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1  can inhibit matrix metalloproteinases (MMPs/gelatinases).
2 hin the relatively large S1' pocket of these gelatinases.
3 se (MMP) activity, in particular that of the gelatinases.
4 ty of vascular endothelial growth factor and gelatinases.
5 e in the levels of matrix metalloproteinases gelatinase A (MMP-2) and gelatinase B (MMP-9) after part
6 NSE) on two matrix metalloproteinases, MMP-2/gelatinase A and MMP-9/gelatinase B, which are known to
7 or both MMP-9 and metalloproteinase-2 (MMP-2/gelatinase A).
8 he expression of metalloproteinase-2 (MMP-2, gelatinase A).
9 used a NIRF substrate for gelatinases (MMP-2/gelatinase-A and MMP-9/gelatinase-B) in apolipoprotein E
10 as of apoE-/- mice produced NIRF signals for gelatinase action, whereas aortas of apoE+/+ mice inject
11  junction of the cushion tissue and impaired gelatinase activities in the muscular component of the i
12  reduced collagen accumulation and increased gelatinase activities in the wounds of estrogen-treated
13 c mice resulted in a significant decrease of gelatinase activity 1 week after AA treatment.
14  D1- and D2-MSNs and astrocytes, and MMP-2,9 gelatinase activity adjacent to cell surfaces was quanti
15  the fsrB mutant produced very low levels of gelatinase activity after prolonged incubation in vitro
16 ceptors with the RGD ligand liberated by MMP gelatinase activity also potentiated cued cocaine seekin
17      As suggested by our data, inhibition of gelatinase activity appears to be a mechanism of action
18 n-null Alport mice, suggesting that elevated gelatinase activity exacerbates glomerular disease progr
19 e antibodies also immunoprecipitated the HMW gelatinase activity from OA SF.
20 of TG2 activity using KCC009 decreases MMP-2 gelatinase activity in cancer cells.
21 roteinase (MMP)-9 activity in vivo and lower gelatinase activity in cerebral microvessels.
22  zymography confirmed that SB-3CT suppressed gelatinase activity in HVC, and histological analysis re
23 otein (BSP) has been shown to induce limited gelatinase activity in latent matrix metalloproteinase-2
24        Our findings demonstrate that the HMW gelatinase activity in OA SF represents a complex of NGA
25 ta in the stroma and increased the amount of gelatinase activity in the epithelium.
26  hepatic matrixmetalloproteinase (MMP)-9 and gelatinase activity increased significantly after sepsis
27 icated that MMP-9 and not MMP-2 mediated the gelatinase activity observed in infiltrating cells.
28 CNSE, anacardic acid, markedly inhibited the gelatinase activity of 3T3-L1 cells.
29              Furthermore, PAF stimulated the gelatinase activity of MMP-2 by activating transcription
30                            Inhibition of the gelatinase activity of MMP9 decreased the number of meta
31       Gelatine zymography revealed different gelatinase activity patterns that, although not linked t
32        AA treatment results in a decrease in gelatinase activity that correlates with the significant
33 ealed that testosterone-induced perivascular gelatinase activity that was most prominent in HVC.
34                                  Blockade of gelatinase activity using a small molecule inhibitor (BA
35                                     Sites of gelatinase activity visualized by NIRF colocalized with
36 ring short-term rhRLX administration (24 h), gelatinase activity was found to be essential for renal
37 13 expression and matrix metalloproteinase 2 gelatinase activity were significantly impaired in Adam1
38 fter prolonged incubation in vitro versus no gelatinase activity with TX5128 and did not show the ext
39 which showed a similar level of aortic valve gelatinase activity, and inflammation between the two gr
40  with markedly reduced tumor uPA expression, gelatinase activity, and prolonged tumor basement membra
41 podosomes in mouse DC are foci of pronounced gelatinase activity, dependent on the enzyme membrane ty
42  GM6001 (100 mg/kg) ameliorated dysregulated gelatinase activity, neutrophil infiltration, production
43 unction was insensitive to the inhibition of gelatinase activity, suggesting that collagen degradatio
44 prase), which exhibited a 7-fold increase in gelatinase activity, whereas levels of dipeptidyl peptid
45 tinoblastoma (RB) tumor burden by modulating gelatinase activity.
46 rix metalloproteinase-2 and -9 and decreased gelatinase activity.
