Anti gene discovery

Sequencing of the human dj-antitrypsin gene in 1984 initiated an explosion in the study of this disease. Transgenic mice were created to study the effects of dj-anti trypsin deficiency, and cell culture studies of the regulation of the gene became possible. In 1992, D. A. Lomas and colleagues (Lomas et al., 1992) showed that the accumulation of abnormal dj-antitrypsin in the ER of the liver was the result of polymerization of dj-antitrypsin.This discovery set the stage for the study of the effects of this polymerized material on the liver, which it is hoped will allow the mechanism of liver disease associated with dj-antitrypsin deficiency to be determined. 

Any step of the viral life cycle can be the target for intervenhon using anti-viral genes. The discovery of co-receptors that are essential for hie viral entry in the cell, but not for cell funchon, has opened the possibility of preventing the viral entry into the cell. These are ideal targets because they prevent the infection of modified cells. CCR5 is the co-receptor that is used by most viral strains [40, 41], while CXCR4 is another co-receptor... 

The discovery of nuclear RARs has introduced a novel method for evaluating the potential carcinostatic activity of a new retinoid [81,84-88], This can be done by measuring the ability of a retinoid either to bind to the RARs [84,85,87,88] or to induce activation of reporter genes via an RAR [81,86-88]. The affinity of retinoids for nuclear receptors in HL-60 cells appears to correlate well with anti-APL activity in vitro [94,95] as discussed in the next section. In general, a good correlation between retinoid carcinostatic activity and ability to bind to or activate retinoic acid receptors appears to exist. 

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