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1  can inhibit matrix metalloproteinases (MMPs/gelatinases).
2 ion of which is dependent on the presence of gelatinase.
3 hin the relatively large S1' pocket of these gelatinases.
4 se (MMP) activity, in particular that of the gelatinases.
5 ty of vascular endothelial growth factor and gelatinases.
6 e in the levels of matrix metalloproteinases gelatinase A (MMP-2) and gelatinase B (MMP-9) after part
7 NSE) on two matrix metalloproteinases, MMP-2/gelatinase A and MMP-9/gelatinase B, which are known to
8 or both MMP-9 and metalloproteinase-2 (MMP-2/gelatinase A).
9 he expression of metalloproteinase-2 (MMP-2, gelatinase A).
10 ctive over stromelysin 1, collagenase 1, and gelatinases A and B, respectively.
11 used a NIRF substrate for gelatinases (MMP-2/gelatinase-A and MMP-9/gelatinase-B) in apolipoprotein E
12  will bind selectively to stromelysin-1 over gelatinase-A which is gratifying given the high degree o
13 as of apoE-/- mice produced NIRF signals for gelatinase action, whereas aortas of apoE+/+ mice inject
14  junction of the cushion tissue and impaired gelatinase activities in the muscular component of the i
15  reduced collagen accumulation and increased gelatinase activities in the wounds of estrogen-treated
16 c mice resulted in a significant decrease of gelatinase activity 1 week after AA treatment.
17  the fsrB mutant produced very low levels of gelatinase activity after prolonged incubation in vitro
18  (50 mg/kg, i.p.) showed reduced hippocampal gelatinase activity after transient global cerebral isch
19      As suggested by our data, inhibition of gelatinase activity appears to be a mechanism of action
20 n-null Alport mice, suggesting that elevated gelatinase activity exacerbates glomerular disease progr
21 e antibodies also immunoprecipitated the HMW gelatinase activity from OA SF.
22 of TG2 activity using KCC009 decreases MMP-2 gelatinase activity in cancer cells.
23 roteinase (MMP)-9 activity in vivo and lower gelatinase activity in cerebral microvessels.
24  zymography confirmed that SB-3CT suppressed gelatinase activity in HVC, and histological analysis re
25 otein (BSP) has been shown to induce limited gelatinase activity in latent matrix metalloproteinase-2
26        Our findings demonstrate that the HMW gelatinase activity in OA SF represents a complex of NGA
27 ar washings was evaluated by zymography, and gelatinase activity in the cornea and conjunctiva was de
28 hy of the proximal jejunum reveals increased gelatinase activity in the intestinal wall after ischemi
29  hepatic matrixmetalloproteinase (MMP)-9 and gelatinase activity increased significantly after sepsis
30 orescence co-localization suggests that this gelatinase activity is derived from MMP-9 released from
31 icated that MMP-9 and not MMP-2 mediated the gelatinase activity observed in infiltrating cells.
32 CNSE, anacardic acid, markedly inhibited the gelatinase activity of 3T3-L1 cells.
33              Furthermore, PAF stimulated the gelatinase activity of MMP-2 by activating transcription
34                            Inhibition of the gelatinase activity of MMP9 decreased the number of meta
35       Gelatine zymography revealed different gelatinase activity patterns that, although not linked t
36        AA treatment results in a decrease in gelatinase activity that correlates with the significant
37 ealed that testosterone-induced perivascular gelatinase activity that was most prominent in HVC.
38                                  Blockade of gelatinase activity using a small molecule inhibitor (BA
39                                     Sites of gelatinase activity visualized by NIRF colocalized with
40 ring short-term rhRLX administration (24 h), gelatinase activity was found to be essential for renal
41                                          The gelatinase activity was localized in the external granul
42               In situ zymography showed that gelatinase activity was mostly co-localized with neurons
43               In situ zymography showed that gelatinase activity was mostly colocalized with neuron-s
44 13 expression and matrix metalloproteinase 2 gelatinase activity were significantly impaired in Adam1
45 fter prolonged incubation in vitro versus no gelatinase activity with TX5128 and did not show the ext
46 which showed a similar level of aortic valve gelatinase activity, and inflammation between the two gr
47  with markedly reduced tumor uPA expression, gelatinase activity, and prolonged tumor basement membra
48 podosomes in mouse DC are foci of pronounced gelatinase activity, dependent on the enzyme membrane ty
49  GM6001 (100 mg/kg) ameliorated dysregulated gelatinase activity, neutrophil infiltration, production
50 unction was insensitive to the inhibition of gelatinase activity, suggesting that collagen degradatio
51 prase), which exhibited a 7-fold increase in gelatinase activity, whereas levels of dipeptidyl peptid
52 tinoblastoma (RB) tumor burden by modulating gelatinase activity.