47 EGF substantially increased endothelial MMP2 gelatinase activity.
48 tivities: dipeptidyl peptidase and a 170-kDa gelatinase activity.
49 ar resistance as a result of upregulation of gelatinase activity.
50  UDCA regulates the expression of TIMP-1 and gelatinases activity in PMA stimulated cells.
51 rococcus faecalis controls the expression of gelatinase and a serine protease via a quorum-sensing me
52                     However, coproduction of gelatinase and cytolysin did not increase virulence addi
53 ment of known virulence traits revealed that gelatinase and cytolysin production accounted for 40.8%
54       Rather, ADAM9 protein is stored in the gelatinase and specific granules and the secretory vesic
55 mulated exocytosis of secretory vesicles and gelatinase and specific granules but not azurophil granu
56 sma membrane/secretory vesicle fractions and gelatinase and specific granules, but not in azurophil g
57 h the gelE gene (pTEX5438) in trans restored gelatinase and translocation, demonstrating that gelatin
58 ree fsr genes also resulted in production of gelatinase and translocation.
59 nt results were found for the expressions of gelatinases and EMMPRIN among the groups demonstrating t
60 ts of CsA on ligature-induced expressions of gelatinases and EMMPRIN in gingival tissues were examine
61 ficantly less gingival protein expression of gelatinases and EMMPRIN than the Lig group.
62 f all legume seeds analyzed, inhibiting both gelatinases and HT29 migration and growth, while pea see
63 member of stromelysins), MMP-9 (considered a gelatinase), and MMP-14 (considered a member of the coll
64 t in the human genome through Western blots, gelatinase, and promoter-reporter assays and incorporate
65 The phage03 gene cluster was also present in gelatinase-and-cytolysin-negative strain E. faecalis JH2
66                                         Both gelatinases are synthesized predominantly by stromal cel
67                             Human neutrophil gelatinase associated lipocalin (NGAL) was found to be i
68 nition using the novel biomarker, neutrophil gelatinase associated lipocalin (NGAL), combined with co
69                     To test if activation of gelatinases associated with seprase could be involved in
70 here was no difference in urinary neutrophil gelatinase-associated liopcalin to creatinine ratios aft
71 rkers of kidney injury, including neutrophil gelatinase-associated lipocalin (NGAL) and podocalyxin,
72 ted whether cystatin C (CysC) and neutrophil gelatinase-associated lipocalin (NGAL) can predict devel
73                             MMP-9/neutrophil gelatinase-associated lipocalin (NGAL) complex is also s
74  electrochemical immunosensor for neutrophil gelatinase-associated lipocalin (NGAL) detection has bee
75 alin-2 (Lcn2) gene, which encodes neutrophil gelatinase-associated lipocalin (NGAL) had the highest f
76                           Urinary neutrophil gelatinase-associated lipocalin (NGAL) has emerged an ea
77 nvestigate the prognostic role of neutrophil gelatinase-associated lipocalin (NGAL) in a large popula
78                                   Neutrophil gelatinase-associated lipocalin (NGAL) is a 25-kDa secre
79                                   Neutrophil gelatinase-associated lipocalin (NGAL) is a diagnostic m
80   Previous research suggests that neutrophil gelatinase-associated lipocalin (NGAL) is a high-quality
81                                   Neutrophil gelatinase-associated lipocalin (NGAL) is a novel renal
82                                   Neutrophil gelatinase-associated lipocalin (NGAL) is a secreted gly
83                                   Neutrophil gelatinase-associated lipocalin (NGAL) is an early marke
84 immunosensor for the detection of neutrophil gelatinase-associated lipocalin (NGAL) is developed by t
85                                   Neutrophil gelatinase-associated lipocalin (NGAL) is expressed and
86 determine the association between neutrophil gelatinase-associated lipocalin (NGAL) levels and cardio
87  = 0.031), and the level of urine neutrophil gelatinase-associated lipocalin (NGAL) was lower (P = 0.
