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- W2146768401 abstract "In rat hepatoma x fibroblast somatic cell hybrids, extinction of rat alpha1-antitrypsin (alpha1AT) gene expression is accompanied by the loss of liver-enriched transcription factors hepatocyte nuclear factor 1 (HNF1alpha) and hepatocyte nuclear factor 4 (HNF4). Previous analysis showed that forced expression of functional HNF1alpha failed to prevent extinction of the rat alpha1AT locus in cell hybrids. Here I show that ectopic co-expression of HNF1alpha plus HNF4 fails to prevent extinction of either rat or human alpha1AT genes in cell hybrids. A 40 kb human alpha1AT minilocus integrated into the rat genome is fully silenced in cell hybrids in the presence of transacting factors. The integrated alpha1AT promoter, but not a viral or ubiquitously active promoter, is repressed 35-fold in the cell hybrids. In addition, position effects also contributed to extinction of many integrated transgenes in a cell type-dependent manner. Finally, internal DNA sequences within the human alpha1AT gene contributed dramatically to the extinction phenotype, resulting in a further 10- to 30-fold reduction in alpha1AT gene expression in cell hybrids. Thus, multiple mechanisms contribute to silencing of tissue-specific gene expression of the alpha1AT gene in cell hybrids." @default.
- W2146768401 created "2016-06-24" @default.
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- W2146768401 date "1999-02-15" @default.
- W2146768401 modified "2023-10-06" @default.
- W2146768401 title "Extinction of alpha1-antitrypsin expression in cell hybrids is independent of HNF1alpha and HNF4 and involves both promoter and internal DNA sequences" @default.
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- W2146768401 doi "https://doi.org/10.1093/nar/27.4.1190" @default.
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