Tuesday , June 22 2021

tuning of cell death: a new component of the machinery of death revealed



An important component of microscopic machinery that drives the cell death has been identified by scientists & # 39; Walter and Eliza Hall Institute.

The study of machinery "pro-death" that causes maridati cells, diseased or unwanted dying, the research team showed that a protein called VDAC2 was critical to the function of & # 39; pro-death protein called Bax .

The team also showed that VDAC2 contributed to the killing of & # 39; certain cancer cells by anti-cancer agents. The research, published today in the journal Nature Communications, Was led by PhD student Dr Chin Hui-San with Professor David Huang, Dr Mark van Delft and Associate Professor Grant Dewson.

SUMMARY

  • The death & # 39; & # 39 cells through; a process known as apoptosis is essential for removing & # 39; unwanted cells, damaged or diseased, and driven by & # 39; Engine & # 39; of & # 39; thin protein.
  • The Bax protein is a major component of cell death machinery, forming part of a complex that takes cells to a "point of no return" in & # 39; apoptotic death.
  • Our researchers have discovered a protein called Bax VDAC2 helping to manage the apoptosis, and can & # 39; play a role in answering the response of cancer cells to anticancer agents.

MACHINERY & # 39; Mortality

Death of apoptotic cells is critical for the development and maintenance of our body, and damages the protein machinery running apoptosis were associated with & # 39; range & # 39; disease. The proteins of the death of defective cells have been linked to both cancer development as well as the resistance of cancer cells to treatment.

a key protein in cell death machinery called Bax, said Dr. van Delft. "Bax help take cells" point & # 39; no return "initiation of apoptotic cell death, which forms pores in the mitochondria, the cell forces. This widens & # 39; the last" executor " demountable cell proteins.

"Understanding how the functions & # 39; Bax may lead to new therapies or promote cell death – b & # 39; applications for diseases such as cancer – or therapeutic to prevent cell death, which the potential to save cells in & # 39; conditions such as neurodegenerative disorders or stroke ", he said.

The team investigated as related protein called Bax and Bak cell kill, knocking function & # 39; different genes using CRISPR technology, said Associate Professor Dewson.

"To our surprise we found that gene was essential for function & # 39; Bax but not Bak, although these two proteins were similar with & # 39; functional and structural way.

"We were able to follow this research to show that the protein, called VDAC2, was a catalyst that helped Bax associate with mitochondria and form pores in their membranes, to kill the cell," said Associate Professor Dewson. "Intisġenti work & # 39; & # 39 days; VDAC2 is to maintain the function of mitochondria, the pumping metabolites in and out of mitochondria."

CELLS DRIVING FOR CANCER DEATH

Failure of cell death machinery is a feature of & # 39; cancer cells, and is linked to the resistance of cancer cells to anticancer treatments, said Professor Huang.

"Bax is important to help anti-cancer agents kill cells – without Bax and his relative Bak, the cancer cells can not pass apoptosja when treated with & # 39; variety & # 39; therapies cancer.

"Our research has shown that Bax VDAC2 is needed to manage the response of cancer cells to agents & # 39; conventional chemotherapy as well mimimati BH3 recently developed," said Professor Huang.

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The research was supported by the National Council of Australian Research Research, the Council of the Victoria Cancer, the Australian Foundation for Research on Cancer, the Leukemia Society and Lymphoma (US) and the Government a & # 39; Victoria. Dr. Chin Hui was supported by San bag & # 39; & # 39 study; PhD from the University & # 39; Melbourne.

Disclaimer & # 39; responsibility: AAAS and EurekAlert! not responsible for the accuracy of & # 39; releases & # 39; news posted on EurekAlert! by contributing institutions or for the use of & # 39; any information via EurekAlert system.


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