88 einase (MMP)-3, MMP-8, MMP-9, and neutrophil gelatinase-associated lipocalin (NGAL) were found in dis
89 interleukin-8 (IL-8), biotin, and neutrophil gelatinase-associated lipocalin (NGAL) were the most rob
90 creted protein 24p3 (lipocalin-2, neutrophil gelatinase-associated lipocalin (NGAL)), which is expres
91 e results with those obtained for neutrophil gelatinase-associated lipocalin (NGAL), a comparator "AK
92     We explored the expression of neutrophil gelatinase-associated lipocalin (NGAL), a marker of tubu
93 lates epithelial cells to express neutrophil gelatinase-associated lipocalin (Ngal), a member of the
94 ss the prognostic value of plasma neutrophil gelatinase-associated lipocalin (NGAL), a novel marker o
95 bodies induced high expression of neutrophil gelatinase-associated lipocalin (NGAL), an iron-binding
96 sferrin (TF), ceruloplasmin (CP), neutrophil gelatinase-associated lipocalin (NGAL), and monocyte che
97 lant patients to evaluate urinary neutrophil gelatinase-associated lipocalin (NGAL), IL-18, and kidne
98                 Median values for neutrophil gelatinase-associated lipocalin (NGAL), interleukin-18 (
99 e novel AKI biomarkers, including neutrophil gelatinase-associated lipocalin (NGAL), kidney injury mo
100     This study measured levels of neutrophil gelatinase-associated lipocalin (NGAL), kidney injury mo
101                             Urine neutrophil gelatinase-associated lipocalin (NGAL), kidney injury mo
102 y concentrations of microalbumin, neutrophil gelatinase-associated lipocalin (NGAL), kidney injury mo
103 with urinary interleukin (IL)-18, neutrophil gelatinase-associated lipocalin (NGAL), kidney injury mo
104                           Urinary neutrophil gelatinase-associated lipocalin (NGAL), monomeric NGAL (
105 ve measures of urine IL-18, urine neutrophil gelatinase-associated lipocalin (NGAL), or plasma NGAL c
106 ve measures of urine IL-18, urine neutrophil gelatinase-associated lipocalin (NGAL), or plasma NGAL c
107 ased immunoassay for detection of neutrophil gelatinase-associated lipocalin (NGAL), which is a new d
108 pecific for human MMP-9 and human neutrophil gelatinase-associated lipocalin (NGAL).
109 from human neutrophils and termed neutrophil gelatinase-associated lipocalin (NGAL).
110 tio (ACR), and urinary and plasma neutrophil gelatinase-associated lipocalin (NGAL); each measurement
111                               The neutrophil gelatinase-associated lipocalin (NGAL, also known as LCN
112 imed to determine whether urinary neutrophil gelatinase-associated lipocalin (uNGAL) can accurately p
113 uating the cut-off level of urine neutrophil gelatinase-associated lipocalin (uNGAL) for diagnosing A
114                           Urinary neutrophil gelatinase-associated lipocalin (uNGAL) has been identif
115                             Urine neutrophil gelatinase-associated lipocalin (uNGAL) has shown promis
116 s, urinary kidney damage markers, neutrophil gelatinase-associated lipocalin 1, and interleukin 6 wer
117  0.0004), and was noninferior for neutrophil gelatinase-associated lipocalin [14.7 mug/L (interquarti
118              (Acute Kidney Injury Neutrophil Gelatinase-Associated Lipocalin [N-GAL] Evaluation of Sy
119 ney injury molecule-1 [KIM-1] and neutrophil gelatinase-associated lipocalin [NGAL]) and oxidative st
120          Lipocalin 2 (Lcn2; 24p3; neutrophil gelatinase-associated lipocalin [NGAL]) is an antimicrob
121 ination) of 4 urinary biomarkers (neutrophil gelatinase-associated lipocalin [NGAL], interleukin [IL]
122 a tubular damage biomarker (urine neutrophil gelatinase-associated lipocalin [uNGAL]), forming a comp
123 ie2 receptor and in urinary MMP-9/neutrophil gelatinase-associated lipocalin activity after cediranib
124 ence in concentrations of urinary neutrophil gelatinase-associated lipocalin after the 2 infusions (P
125 ermined the prognostic utility of neutrophil gelatinase-associated lipocalin and creatinine, alone an
126     These include a plasma panel (neutrophil gelatinase-associated lipocalin and cystatin C) and a ur
127 ciated with AKI severity, and for neutrophil gelatinase-associated lipocalin and cystatin C, with poo
128                                   Neutrophil gelatinase-associated lipocalin and liver fatty acid-bin
129                             Serum neutrophil gelatinase-associated lipocalin and serum interleukin-18
130                           Urinary neutrophil gelatinase-associated lipocalin and urinary kidney injur
131 rognostic utility of both urinary neutrophil gelatinase-associated lipocalin and varying creatinine-b
132                             Serum neutrophil gelatinase-associated lipocalin at day 3 was lower in th
133     The upper quartile of urinary neutrophil gelatinase-associated lipocalin best predicted the prima
134 um creatinine, interleukin-6, and neutrophil gelatinase-associated lipocalin concentrations.
