Game changer

I'll apologise now for the geek-out, but sometimes a little piece of science comes around that sets my nerd-senses tingling.  One such event happened a few days ago, and I'm still working it into my world view - this is a game changer (at least in the little corner of the scientific world in which I live.  Sorry, but I need to yell for a second:

INTEGRINS CAN ENGAGE G-PROTEINS!!!!!!!

Not impressed?  You should be - unless, of course, you don't know what integrins or g-proteins are.

As per usual, some background first.
Cells need to stick to things, otherwise we wouldn't exist - instead of a person reading this, you'd be a blob of gelatinous goo if your cells didn't stick together.  One of the more important molecules that does this is called an integrin (image to right).  What makes these special is that they can be turned on/off (called inside-out signalilng), and they also let the cell know if they have bound to something (called outside-in signaling).

G Proteins are something else - they are a family of proteins used by our cells to transmit signals.  In the case of this study the particular G-protein involved is one that normally binds to "G-Protein Coupled Receptors", which are the most common type of receptor used by our bodies to respond and detect stimuli.  Your immune system uses them to respond to some kinds of bacterial products, they're what allow for you to taste, feel, smell and see.  They allow your nerves to work, your blood pressure to change, and they let your blood clot when you get a cut.

So what is so amazing about integrins interacting with G-Proteins?  Its amazing because this shouldn't happen - numerous signalling molecules have been implicated in integrin signalling, but nothing that looks like a G-Protein.  Likewise, G-proteins are not known to interact with anything other than a G-Protein coupled receptor.

OK, that was a lot of background, so what did these guys discover?

As I mentioned above, integrins are involved in the clotting of our blood.  One integrin in particular - alphaIIb beta3 - helps hold those clots together.  Later, once the wounds has healed, the platelets in the clot use the same integrin to controct the clot, thus re-opening the blood vessel to blood flow.  In platelets floating around in your blood this integrin is usually turned off - it won't stick. 
But when our blood clots a protein called thrombin is activated, and in turn activates on of those G-Protein Coupled Receptors I mentioned above, which in turn activates a G-protein.

Once active, that G-protein moves around the cell, turning on and off various biological processes needed to make a clot.  Here is the first amazing thing this study found - one of the things that gets turned on is alphaIIb beta3, by directly interacting with the G-protein.  This allows the platelet to bind the clot.  The second amazing thing occurs later on - when the integrin binds to the clot it re-activates the G-protein; sending a signal into the cell which causes the platelet to contract.

OK, so maybe that's not as exciting as it originally seemed, but I did that kinda work back during my PhD - but I didn't get into science...

Gong H, Shen B, Flevaris P, Chow C, Lam SC, Voyno-Yasenetskaya TA, Kozasa T, & Du X (2010). G protein subunit Galpha13 binds to integrin alphaIIbbeta3 and mediates integrin "outside-in" signaling. Science (New York, N.Y.), 327 (5963), 340-3 PMID: 20075254