-Fluorouracil-resistant colorectal cancer
Volume 11, Issue 31 from @Oncotarget reported that TQ decreased the expression levels of colorectal stem cell markers CD44 and Epithelial Cell Adhesion Molecule Ep CAM and proliferation marker Ki67 in colonospheres derived from both cell lines and reduced cellular migration and invasion.

Oncotarget: Th1 cytokines potentiate apoptosis of breast cancer cells and suppress tumor growth
Volume 11, Issue 30 of Oncotarget reported that previously, the authors showed that anti-estrogen drugs combined with a dendritic cell-based anti-HER-2 vaccine known to induce strong Th1-polarized immunity dramatically improved clinical response rates in patients with HER-2pos/ERpos early breast cancer.

Opening an autophagy window as the apoptosis door starts to close
Tokyo Medical and Dental University (TMDU) researchers have successfully attached the cancer cell-targeting antibody Trastuzumab to a previously reported supermolecule that induces autophagic cell death.

Stop Livin to make lymphoma cells stop living
Researchers at the University of Tsukuba have shown that the protein Livin, an inhibitor of apoptosis or programmed cell death, mediates resistance to immunotherapy in some lymphoma variants.

Protein causes mutations that lead to breast cancer cell aggression
In her previous research, University of Alberta biochemist Ing Swie Goping identified that the protein, BCL-2 interacting killer (BIK), was associated with relapses in breast cancer patients.

Shigella prevents infected cells from sacrificing themselves for the greater good
Researchers from Tokyo Medical and Dental University (TMDU) investigated how Shigella survive and multiply to cause severe inflammatory colitis.

Bacteria can 'outsmart' programmed cell death
To be able to multiply, bacteria that cause diarrhoea block mediators of programmed cell death, a new study in 'Nature Microbiology' shows.

High expression of apoptosis protein (Api-5) in chemoresistant triple-negative breast cancers: an innovative target
78 TNBC biopsies from patients with different responses to chemotherapy were analysed for API-5 expression before any treatment.

High expression of apoptosis protein (Api-5) in chemoresistant triple-negative breast cancers
78 TNBC biopsies from patients with different responses to chemotherapy were analysed for API-5 expression before any treatment.

Researchers describe a mechanism inducing self-killing of cancer cells
A KAIST research team has developed helical polypeptide potassium ionophores that lead to the onset of programmed cell death.

Read More: Apoptosis News and Apoptosis Current Events
Brightsurf.com is a participant in the Amazon Services LLC Associates Program, an affiliate advertising program designed to provide a means for sites to earn advertising fees by advertising and linking to Amazon.com.