Coincidentally, this paper came up in conversation last week -- I didn't realize it was the paper until I got to the methods section though. Coincidence? Or is Ben reading too many papers?
The paper in question is this one from Pei-Wen Chen et al., in JBC a few months ago and it deals with figuring out what the Art GTPase-activating Protein, ASAP1 does in cytoskeletal remodeling.
Rapid background -- Cancer cells have totally whacked out cytoskeletal stuff. You can do really simple stains of just actin with colloidin or whatever and tell the cancer cells are a mess. People have been trying to figure out a pattern in the madness with all sorts of microscopy and things forever. Actually, if you are interested this is a super solid open access review on the topic.
Great approaches to the cytoskeletal approach are 2 of my favorite lab things to do -- proteomics! and immunocytochemistry (ICC/IHC)
In this paper, they are focued on focal adhesions. This is where a bunch of actin builds up to have a ton of structural strength and is the central point of the remodeling (this can also be the starting point for a cell moving -- construct a focal adhesion and move the cell toward or away from it). Focal adhesions can be modelated by several players.
In this study, this group looks at a relative new player ASAP1 and how the activity of this protein might explain some what appeared to be randomness in this remodeling.
They do this by knocking down ASAP1 and by using fibronectin to drive remodeling with/without the protein. Nice ICC and nice LTQ proteomics confirms the active players. All in all, just a nice study out of the NIH that fills in a gap in the remodeling process that might allow some of the other puzzle pieces to fall into place!
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