135 duced sC5b-9, and reduced urinary neutrophil gelatinase-associated lipocalin in the first week posttr
136 /kg/h for >/=12 hours) and plasma neutrophil gelatinase-associated lipocalin level higher than 150 ng
137 n our adjusted models, enrollment neutrophil gelatinase-associated lipocalin level was independently
138 iscriminatory power of enrollment neutrophil gelatinase-associated lipocalin level was the greatest (
139                             Serum neutrophil gelatinase-associated lipocalin levels are strongly pred
140 mbining both DeltaSCr-initial and neutrophil gelatinase-associated lipocalin measured 3 hours after c
141 oline assay and quantification of neutrophil gelatinase-associated lipocalin mRNA.
142 come was noninferiority for urine neutrophil gelatinase-associated lipocalin on the day after surgery
143                             Urine neutrophil gelatinase-associated lipocalin remained independently a
144 ylcarnitine linked with levels of neutrophil gelatinase-associated lipocalin representing acute tubul
145 ve iron, interleukin (IL)-18, and neutrophil gelatinase-associated lipocalin to predict PNF and DGF i
146 in, redox-active iron, IL-18, and neutrophil gelatinase-associated lipocalin to predict viability of
147 otic pathways, and no increase in neutrophil gelatinase-associated lipocalin to suggest tubular injur
148 .8 +/- 10.1 mg/dL, P < 0.05), and neutrophil gelatinase-associated lipocalin urine protein (55.6 +/-
149                           Urinary neutrophil gelatinase-associated lipocalin was measured at baseline
150 ted in intrinsic AKI, but urinary neutrophil gelatinase-associated lipocalin was most useful (81% spe
151                             Urine neutrophil gelatinase-associated lipocalin was the most sensitive m
152                 Combining urinary neutrophil gelatinase-associated lipocalin with a novel creatinine-
153          Others were plasma NGAL (neutrophil gelatinase-associated lipocalin) and NT-proBNP (N-termin
154 f novel urinary biomarkers (e.g., neutrophil gelatinase-associated lipocalin) in this patient group.
155 ycoproteins (e.g., cadherin 5 and neutrophil gelatinase-associated lipocalin) typically circulate in
156 h as kidney injury molecule-1 and neutrophil gelatinase-associated lipocalin).
157 tion between the concentration of neutrophil gelatinase-associated lipocalin, an established AKI biom
158 kers kidney injury molecule-1 and neutrophil gelatinase-associated lipocalin, and doses>/=0.005 mg/kg
159  role of serum cystatin C (Scyc), neutrophil gelatinase-associated lipocalin, and interleukin-18 in p
160 tive tissue growth factor (CTGF), neutrophil gelatinase-associated lipocalin, and kidney injury molec
161                       Biomarkers, neutrophil gelatinase-associated lipocalin, and kidney injury molec
162 T components (elastase, histones, neutrophil gelatinase-associated lipocalin, and proteinase-3) were
163 f high-mobility group protein B1, neutrophil gelatinase-associated lipocalin, and S100B were higher i
164 arkers of renal injury, including neutrophil gelatinase-associated lipocalin, CXCL1, and CXCL2.
