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1 ine-rich proteins, cystatins, statherin, and histatins.
2 s characteristic of PRP-1, PRP-2, PIF-s, and histatins.
3 basic proline-rich proteins, statherin, and histatins.
4 es containing amylase, PRPs, statherins, and histatins.
5 P) patients, the antimicrobial peptide (AMP) histatin 1 (HTN1) was found to be the most differentiall
9 zymatic cleavage sites as K(13) and K(17) in histatin 1, R(22), Y(24), and R(25) in histatin 3, and Y
11 beta, secretory IgA, and lower lysozyme, and histatins 1 and 5 were found in patients with cirrhosis,
15 The effects of zoledronic acid (1-100 uM), Histatin-1 (10 uM), or their combination was evaluated i
16 The aims of this study were to determine if histatin-1 (H1) is present in normal human tears and whe
17 itulated in endothelial cells (EA.hy926), as Histatin-1 counteracted cytotoxic and antimigratory effe
22 observations highlight the potential use of Histatin-1, in the design of novel therapies aiming to p
24 ntage, we genetically engineered variants of histatin 3 with one, two, three, or four copies of the f
25 7) in histatin 1, R(22), Y(24), and R(25) in histatin 3, and Y(10), K(11), R(12), K(13), H(15), E(16)
33 ther pathogenic fungi by the catonic protein Histatin 5 (Hst 5) is loss of cytoplasmic small molecule
39 in these functional characteristics between histatin 5 and dh-5 on the one hand and dhvar1, dhvar4,
41 dritic cells both demonstrated that 20.0 muM histatin 5 attenuated (p < 0.05) 0.02 muM HagB-induced C
45 more resistant to the antimicrobial peptide histatin 5 but showed essentially normal responses to th
46 hese data indicate that the salivary protein histatin 5 exerts its antifungal function through a mech
49 al proteases, a detailed characterization of histatin 5 inhibition of gingipains from Porphyromonas g
50 e potential mechanistic relationship between histatin 5 interference with the respiratory apparatus a
52 nhibition of the Arg-gingipain revealed that histatin 5 is a competitive inhibitor, affecting only th
54 n that the human salivary antifungal peptide histatin 5 is taken up by Candida albicans cells and ass
56 ing residues 1 to 14 and residues 4 to 15 of histatin 5 showed much lower inhibitory activities (IC50
57 d specifically designed synthetic analogs of histatin 5 to elucidate the role of peptide amphipathici
59 Using biotinylated gelatin as a substrate, histatin 5 was found to inhibit the activity of the host
60 ree peptides containing different regions of histatin 5 were synthesized and tested as inhibitors of
62 re dh-5, comprising the functional domain of histatin 5, and dhvar1 and dhvar4, both designed to maxi
65 peptin, antipain, and EDTA could not prevent histatin 5, statherin, or PRP1 degradation in whole sali
67 nonrespiring yeast cells are insensitive to histatin 5, the potential mechanistic relationship betwe
73 r candidacidal activity by using recombinant histatin-5 and its variants produced in Escherichia coli
75 such as Lys-13 and Arg-22 in the sequence of histatin-5 are, indeed, important for candidacidal activ
76 gnificantly less potent than the recombinant histatin-5 as well as m71, indicating that Arg-22 is cru
77 ignificantly less effective than recombinant histatin-5 in killing Candida albicans, suggesting that
78 ns with affinity tags at the N-terminus, and histatin-5, a peptide with multiple histidine residues.
80 wever, are comparable to that of recombinant histatin-5, indicating that Arg-12, Lys-17, His-19, and
81 nce for a comprehensive mechanistic model of histatin-5-provoked yeast cell death in which oxygen rad
87 line-rich proteins, statherin, and the major histatins are capable of undergoing crosslink reactions
91 roline-rich proteins (PRPs), statherins, and histatins but not MG1, sIgA, secretory component, or cys
92 tatherin, and some of the lysines present in histatins, could participate in the crosslink reaction.
95 oring of the appearance and disappearance of histatin fragments yielded the identification of the fir
101 ylase, proline-rich proteins, statherin, and histatins in salivary secretions, and the aim of this st
102 rly perfect correlation was observed between histatin-induced inhibition of respiration and cell kill
103 ,6,6-tetramethylpiperidine-N-oxyl, abolished histatin-induced ROS formation in isolated mitochondria.
104 n components of saliva, including cystatins, histatins, lysozyme, and isoforms and/or fragments of al
105 Components identified in pellicle included histatins, lysozyme, statherin, cytokeratins, and calgra
107 e rate and mode of degradation of individual histatin proteins in whole saliva to establish the impac
108 consistent with the presence of lysozyme and histatins, respectively, which may represent the major c
113 line-rich proteins, statherin, and the major histatins, whereas a glutamine-containing dansylated pep
114 uates the structure-function relationship of histatins with regard to their candidacidal activity by