Key step in the 'puncture' mechanism of cell death revealed

May 12, 2008

A team of medical researchers led by Dr Ruth Kluck at Melbourne’s Walter and Eliza Hall Institute (WEHI) has discovered a key step in the mechanism by which cells destroy themselves. In this process, called “apoptosis”, certain proteins cause the cell to self-destruct by puncturing its “power plant.” How the proteins do this has been clarified by the WEHI team. The discovery is an important step towards the identification of targets for drugs designed to regulate cell death.

Dr Kluck and her colleagues explore how cells engineer their own destruction. Properly regulated cell death is actually essential for good health. This is because our cells naturally have a limited life span. The worn out, damaged or unnecessary cells in our bodies are eliminated at the rate of one million per second and replaced by the same number of new cells for as long as we live.

If a cell fails to die when it reaches its “use-by” date, it may go on to multiply uncontrollably and form a cancer. Conversely, a person in whom too many cells self-destruct may develop a degenerative disease such as Alzheimer’s.

The cell’s self-destruction is driven by a protein called Bak that acts by puncturing the membrane of the mitochondria - the cell’s power plant. Once this power plant is wrecked, the cell is doomed.

But how does Bak do this? The crux seems to be the way Bak can bind to itself and form complexes that damage the mitochondrial membrane. Dr Kluck and colleagues have discovered that cellular distress signals cause one segment of Bak to flip out and insert neatly into a groove on another Bak molecule. The Bak doublet then forms the larger complexes that can puncture the mitochondria and provoke the cell’s self-destruction.

This insight into how apoptosis starts will assist in the development of drugs that can flick on the apoptosis “switch” to kill cancer cells more effectively. The development of drugs with the opposite effect is also important: to “switch off” unwarranted apoptosis in degenerative disorders.

Source: Research Australia

Explore further: CNIO researchers show that telomeres are linked to the origins of idiopathic pulmonary fibrosis

Related Stories

Functioning brain follows famous sand pile model

Jun 22, 2015

One of the deep problems in understanding the brain is to understand how relatively simple computing units (the neurons), collectively perform extremely complex operations (thinking).

S. Korea to revive stem cell research after scandal

Sep 19, 2011

President Lee Myung-Bak promised Monday to spend some $89 million restoring South Korea's reputation as a leader in stem cell research, five years after a scandal tarnished its reputation.

Overcoming tumor resistance to anti-cancer agent TRAIL

Mar 22, 2010

The TRAIL ligand is a promising anticancer agent that preferentially kills tumor cells without apparent damage to healthy cells. Many cancers exhibit resistance to TRAIL, however, thus limiting its therapeutic potential. ...

Recommended for you

Researchers reveal a genetic blueprint for cartilage

49 minutes ago

Cartilage does a lot more than determine the shapes of people's ears and noses. It also enables people to breathe and to form healthy bones—two processes essential to life. In a study published in Cell Re ...

Latent virus and life expectancy

4 hours ago

The telomeres are repetitive DNA sequences at each end of our chromosomes. Studies show that in every cell division, the telomere is shortened. As a result, the telomere limits the cell to a fixed number of divisions and ...

User comments : 1

Adjust slider to filter visible comments by rank

Display comments: newest first

E_L_Earnhardt
not rated yet May 13, 2008
Wrong direction! Reduce temperature of the cell to slow mitosis! Cyroablation is the way to kill it if you must! Multiply "Bak" and you doom the race! Mitochondria are our best friends!

Please sign in to add a comment. Registration is free, and takes less than a minute. Read more

Click here to reset your password.
Sign in to get notified via email when new comments are made.