Chinese Scientists Uncover Secrets of Human Cell Senility

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Last updated at: (Beijing Time) Thursday, January 31, 2002

Chinese Scientists Uncover Secrets of Human Cell Senility

Chinese scientists say they have determined the P16 gene is the key link in the genetic program of cell senility, a major step in deciphering the secret of the human cell senility.

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Chinese scientists say they have determined the P16 gene is the key link in the genetic program of cell senility, a major step in deciphering the secret of the human cell senility.

Scientists described this genetic discovery as an original contribution to Chinese research on the mechanism of aging opening up a new path for the scientific community to decode the secret of human cell senility.

The discovery was made by a group of experts headed by Tong Tanjun and Zhang Zongyu, professors from the Medical Department of Beijing University.

The research program adopts universally acknowledged model of human cell senility. By studying gene P16's functions, the scientists found that the p16 gene can affect the life span of cells and the cellular biological clock length, and the reduction of negative control is an important cause of over expression of the P16 gene in replicative cellular aging.

The experts also prove by four different means that controlling the expression of the P16 gene does not only prolong the life span of the cell and reduce the level of aging but also slow down the shortening of cellular biological clock length. "The opposite results will be made if we strengthen the expression of P16 gene," said the experts.

Professor Tong said cellular aging is the basic unit of cell senescence, and the common foundation for geriatric diseases.

"Our research has shown at least the life span of some human cells can be regulated through recombinant DNA technique," he said.

P16 , a 15kD protein (148 amino acids), is also known as CDK4I, P16-INK4, P16-INK4A, multiple tumor suppressor 1 (MTS1). P16 is encoded by the gene cdkn2a or cdkn2.

P16 forms a heterodimer with cyclin-dependent kinase 4 and 6 thereby preventing their interaction with cyclin D both in vitro and in vivo. Thus, P16 acts as a negative regulator of the proliferation of normal cells. P16 (cdkn2) mutations are involved in tumor formation in a wide range of tissues. cdkn2a is homozygously deleted, mutated, or otherwise inactivated in a large proportion of tumor cell lines and some primary tumors, including melanomas and tumors of the biliary tract, pancreas, and stomach.

By PD Online Staff Li Yan

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