Hi everyone,
I am currently doing a masters in Architecture and have to research the topic of vinca alkaloids in a lot of depth - just to let you know I am not from a scientific background so apologies if I get anything wrong!
I have done a lot of research in to the method of action of vinblastine and vincristine (I am studying the Madagascan periwinkle in an attempt to produce a design based on bio-mimicry) as microtubule inhibitors, but my tutors would like for me to know exactly HOW the vinca alkaloids disrupt the polymerisation of the tubulin in order to kill the microtubules and prevent further mitosis of the cancerous cells.
Here is what I THINK is happening! : I have read that microtubules have dynamic instability due to their nature of being required to grow/shrink as they please. This leads me to believe that the bonds between the alpha tubulin and the beta tubulin are not that strong, and so the molecules of the vinca alkaloids bind to the beta tubulin effectively sealing the microtubule structure, so that no more alpha tubulin can bind and therefore the microtubule cannot grow, loses all dynamic movement and eventually dies.
If this is what is happening, what causes the molecules of the vinca alkaloids to bind faster to the beta tubulin than the alpha tubulin can? It seems to me that alpha and beta tubulin are designed to polymerize, and therefore I can't work out why the vinca alkaloid would be a better match for the beta tubulin ?
I'm really sorry if this is a little muddled, or if I am completely wrong about any of the above, but if anyone has any knowledge - or can point me in the direction of any publications - on the EXACT method in which vinca alkaloids destroy microtubules I will be forever grateful.
Thanks so much!