165 jury proteins (osteopontin [OPN], neutrophil gelatinase-associated lipocalin, cystatin C, trefoil fac
166 f the MR and downstream molecules neutrophil gelatinase-associated lipocalin, galectin-3, and lipocal
167 els of the iron acceptor proteins neutrophil gelatinase-associated lipocalin, hemopexin, and transfer
168 ls of novel biomarkers, including neutrophil gelatinase-associated lipocalin, high-mobility group pro
169   Kidney injury biomarker levels (neutrophil gelatinase-associated lipocalin, IL-18, and kidney injur
170 ollowing five urinary biomarkers: neutrophil gelatinase-associated lipocalin, IL-18, kidney injury mo
171  highest tertiles of peak urinary neutrophil gelatinase-associated lipocalin, IL-18, KIM-1, liver fat
172 nd cystatin C) and a urine panel (neutrophil gelatinase-associated lipocalin, interleukin 18, and kid
173              A biomarker panel of neutrophil gelatinase-associated lipocalin, interleukin-1ra, and Pr
174 er surgery) urine interleukin 18, neutrophil gelatinase-associated lipocalin, kidney injury molecule
175 e injury biomarkers microalbumin, neutrophil gelatinase-associated lipocalin, kidney injury molecule-
176 dy, 5 urinary biomarkers (urinary neutrophil gelatinase-associated lipocalin, kidney injury molecule-
177 tamyl transpeptidase, cystatin C, neutrophil gelatinase-associated lipocalin, kidney injury molecule-
178 ge markers of renal injury (urine neutrophil gelatinase-associated lipocalin, kidney injury molecule-
179 n and blood flow, whereas GFR and neutrophil gelatinase-associated lipocalin, monocyte chemoattractan
180  we measured renal vein levels of neutrophil gelatinase-associated lipocalin, monocyte chemoattractan
181                                   Neutrophil gelatinase-associated lipocalin, myeloperoxidase, and in
182 dney injury molecule-1, KIM-1 and neutrophil gelatinase-associated lipocalin, NGAL), kidney growth, a
183 gen activator receptor, suPAR and neutrophil gelatinase-associated lipocalin, NGAL.
184  (SCN; also known as lipocalin-2, neutrophil gelatinase-associated lipocalin, or 24p3) into the urina
185 d, the optimal 3-marker panel was neutrophil gelatinase-associated lipocalin, protein C, and interleu
186 sments of blood urea nitrogen and neutrophil gelatinase-associated lipocalin, respectively.
187 nd human homologues 24p3/lcn2 and neutrophil gelatinase-associated lipocalin, show great functional d
188                        Renal vein neutrophil gelatinase-associated lipocalin, tumor necrosis factor-a
189 of recombinant wild-type sequence neutrophil gelatinase-associated lipocalin, wild-type cys(98)-24p3/
190 ted induction of c-fos, junb, and neutrophil gelatinase-associated lipocalin.
191 a marker of neutrophil activation neutrophil gelatinase-associated lipocalin.
192 n of kidney injury molecule-1 and neutrophil gelatinase-associated lipocalin.
193 ated the expression of NGAL/LCN2 (neutrophil gelatinase-associated lipocalin/lipocalin 2), a secreted
194  (SCN; also known as lipocalin 2, neutrophil gelatinase-associated lipocalin/NGAL, or 24p3).
195 adhesion molecule, periostin, and neutrophil gelatinase-associated lipocalin; and a two-fold decrease
196 ney injury molecule-1], and NGAL [neutrophil gelatinase-associated lipocalin]) were evaluated (N=105)
197 e elastase (matrix metalloproteinase-12) and gelatinase B (matrix metalloproteinase-9).
198  metalloproteinases gelatinase A (MMP-2) and gelatinase B (MMP-9) after partial hepatectomy.
199               The effect of Brij-35 on human gelatinase B (MMP-9), matrilysin (MMP-7), and membrane-t
200 ate that a Plg cascade synergizes with MMP-9/gelatinase B in vivo during dermal-epidermal separation
201 urvival can be improved by inhibiting MMP-9 (gelatinase B) activity.
202 nd activation of metalloproteinase-9 (MMP-9, gelatinase B) in a well-established steatotic rat liver
203 gated the role of metalloproteinase-9 (MMP-9/gelatinase B) in liver ischemia/reperfusion (I/R) injury
204 d cord and matrix metalloproteinase-9 (MMP-9/gelatinase B), expressed by infiltrating monocytes.
205 lloproteinases, MMP-2/gelatinase A and MMP-9/gelatinase B, which are known to have critical roles in
206 of the extracellular matrix-degrading enzyme gelatinase B/matrix metalloproteinase-9 (Mmp-9) on islet
207 kage within 30-60 min, likely independent of gelatinase B/MMP-9 activities.
208                               Although MMP-9/gelatinase-B is an important component of these TGF-beta
209 or gelatinases (MMP-2/gelatinase-A and MMP-9/gelatinase-B) in apolipoprotein E-deficient (apoE-/-) mi
210 expression of matrix metalloproteinase MMP-9/gelatinase-B.
