Does transcriptional profiling reveal functional links between RasGrf1 and Pttg1 in pancreatic beta cells?
The specific transcriptional profile and signaling behavior of RasgGrf1 KO pancreatic islets, together with the dominance of Pttg1 over RasGrf1 with regards to the generation of these phenotypes in mouse pancreas, suggest that RasGrf1 is an important upstream component of signal transduction pathways regulating Pttg1 expression and controlling beta cell development and physiological responses.
The postsurgical corpus callosum increase might be the result of decompression, re-expansion and increase of interstitial fluid, although it may also be caused by differences in shape due to cerebral reorganisation.