These issues include: the determination of regenerative capacity; the importance of stem cells, dedifferentiation and transdifferentiation; how regenerative signals are initiated and targeted; and the mechanisms that control regenerative proliferation and patterning.
Thus, how these multiple signals are initiated and specified to regulate MAPK are obvious important questions to investigate.
Classically, cAMP signals are initiated by the binding of a specific extracellular ligand to a G-protein-coupled receptor (GPCR) that is linked to a heterotrimeric G-protein containing a Gαs subunit.
Signals are initiated by extracellular interactions of the Notch receptor with Delta/Serrate/Lag-2 (DSL) ligands, whose structure is highly conserved throughout evolution.
High-resolution spatiotemporal analysis revealed that Ca2+ influx signals were initiated with different latencies at discrete cellular regions and were propagated along the N19 cell body and processes.
However, upon severe tissue damage that disrupts the epithelium, both stress and polarity signals are initiated to effect repair pathways (see below).
CD137 ligand signaling was initiated as previously described for human peripheral monocytes.
Ice-cold rested cells and beads were span together and signaling was initiated by transfer to 37°C.
The role of flotillin-1 in TLR-induced signaling in human umbilical vein endothelial cells (HUVEC) was studied by shRNA and TLR signaling was initiated by selective agonists.
The [Ca 2+] i signal was initiated when the tip came into contact with the cell and was maximum at the maximum deflection.
