J. Shefcyk

TL;DR: The ability of phorbol 12-myristate 13-acetate to initiate neutrophil responses similar to those produced by the chemotactic factor without causing a rise in the level of intracellular free calcium suggests two possibilities; that there is a second messenger in addition to calcium or that it activates the cells at a point distal to calcium mobilization.

TL;DR: The results reported here suggest that the activity of the Na+/H+ antiport in neutrophils is regulated by protein kinase C; that the G-protein system, either directly or indirectly, is involved in the stimulus-response coupling sequence in these cells; and that the toxin acts at, or prior to, the steps responsible for the activation of phospholipase C.

TL;DR: It is suggested that a rise in the intracellular concentration of free calcium is neither necessary nor sufficient for the stimulated increase in cytoskeletal-associated actin and a possible relationship between the lipid remodeling stimulated by chemoattractants and the increased cytOSkeletal actin is discussed.

TL;DR: P pertussis toxin acts at an early step in the signal transduction and does not affect the sequence of reactions initiated by the activation of the protein kinase C, and the guanine nucleotide regulatory protein Gi, but not Gs, is closely involved in signalTransduction in these cells.

TL;DR: The inhibitory action of high osmolarity on the fMet-Leu-Phe and leukotriene B4 induced stimulation of cytoskeletal actin is discussed in terms of the possibility that the addition of high molarity, either directly or through activation of protein kinase C, causes receptor uncoupling.