Gene scene

Article Abstract:

A protein has been identified that prevents genetic material from replicating, a discovery with important implications for treating diseases such as cancer and AIDS that are associated with uncontrolled cell growth. Isolated initially from the bacterium Escherichia coli, the protein is believed to be present in all living systems. Years of research by Arthur Kornberg concerning the ''on-switch'' for bacterial replication earned him the Nobel Prize in medicine in 1959, but finding the off-switch has proved more difficult for him. In the current report, co-authored by Deog Su Hwang, a protein that binds to the site where replication starts is described. It appears to prevent the proteins that initiate replication from working. The gene controlling the off-switch protein has been named iciA (inhibitor of chromosome initiation A), and it may be the first of many such agents. The amino acid sequence of the protein and the nucleotide sequence of the gene will be described in forthcoming reports. Such information will facilitate research on proteins with similar functions. Besides the potential therapeutic implications of the discovery, the fact that this is the first ici gene discovered shows how little scientists know about the basic chemical processes that control life. (Consumer Summary produced by Reliance Medical Information, Inc.)

Research, Bacterial genetics, Genetic regulation, Chromosome replication, Cell division, Kornberg, Arthur

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First gene therapy for inherited hypercholesterolemia a partial success

Article Abstract:

Gene therapy may be an effective treatment for individuals suffering from severe familial hypercholesterolemia, or increased blood levels of cholesterol. Familial hypercholesterolemia is an inherited disorder caused by the absence of the receptor for low density lipoprotein (LDL). The severity of familial hypercholesterolemia depends on the number of defective LDL receptor genes. Gene therapy for familial hypercholesterolemia involves the insertion of the gene for the LDL receptor into the patient's liver cells. A 29-year-old woman was the first patient to undergo gene therapy for severe familial hypercholesterolemia. Her blood levels of LDL cholesterol have decreased by 20% to 40% since undergoing gene therapy. She has not been treated with any drugs to lower her blood levels of cholesterol during this time. A liver biopsy revealed that the LDL receptor gene is functioning in this patient.

Usage, Genetic aspects, Gene therapy, Hypercholesterolemia

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Gene scene: a master control switch for myogenesis muscles its way into the clinic

Article Abstract:

MyoD, the gene that directs the formation of skeletal muscle in the developing embryo, may be useful in diagnosing fetal muscle diseases. Amniocytes, fetal cells in amniotic fluid that can be collected by amniocentesis, will turn into muscle cells if MyoD is added to their DNA. These cells then produce muscle proteins such as dystrophin, which could be isolated and analyzed for deficiencies. Patients with rhabdomyosarcoma, a malignant tumor of skeletal muscle, may have lost a tumor suppressor gene that interacts with MyoD. This tumor can also be diagnosed early by testing tumor tissue for the presence of the MyoD protein. MyoD could assist in the delivery of healthy genes to patients with genetic disorders using muscle cells. MyoD can also convert some malignant muscle tumors to healthy muscle tissue.

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