Ruoyan’s paper on “Analysis of the FGFR Signalling Network with Heparin as Co-Receptor: Evidence for the expansion of the core FGFR signaling network” is out.
I am rather late with this post – the paper came out a month ago and I am usually quicker off the mark. The analysis was developed by Ed Yates, as part of our ambition to try to unravel the question of specificity of function, using the fibroblast growth factors (FGFs) as our model. A good model I would argue. Invertebrate animals have two or three FGFs, mammals 22, of which 18 count as “true” or “real” FGFs, that is they are extracellular effectors. What is particularly intriguing is that different FGFs do quite different things, at least according to the labels we use to describe molecular function. Some are outright hormones, while others are morphogens, and so on. The analysis takes in the specificity of FGFs for their different receptors and for their co-receptor heparan sulfate, using heparin as a model for the latter. Despite specificity being rather loose, so not simply 1 to 1, it is there and seems to reflect the evolution of the FGFs.
This is a first instalment. Ruoyan’s successors in the lab are working their way through the FGFs we have not analysed. By the time we make our biennial pilgrimage to the next FGF Gordon Research Conference in March 2014 we will have a lot more to say on this front.