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UCLA Scientists Find New Data To Prevent Transcription Of Cancer Cells

Research done at the UCLA Jonsson Comprehensive Cancer Center has identified an important protein named transcription factor TAF12, which has an important role in the formation of a preinitiation complex. This preinitiation complex is known to have more than one hundred proteins, which are required for the transcription of protein-coding genes.

According to the research, when the TAF12 factor is eliminated, the complete preinitiation complex is destroyed and the genome-wide transcription is downgraded to a large extent.

These findings are very important as the research can lead to cancer therapies, which concentrate on TAF12, thus ending transcription in cancer cells and reducing the growth of cancerous cells. Earlier, other research has shown TAF12 to be responsible for the spread of acute myeloid leukemia in mice.

Commenting on the developments, Michael Carey, Professor of Biological Chemistry and Director of the Gene Regulation Program at the Jonsson Cancer Center, said, ""Identifying TAF12 as the cornerstone of the preinitiation complex allowed us to eliminate preinitiation complexes in the cell, and that has not been done before."

Over the last few years, there has been lot of advancement in studying how the genome is organized and understanding the structures of transcription factors. However, the precise details of how enhancers communicate with promoters, which are the genetic elements that control transcription in human and mouse genomes, to turn on genes, has still not been fully understood.

In this study, UCLA researchers tried to identify the key proteins in the co-activators to see if this knowledge of gene regulation and transcription could be eventually applied to cancer therapeutics. The researchers conducted an shRNA knockdown screen to pinpoint important proteins in gene transcription in mouse embryonic stem cells. A technique known as auxin-inducible degradation was used to remove the identified transcription factor to know the effects on formation of preinitiation complexes throughout the genome.

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