211 If the plasmid-containing host also produces gelatinase, bacteriocin cannot be detected.
212 opment of a sensor platform for detection of gelatinases based on porous silicon photonic films.
213                                              Gelatinase belongs to the M4 family of bacterial zinc me
214 sor histidine kinase, upon activation by the gelatinase biosynthesis-activating pheromone (GBAP) pept
215     GFP reporter assays confirmed that GBAP (gelatinase biosynthesis-activating pheromone) quorum non
216 -MMP-9 complex was reconstituted in vitro in gelatinase buffer.
217  biofilm formation through the production of gelatinase, but the mechanism has been hitherto unknown.
218 ce of the initial, transient upregulation of gelatinase by AA injection is unknown, and further studi
219 teinase (MMP)-2 and MMP-9, are extracellular gelatinases capable of degrading another amyloidogenic p
220 provide the first evidence for inhibition of gelatinase catalytic activity by anacardic acid, providi
221 rix metalloproteinase-2 (MMP-2)-an important gelatinase closely associated with tumor aggressiveness
222 ival tissue of the untreated arthritic rats, gelatinase, collagenase, TNF-alpha, and IL-1beta were al
223 little or no translocation and no detectable gelatinase, confirming the importance of both fsr and ge
224 lated targets include other factors, besides gelatinase, described as important for biofilms (BopD),
225 gest that a critical balance between the two gelatinases determines the outcome of inflammatory respo
226  gradients established through the action of gelatinases (eg, matrix metalloproteinase 9), which degr
227                      Eyes were evaluated for gelatinase expression and activity by gel and in situ zy
228 u zymography of retinal tumors showed strong gelatinase expression and activity within transgenic RB
229  rat thermal injury model is associated with gelatinase expression and activity.
230                 Here we show that glomerular gelatinase expression, specifically matrix metalloprotei
231 x metalloproteinase (MMP)-9, a member of the gelatinase family of MMPs, mediates leukocyte migration
232 e, confirming the importance of both fsr and gelatinase for E. faecalis translocation.
233                       Here we show that both gelatinase (GelE) and serine protease (SprE) contribute
234 ion by E. faecalis OG1RF; these mutants lost gelatinase (GelE) and serine protease (SprE) production
235 tion mutant (TX5128), which produces neither gelatinase (GelE) nor the cotranscribed (in the wild typ
236                                              Gelatinase (GelE) purified from E. faecalis V583 was use
237             The endocarditis antigen (efaA), gelatinase (gelE), collagen-binding protein (ace), and a
238 fratricide as the governing principle behind gelatinase (GelE)-mediated cell death and eDNA release.
239 duction of an extracellular metalloprotease, gelatinase (GelE).
240 E. faecalis V583 and E. faecalis lacking the gelatinase gene (gelE).
241 nules, whereas the later-formed specific and gelatinase granules and secretory vesicles contained com
242 il granules to specific granules and then to gelatinase granules, suggesting temporal changes in the
243 eriodontal bone loss with the expressions of gelatinases (i.e., matrix metalloproteinase [MMP]-2 and
244     Zymographic analysis showed that the HMW gelatinase in OA SF comigrated with a purified NGAL-MMP-
245                            Activation of MMP gelatinase in the extracellular space is necessary for a
246    We therefore investigated the role of the gelatinases in neuronal addition to the HVC of adult fem
247 s study, we first examined the expression of gelatinases in vivo using a collagenase-induced mouse mo
248 ed by a compartmental redistribution of this gelatinase, in which intracellular retention resulted in
249                                    Moreover, gelatinase inhibition resulted in a significant increase
250   Carbamate 5b was metabolized to the potent gelatinase inhibitor 2, which was present at therapeutic
251 -MMP-9 neutralizing antibody or with a broad gelatinase inhibitor for both MMP-9 and metalloproteinas
252 tudy was to identify and develop a selective gelatinase inhibitor for imaging active MMP2/MMP9 in viv
253 ated testosterone-implanted females with the gelatinase inhibitor SB-3CT.
254       In contrast, mice treated with a broad gelatinase inhibitor showed rather inferior protection a
255                                              Gelatinase inhibitor treatment abolished NIRF signals in
256 erivatives of SB-3CT, a selective and potent gelatinase inhibitor, were synthesized and evaluated.
