Sandbox Reserved 592: Difference between revisions
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The physiological state of a cell depends on the physiological state of the genes which defines the function of the cell. Unregulated expression of genes in the cell leads to physiological and morphological change of the cell. Euchromatin and heterochromatin define the physiological state of a cell. Mutations and knockout studies of SUV39H1 in mice have shown to increase genomic instability. The instability arises from the inability of SUV39H1 to form heterochromatin. Since the enzyme could not methylate the nucleosomes and transform a euchromatin state into a heterochromatin state, certain genes were highly expressed, which lead to the instability of cells <ref>PMID:22583735</ref>. | The physiological state of a cell depends on the physiological state of the genes which defines the function of the cell. Unregulated expression of genes in the cell leads to physiological and morphological change of the cell. Euchromatin and heterochromatin define the physiological state of a cell. Mutations and knockout studies of SUV39H1 in mice have shown to increase genomic instability. The instability arises from the inability of SUV39H1 to form heterochromatin. Since the enzyme could not methylate the nucleosomes and transform a euchromatin state into a heterochromatin state, certain genes were highly expressed, which lead to the instability of cells <ref>PMID:22583735</ref>. | ||
Further knockout studies of SUV39H1 have shown that length of telomeres in mice and pigs have increased. The increase in the length of the telomeres also increases tumor genesis in pigs and mice. The previous studies, however, did not show a significant telomere growth in human cells. The results may indicate an epigenetic regulation that is more similar between pigs and mice than human <ref>PMID:11701123</ref>. | Further knockout studies of SUV39H1 have shown that length of telomeres in mice and pigs have increased. The increase in the length of the telomeres also increases tumor genesis in pigs and mice. The previous studies, however, did not show a significant telomere growth in human cells. The results may indicate an epigenetic regulation that is more similar between pigs and mice than human <ref>PMID:11701123</ref>. | ||
The results from previous studies in knockout mice further support cancer related symptoms. In colorectal cancer (CLC), Unregulated SUV39H1 lead to the gene silencing of tumor suppressor genes of CLC. The silencing of the tumor suppressor gene leads to the proliferation and subsequent promotion of CLC (Shown in Figure 5). Chaetocin was shown to inhibit SUV39H1 from binding to H3K9. There is also siRNA and other gene therapies which showed inhibition of SUV39H1. | The results from previous studies in knockout mice further support cancer related symptoms. In colorectal cancer (CLC), Unregulated SUV39H1 lead to the gene silencing of tumor suppressor genes of CLC. The silencing of the tumor suppressor gene leads to the proliferation and subsequent promotion of CLC (Shown in Figure 5). Chaetocin was shown to inhibit SUV39H1 from binding to H3K9. There is also siRNA and other gene therapies which showed inhibition of SUV39H1 <ref>PMID:22194015</ref>. | ||
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