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1 ole in degrading bacterial and mitochondrial N-formylated peptides.
2 ce phenol-soluble modulins (PSMs), which are N-formylated peptides.
3 asin-deficient mice, even in the presence of N-formylated peptides.
4 s Ib molecule with a high propensity to bind N-formylated peptides.
5                       The lack of endogenous N-formylated peptide allows discovery of novel pathogen-
6 in nociceptor neurons, in part via bacterial N-formylated peptides and the pore-forming toxin alpha-h
7 + T cells, which recognize short hydrophobic N-formylated peptides, appear to comprise a substantial
8 tide deformylase using a series of synthetic N-formylated peptides as substrates.
9                               Although three N-formylated peptides derived from L. monocytogenes are
10 ned whether hPepT1 could transport the model n-formylated peptide fMLP and, if so, whether such cellu
11 ed by prior exposure to the chemoattractants N-formylated peptides (fMLP) or a complement cleavage pr
12 f the fifth component of complement (C5a) or n-formylated peptides (formylmethionylleucylphenylalanin
13  complex (MHC) class Ib molecule H2-M3 binds N-formylated peptides from mitochondria and bacteria.
14 he cell surface by addition of high-affinity N-formylated peptides from mitochondria and listeria.
15                   Upon addition of exogenous N-formylated peptides, M3 trafficks rapidly to the cell
16        Pseudopod growth was stimulated using N-formylated peptide (N-formyl-methionyl-leucyl-phenylal
17 AMPs), such as mitochondrial DNA (mtDNA) and N-formylated peptides (NFPs), are elevated in patients w
18 , whereas tapasin is critical for loading of N-formylated peptides onto the intracellular pool of M3.
19 e to the classic bacterial chemoattractants, n-formylated peptides, or other soluble bacterial factor
20 ein is catalytically active in deformylating N-formylated peptides, shares many of the properties of
21 Purified deformylase is highly active toward N-formylated peptide substrates.
22 ass Ib molecule that preferentially presents N-formylated peptides to CD8(+) T cells.
23         MHC class Ib molecule H2-M3 presents N-formylated peptides to CD8+ CTLs.
24 lity complex class Ib molecule that presents N-formylated peptides to cytotoxic T cells.
25                                  Addition of N-formylated peptides to TAP(o) cells stabilizes M3 in t
26                             Blood amounts of N-formylated peptides, which are endogenous agonists of
27 le of the mouse with a unique preference for N-formylated peptides, which may come from the N-termini