User:David K. Barclay/Notebook/Controlling Pancreas Cell Fate Using Transcription Factors

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==Controlling Pancreas Cell Fate Using Transcription Factors==
==Controlling Pancreas Cell Fate Using Transcription Factors==
* Controlling pancreas cell fate using transcription factors. Cell fate is defined as switching alpha (α) pancreas cells into beta (β) cells, the difference between the two is secretion of glucagon (α) and insulin (β).
* Controlling pancreas cell fate using transcription factors. Cell fate is defined as switching alpha (α) pancreas cells into beta (β) cells, the difference between the two is secretion of glucagon (α) and insulin (β).
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* Pc-TF is a synthetically created fusion protein. The protein is a fusion of a transcription activation domain with a Polycomb chromodomain taken from PRC1 (H3K27me3 repressive complex). The binding of Pc-TF to H3K27me3 opens the gene and upregulates transcription of the gene. This upregulates the previously silenced gene. In pancreas cells, this would have the effect of switching cell fate from α to β. Αlpha cells are seen as undifferentiated cells, making it very possible for the cells states to be switched with this upregulation of gene targets repressed by H3K27me3 PRC1 binding.
==Notes==
==Notes==

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Controlling Pancreas Cell Fate Using Transcription Factors

  • Controlling pancreas cell fate using transcription factors. Cell fate is defined as switching alpha (α) pancreas cells into beta (β) cells, the difference between the two is secretion of glucagon (α) and insulin (β).
  • Pc-TF is a synthetically created fusion protein. The protein is a fusion of a transcription activation domain with a Polycomb chromodomain taken from PRC1 (H3K27me3 repressive complex). The binding of Pc-TF to H3K27me3 opens the gene and upregulates transcription of the gene. This upregulates the previously silenced gene. In pancreas cells, this would have the effect of switching cell fate from α to β. Αlpha cells are seen as undifferentiated cells, making it very possible for the cells states to be switched with this upregulation of gene targets repressed by H3K27me3 PRC1 binding.

Notes

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27 October 2014

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