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编号:144411
脱发基因的功能被识别
http://www.100md.com 2001年10月25日 好医生
     NEW YORK, Oct 23 (Reuters Health) - Scientists have figured out the normal role of a gene that causes rare forms of hair loss when it is mutated.

    Although the gene has so far been linked only to rare forms of hair loss, the research eventually may point the way to a better understanding of the genetic causes of common baldness, one of the study's authors told Reuters Health.

    Mutations in a gene called hairless can cause rare forms of hair loss, including a condition called alopecia universalis, which causes the sudden loss of all body hair.

    "But until now no one knew what the normal function of the gene was," Dr. Catherine C. Thompson of the Kennedy Krieger Research Institute at Johns Hopkins University in Baltimore, Maryland, told Reuters Health.

    According to Thompson, she and her colleagues have discovered that the protein encoded by the hairless gene is a "transcriptional corepressor" for thyroid hormone receptors. Their findings are published in the October issue of Genes and Development.

    "This means that it acts together with thyroid hormone receptors to turn off the expression of certain genes," she explained. Thyroid hormone receptors have the capacity to activate, or turn on, as well as repress, or turn off, the expression of certain genes, Thompson explained. Hairless seems to influence hormone thyroid receptors when they repress genes, she said.

    Now that it is clear that the hairless protein is involved in the expression of certain genes, the next step will be to figure out which genes hairless regulates, Thompson noted. "These genes, or the proteins they encode, may become targets for therapy," she said.

    Even though hairless has been linked only to rare forms of hair loss, not common baldness, "it is likely that both occur through a similar mechanism," Thompson said.

    "By understanding how hairless works, we may discover features common to other types of hair loss," she added.

    SOURCE: Genes and Development 2001;15:2687-2701., http://www.100md.com