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ÇóÖú·ÒëÏÂÃæÒ»¶ÎÎÄ×Ö Ó¢ÒëÖУº Studies of a newly discovered receptor or endogenous ligand are often confounded by incomplete knowledge of the exact role of that receptor or ligand. One of the most powerful of the new genetic techniques is the ability to breed animals (usually mice) in which the gene for the receptor or its endogenous ligand has been "knocked out," ie, mutated so that the gene product is absent or nonfunctional. Homozygous "knockout" mice will usually have complete suppression of that function, while heterozygous animals will usually have partial suppression. Observation of the behavior, biochemistry, and physiology of the knockout mice will often define the role of the missing gene product very clearly. When the products of a particular gene are so essential that even heterozygotes do not survive to birth, it is sometimes possible to breed "knockdown" versions with only limited suppression of function. Some patients respond to certain drugs with greater than usual sensitivity. (Such variations are discussed in: Drug Biotransformation.) It is now clear that such increased sensitivity is often due to a very small genetic modification that results in decreased activity of a particular enzyme responsible for eliminating that drug. Pharmacogenomics (or pharmacogenetics) is the study of the genetic variations that cause individual differences in drug response. Future clinicians may screen every patient for a variety of such differences before prescribing a drug. |
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