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. 2013 Apr 2;14(4):7193–7230. doi: 10.3390/ijms14047193

Table 1.

Intracellular signaling cascades triggered by microbe-derived peptides.

Ligand Origin Selectivity Cells Effects Ref. Potency
Hp(2–20) H. pylori FPR2, FPR3
FPR2
Mon.; Lymph.
MKN-28, AGS
O2−. generation; apoptosis; chemotaxis; proliferation; VEGF secretion; ERKs, Akt and STAT3 activation [6,9] pEC50 = 6.52
F peptide HIV-1 FPR2 Mon.; Neutr. chemotaxis; Ca2+ mobilization; desensitization CCR5 and CXCR4 [7,10] pEC50 = 5.00
V3 peptide HIV-1 FPR2 Mon.; Neutr. chemotaxis; Ca2+ mobilization; desensitization CCR5 [11] pEC50 = 5.82
T21/DP107 HIV-1 FPR2 Mon.; Neutr. chemotaxis; Ca2+ mobilization; [12] pEC50 = 6.30
N36 peptide HIV-1 FPR2 Mon.; Neutr. chemotaxis; Ca2+ mobilization; desensitization chemokine receptors; increased expression of TRAIL; NFκB activation; apoptosis [13,14] pEC50 = 5.00
PSMs Peptide toxins FPR2 Neutrophils Ca++ mobilization; chemotaxis; IL-8 release; NADPH oxidase activation [15,16] pEC50 = 8.67

FPR, formyl-peptide receptor; Mon., monocytes; Lymph., lymphocytes; Neutr., neutrophils; VEGF, vascular endothelial growth factor; ERK, extracellular signal-regulated kinase; Akt, protein kinase B; STAT3, signal transducer and activator of transcription 3; TRAIL, tumor necrosis factor-related apoptosis-inducing ligand; NADPH, nicotinamide adenine dinucleotide phosphate; pEC50, negative logarithm of the EC50.