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The study from 1983 focused on human epidermal transglutaminase, an enzyme crucial for epidermal terminal differentiation. It required calcium or strontium and a free sulfhydryl group, similar to liver transglutaminase, but unlike plasma transglutaminase, it did not need proteolytic activation. The enzyme's activity increased significantly after treatment with organic solvents, heat, and chaotropic reagents, although these treatments did not change its molecular weight or immunologic properties. The research aimed to develop monoclonal antibodies for detailed structural analysis and to explore safe methods for modulating the enzyme's function in human epidermal diseases.

The study involved generating a transgenic mouse line overexpressing the SSAT gene under a mouse metallothionein I promoter, leading to significant changes in tissue polyamine pools and delayed permanent hair loss compared to previous models. The liver was notably affected, with altered polyamine levels. Despite high SSAT mRNA levels, enzyme activity was only moderately increased unless induced by ZnSO4 or the polyamine analogue DENSPM, which caused a dramatic increase in enzyme activity and depletion of liver polyamines, resulting in high mortality and liver damage. The findings suggested that SSAT overexpression made the mice highly sensitive to polyamine analogues, indicating a post-transcriptional regulation mechanism.

The study introduced the rat ornithine transcarbamylase (OTC) gene into OTC-deficient spf-ash mice, resulting in significant improvements in enzyme activity and metabolic markers. Hemizygous spf-ash mice with the transgene exhibited liver OTC activity about twice that of nontransgenic counterparts and small intestinal OTC activity 6 times higher, reaching 12% and 27% of control levels, respectively. These transgenic mice displayed normal hair growth, nearly normalized urinary orotic acid excretion, and normalized serum citrulline concentration, indicating a successful correction of the OTC deficiency.

The study involved generating a transgenic mouse line overexpressing the SSAT gene under a mouse metallothionein I promoter, leading to significant changes in tissue polyamine pools and delayed permanent hair loss compared to previous models. The liver was notably affected, with drastic reductions in spermine and increases in putrescine. Despite high levels of SSAT mRNA, enzyme activity was only moderately elevated unless induced by ZnSO4 or the polyamine analogue DENSPM, which caused a massive increase in enzyme activity and depletion of spermidine and spermine pools. This treatment led to high mortality and liver damage, indicating that SSAT overexpression made the mice highly sensitive to polyamine analogues, suggesting a post-transcriptional regulation mechanism.