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. 2008 Jul 29;84(4):1075–1081. doi: 10.1189/jlb.0706462

Fig. 4.

Fig. 4.

Human PMNs as a source of endogenous (i.e., CMP-inhibitable) ST activity. Although pretreatment of PMNs with sialidase and exogenous ST provided maximal ST activity (A, MFI=406 vs.165 with CMP), a strong signal was evident when exogenous ST was added to PMNs unexposed to sialidase pretreatment (B, MFI=310 vs. 167 with CMP). When PMNs were pretreated with sialidase, and intact, untreated PMNs were added as an endogenous source of ST, readily detectable ST activity was evident (C, MFI=295 vs. 141 with CMP). When an aliquot of intact, untreated PMNs was added to PMNs that were not exposed to sialidase, a lesser but distinct signal was apparent (D, MFI=266 vs. 131 with CMP). Transferase activity (shaded peaks) was compared in each case with PMNs, in which no exogenous ST was added and in the presence of the specific ST inhibitor, CMP (0.3 mM final concentration; open peaks).