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1 a mechanism that was partially prevented by peptidase inhibitors.
2 indicates that it represents a new family of peptidase inhibitors.
3 behavioral and neurochemical effects of the peptidase inhibitors.
4 a subtractive strategy using class-specific peptidase inhibitors.
5 omain related to the Kunitz family of serine peptidase inhibitors.
6 We found that four splice variants of the peptidase inhibitor 16 (PI16) mRNA are among the most hi
8 CCL20, S100A7/A8/A9, DEFB4, lipocalin 2, and peptidase inhibitor 3 (p < 0.05), indicating a positive
10 kines (IL-12p40, IL-13, IL-22, CCL17, CCL18, peptidase inhibitor 3 [PI3]/elafin, and S100As) showed c
11 two negative control genes (cytochrome b and peptidase inhibitor 3) show no significant association.
12 (ie, IL-13, IL-22, CCL17, S100As, and elafin/peptidase inhibitor 3), and modulation of epidermal hype
13 imicrobials (IL-17A, IL-19, CCL20, LL37, and peptidase inhibitor 3/elafin), TH9/IL-9, IL-33, and inna
15 heters that were used to inject a mixture of peptidase inhibitors (amastatin, captopril and phosphora
16 ion in addition to 19 putative peptidases, 9 peptidase inhibitors and 7 C-type lectins that may funct
17 Serpins compose the largest superfamily of peptidase inhibitors and are well known as regulators of
18 nto differential distribution of peptidases, peptidase inhibitors and other potential allergenic prot
19 epE is not inhibited by any of the classical peptidase inhibitors, and its amino acid sequence does n
21 ses and identified IL-1 cytokines and serine peptidase inhibitors as the most dysregulated esophagus-
22 ress several extracellular and intracellular peptidase inhibitors, as well as other molecules that ar
23 (Nqo1), peroxiredoxin-4 (Prdx4), and serine peptidase inhibitor b1b (Serpinb1b) and represses the ex
24 ced MOR-1 internalization in the presence of peptidase inhibitors, but little or no internalization i
25 ngs demonstrate that the application of NAAG peptidase inhibitors can reduce the deleterious motor an
26 tentially interdependent induction of serpin peptidase inhibitor, clade A member 3 (SERPINA3) and int
27 coding alpha-1 antitrypsin, SERPINA1 (serpin peptidase inhibitor, clade A, member 1), in determining
29 r studies indicate that serine (or cysteine) peptidase inhibitor, clade A, member 3N (SerpinA3N) may
31 mily member 1 (CLCA1), periostin, and serine peptidase inhibitor, clade B (ovalbumin), member 2 (serp
34 mutations were found in the SERPINF1 (Serpin Peptidase Inhibitor, Clade F) gene which encodes PEDF (p
35 8 (MTRNRL8), interleukin-8 (IL8), and serpin peptidase inhibitor, clade H (SERPINH1) and chemokine li
37 rally different HsPDF inhibitors and control peptidase inhibitors confirmed that inhibition of HsPDF
39 red on apolipoprotein E, jun, leptin, serpin peptidase inhibitor E type 1 and peroxisome proliferator
41 also differs from human in resisting tryptic peptidase inhibitors (e.g., aprotinin), while favoring a
42 in encoded by one of these genes, epididymal peptidase inhibitor (EPPIN), and associations found betw
43 ression of anti-inflammatory genes mainly of peptidase inhibitor families is upregulated in LL neutro
45 elevated expression of mucin-5B and several peptidase inhibitors, higher abundance of common commens
46 ue secretory signal peptide and a 90-residue peptidase inhibitor I9 domain in addition to the 283-res
47 es to show the involvement of peptidases and peptidase inhibitors in biological pathways have been cr
48 f small-molecule inhibitors in the tables of peptidase-inhibitor interactions, a table of known cleav
49 along with the known substrate cleavages and peptidase-inhibitor interactions, and a link to the KEGG
50 tion of known substrate cleavages; tables of peptidase-inhibitor interactions; and dynamically genera
51 o synthesize both enantiomers of an aspartic peptidase inhibitor intermediate, 3-hydroxy-4-phenylpipe
52 al microglia or adult microglia treated with peptidase inhibitors into spinal cord lesions of adult m
54 or-knockout lines for the ecotin-like serine peptidase inhibitor (ISP2; Deltaisp2/isp3), an inhibitor
58 In this study, we identified SPINT2 (serine peptidase inhibitor Kunitz type 2), a proteolytic inhibi
59 iation between low circulating plasma serine peptidase inhibitor Kunitz type-1 (SPINT1) concentration
60 lactate dehydrogenase B), and SPINT2 (serine peptidase inhibitor, Kunitz type 2) (all P < 0.001).
61 owing study, rats were administered the NAAG peptidase inhibitor PGI-02776 (10mg/kg) 30 min following
64 on- and migration-related proteins including peptidase inhibitors, proteases, receptors, and integrin
65 ction/antimicrobial activity/detoxification, peptidase inhibitors, protein digestion (cysteine-, aspa
67 Inhibition of the GCP II enzyme with NAAG peptidase inhibitors reduces the concentration of glutam
69 previously reported that secretory leukocyte peptidase inhibitor (SLPI) is regulated by the AR in a l
70 ike peptide 1 (GLP1) mimetics and dipeptidyl peptidase inhibitors that enhance GLP1 receptor activati
71 to elicit internalization were unaffected by peptidase inhibitors, the opioids released by veratridin
72 for enkephalin activity, we applied specific peptidase inhibitors to determine which peptidase(s) reg
74 oral effects and support the conclusion NAAG peptidase inhibitors warrant further study as a novel an
75 ty protein group B1 and serine (or cysteine) peptidase inhibitor were only enriched in the presence o
76 ence of cysteine and aspartic peptidases and peptidase inhibitors, whereas other peptidase families w
77 ly 180-kDa multidomain membrane-anchored pan-peptidase inhibitor, which is cleaved by host endopeptid
78 hat will help in the design of additional DD-peptidase inhibitors with the potential to serve as lead
79 gned di-ester prodrug of the urea-based NAAG peptidase inhibitor ZJ-43, was tested for neuroprotectiv
80 pothesis that two structurally distinct NAAG peptidase inhibitors, ZJ43 and 2-(phosphonomethyl)pentan