Gene's novel role may provide key to treating liver and neurodegenerative diseases

'FAIM' gene research conducted by Singapore scientists

06-Jul-2009 - Singapore

Scientists at Singapore's Bioprocessing Technology Institute (BTI) have made a novel discovery about how the gene, "Fas-apoptosis inhibitory molecule" (FAIM), protects both immune and liver cells from apoptosis, or programmed cell death.

The scientists, Jianxin Huo, Ph.D., and Shengli Xu, Ph.D., also discovered that this process may possibly be manipulated for clinical application and proposed the first-to-be-published in-animal model to study the role of FAIM in detail. FAIM triggers a mechanism that ultimately impedes an important pathway to apoptosis, which is mediated by a key protein called Fas. Using their mouse model, the scientists elucidated part of the sequence of molecular events that regulates Fas-mediated apoptosis. They found that FAIM functioned as a key switch in the Fas cell death circuit, which could be turned up or down to prolong or decrease cell survival.

Therefore, in principle, this gene could make a good target for drug intervention in either liver cirrhosis in which the target is to prolong cell survival, or in cancer in which the goal is to induce tumour cell death.

BTI Scientific Director Lam Kong Peng, Ph.D., who heads the immunology group that conducted the research, said, "We had earlier identified FAIM to be valuable in increasing the yield of biologics, and that had been one of the main focuses of BTI's research until now. We were extremely pleased to be able to establish that FAIM's function is preserved across both liver and immune cells, as this underscores its critical role in regulating cell death in disease."

The immunology team at BTI, one of the research institutes sponsored by Singapore's A*STAR (Agency for Science, Technology and Research), aims to further characterize the role of FAIM in liver cancer and other debilitating diseases.

Original publication: J. Huo, S. Xu, K. Guo, Q. Zeng and K-P Lam; "Genetic deletion of faim reveals its role in modulating c-FLIP expression during CD95-mediated apoptosis of lymphocytes and hepatocytes"; Cell Death and Differentiation 2009.

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