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posted by janrinok on Sunday November 10 2019, @09:44AM   Printer-friendly
from the thar-she-goes! dept.

Arthur T Knackerbracket has found the following story:

Scientists have for the first time seen how the MYC protein, which plays a central role in cancer, binds to a key protein and controls important functions in the cell. The study, published in Nature Structural and Molecular Biology, is a collaboration between scientists at Linköping University, Sweden, and the Princess Margaret Cancer Center in Toronto, Canada. The new discovery may in the long term help in the development of new cancer drugs that disrupt the function of MYC in tumour cells.

The MYC protein regulates many important functions in healthy cells. But MYC is often extremely overactive in aggressive tumours, where its function can be likened to that of an accelerator pedal that has got stuck. The mechanisms by which MYC functions in the cell are largely unknown. The scientists who carried out the present study, therefore, wanted to find out how the transcription factor MYC interacts with another protein, the TATA-binding protein (abbreviated "TBP"). TBP acts as a starting button for the expression of many genes in the cell.

MYC, however, has proved to be elusive for structural biologists. It is what is known as a "disordered" protein, which constantly shifts between different structures in a very dynamic manner. MYC can bind to over 300 different proteins in the cell. The key to MYC being able to interact with so many other proteins so rapidly is probably its adaptability and its ability to change structure in a flash.

[...] The scientists have not been able to directly image the dynamic binding site that has the greater biological function at atomic resolution yet. For this reason, they combined data from different methods and carried out advanced calculations in a supercomputer to model the interaction between the two proteins. They used AI to home in on the structure that agrees best with the observed data and in this way identified a previously unknown binding site. The researchers believe that MYC helps to increase gene expression by making it easier to place TBP at the correct location on the DNA.

Journal: Yong Wei, Diana Resetca, Zhe Li, Isak Johansson-Åkhe, Alexandra Ahlner, Sara Helander, Amelie Wallenhammar, Vivian Morad, Brian Raught, Björn Wallner, Tetsuro Kokubo, Yufeng Tong, Linda Z. Penn, Maria Sunnerhagen. Multiple direct interactions of TBP with the MYC oncoprotein[$]. Nature Structural & Molecular Biology, 2019; DOI: 10.1038/s41594-019-0321-z


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  • (Score: 3, Informative) by Rupert Pupnick on Sunday November 10 2019, @01:22PM

    by Rupert Pupnick (7277) on Sunday November 10 2019, @01:22PM (#918582) Journal

    MYC is implicated in about 500,000 cases in the US a year, which is a little more than 1/4 of the US total, according to a related article on the site.

  • (Score: 1) by RandomFactor on Sunday November 10 2019, @04:09PM (1 child)

    by RandomFactor (3682) Subscriber Badge on Sunday November 10 2019, @04:09PM (#918618) Journal

    The next step was to see whether the structure they had found played a role in the protein's biological function. The scientists created mutations of MYC in which different features of the binding site had been removed. They then investigated how the function of the protein, and how cell growth and survival, were affected.

    "We have shown that both binding sites influence MYC activity and affect cell growth and proliferation. Breaking the interaction between MYC and TBP dramatically decreases the ability of the cells to survive," says Maria Sunnerhagen.

    Translation - it sounds like disrupt this and cancer growth, at the very least, slows.

    Changing aggressive cancers into slower moving ones certainly has potential.

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    • (Score: 2) by HiThere on Sunday November 10 2019, @06:19PM

      by HiThere (866) Subscriber Badge on Sunday November 10 2019, @06:19PM (#918660) Journal

      Welllllll.......yes, but. It also sounds like this may be very disruptive to normal cells. It's something that needs to be checked out, but don't depend on it yet.

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