257 tinase and translocation, demonstrating that gelatinase is important for E. faecalis translocation.
258                  These results indicate that gelatinase is important for the successful in vitro tran
259                                              Gelatinase is synthesized as a preproenzyme consisting o
260 gest that of the two enterococcal proteases, gelatinase is the principal mediator of pathogenesis in
261 ve also been described for elastase, MMP-13, gelatinases, mast cell proteases and proteases derived f
262 studies suggested a detrimental role for the gelatinase matrix metalloproteinase (MMP)-9 in ICH, the
263 an also modulate the extracellular levels of gelatinases (matrix metalloproteases, MMPs) and potentia
264                                              Gelatinases, matrix metalloproteinase (MMP)-2, and MMP-9
265 veral MMPs, including collagenase MMP-13 and gelatinase MMP-9.
266 uraged us to investigate the activity of the gelatinases MMP-2 and MMP-9 in both cell lines.
267                      ROS, nitrotyrosine, and gelatinase (MMP-2 and MMP-9) zymogen activity markedly i
268                                   The 92-kDa gelatinase (MMP-9) expression is prerequisite for tissue
269                           Because the 92-kDa gelatinase (MMP-9) is a known mediator of tumor cell inv
270                                         Both gelatinases (MMP-2 and -9) and membrane-type 1 MMP (MMP-
271                                              Gelatinases (MMP-2 and MMP-9(Delta444-707)) appear incap
272 D-336, a novel highly selective inhibitor of gelatinases (MMP-2 and MMP-9) and MMP-14, accelerates di
273 ue has high affinity and selectivity for the gelatinases (MMP-2 and MMP-9) and represents a new class
274 erotic plaques, we used a NIRF substrate for gelatinases (MMP-2/gelatinase-A and MMP-9/gelatinase-B)
275 iovascular remodeling, and MMPs, such as the gelatinases (MMP-9 and MMP-2), have been identified in t
276                                    The other gelatinase, MMP-2, is not involved in morphine dependenc
277     Here, we expand our study toward another gelatinase, MMP-2, using molecular dynamics simulations.
278 e interstitial collagenase MMP-1 and the two gelatinases, MMP-2 and MMP-9, but not the membrane-tethe
279                                          The gelatinases, MMP-2 and MMP-9, digest the endothelial bas
280                                              Gelatinases MMP2 and MMP9 are of particular interest bec
281             CsA inhibited the expressions of gelatinase MMPs and EMMPRIN and partially prevented the
282 d@C82(OH)22 is distinguished between the two gelatinase MMPs with atomic details, but also shed light
283                       To assess the possible gelatinase modulation after AA treatment, a single subco
284 of which have gelE but not fsrA or fsrB, are gelatinase negative, and do not translocate), resulted i
285 spin-coating gelatin, a substrate protein to gelatinases, onto the porous silicon, which forms a thin
286  digestion products of gelatin by the active gelatinase present in the sample are able to enter the p
287 tin zymography studies on these two secreted gelatinases, present in the conditioned media from 3T3-L
288 proteinases (TIMPs) and did not activate pro-gelatinases (pro-MMP-2 and pro-MMP-9) even in the presen
289 more, introduction of fsr genes into two non-gelatinase-producing E. faecalis isolates, the well-char
290 gative, and do not translocate), resulted in gelatinase production by these strains and restored tran
291 ontact allergen-induced cytokine production, gelatinase release, and reactive oxygen species producti
292     The results suggest that the E. faecalis gelatinase requires C-terminal processing for full activ
293  metalloelastase) efficiently hydrolyzed the gelatinase-selective alpha1(V)436-447 fluorescent triple
294 , adherence (Epb pili), virulence (cps loci, gelatinase, SprE) and antibiotic resistances (IsaA, tetM
295 e of metalloproteinase 9 (MMP-9), a secreted gelatinase that is consistently up-regulated in both ani
296 f Western immunoblotting showed that the HMW gelatinase was also recognized by antibodies specific fo
297 lis is a secreted bacterial protease, termed gelatinase, which has been shown to contribute to the pr
298 -130-kd band for high molecular weight (HMW) gelatinase, which has not been characterized.
299                               Activating MMP gelatinases with tissue plasminogen activator potentiate
300                             In addition, our gelatinase zymography and fluorescence data confirmed th

 
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