53 rix metalloproteinase-2 and -9 and decreased gelatinase activity.
54 EGF substantially increased endothelial MMP2 gelatinase activity.
55 tivities: dipeptidyl peptidase and a 170-kDa gelatinase activity.
56 ar resistance as a result of upregulation of gelatinase activity.
57  UDCA regulates the expression of TIMP-1 and gelatinases activity in PMA stimulated cells.
58 rococcus faecalis controls the expression of gelatinase and a serine protease via a quorum-sensing me
59                     However, coproduction of gelatinase and cytolysin did not increase virulence addi
60 ment of known virulence traits revealed that gelatinase and cytolysin production accounted for 40.8%
61 tant rendered defective in the expression of gelatinase and serine protease as the result of a polar
62       Rather, ADAM9 protein is stored in the gelatinase and specific granules and the secretory vesic
63 mulated exocytosis of secretory vesicles and gelatinase and specific granules but not azurophil granu
64 sma membrane/secretory vesicle fractions and gelatinase and specific granules, but not in azurophil g
65 h the gelE gene (pTEX5438) in trans restored gelatinase and translocation, demonstrating that gelatin
66 ree fsr genes also resulted in production of gelatinase and translocation.
67 nt results were found for the expressions of gelatinases and EMMPRIN among the groups demonstrating t
68 ts of CsA on ligature-induced expressions of gelatinases and EMMPRIN in gingival tissues were examine
69 ficantly less gingival protein expression of gelatinases and EMMPRIN than the Lig group.
70 f all legume seeds analyzed, inhibiting both gelatinases and HT29 migration and growth, while pea see
71 sed inhibitors that show high selectivity to gelatinases and MMP-14 (inhibitor 3) and to only MMP-2 (
72 trix metalloproteinases (i.e., collagenases, gelatinases) and neutrophil elastase activities.
73 member of stromelysins), MMP-9 (considered a gelatinase), and MMP-14 (considered a member of the coll
74 t in the human genome through Western blots, gelatinase, and promoter-reporter assays and incorporate
75 ficant synergistic reduction of collagenase, gelatinase, and serpinolytic (alpha1-PI degrading) activ
76 The phage03 gene cluster was also present in gelatinase-and-cytolysin-negative strain E. faecalis JH2
77                                         Both gelatinases are synthesized predominantly by stromal cel
78                             Human neutrophil gelatinase associated lipocalin (NGAL) was found to be i
79                     To test if activation of gelatinases associated with seprase could be involved in
80 here was no difference in urinary neutrophil gelatinase-associated liopcalin to creatinine ratios aft
81 ted whether cystatin C (CysC) and neutrophil gelatinase-associated lipocalin (NGAL) can predict devel
82                             MMP-9/neutrophil gelatinase-associated lipocalin (NGAL) complex is also s
83  electrochemical immunosensor for neutrophil gelatinase-associated lipocalin (NGAL) detection has bee
84                           Urinary neutrophil gelatinase-associated lipocalin (NGAL) has emerged an ea
85 nvestigate the prognostic role of neutrophil gelatinase-associated lipocalin (NGAL) in a large popula
86                                   Neutrophil gelatinase-associated lipocalin (NGAL) is a 25-kDa secre
87   Previous research suggests that neutrophil gelatinase-associated lipocalin (NGAL) is a high-quality
88                                   Neutrophil gelatinase-associated lipocalin (NGAL) is a novel renal
89                                   Neutrophil gelatinase-associated lipocalin (NGAL) is a secreted gly
90     We tested the hypothesis that neutrophil gelatinase-associated lipocalin (NGAL) is an early bioma
91                                   Neutrophil gelatinase-associated lipocalin (NGAL) is an early marke
92 immunosensor for the detection of neutrophil gelatinase-associated lipocalin (NGAL) is developed by t
93                                   Neutrophil gelatinase-associated lipocalin (NGAL) is expressed and
94 determine the association between neutrophil gelatinase-associated lipocalin (NGAL) levels and cardio
95 einase (MMP)-3, MMP-8, MMP-9, and neutrophil gelatinase-associated lipocalin (NGAL) were found in dis
96 interleukin-8 (IL-8), biotin, and neutrophil gelatinase-associated lipocalin (NGAL) were the most rob
97 creted protein 24p3 (lipocalin-2, neutrophil gelatinase-associated lipocalin (NGAL)), which is expres
98 e results with those obtained for neutrophil gelatinase-associated lipocalin (NGAL), a comparator "AK
99     We explored the expression of neutrophil gelatinase-associated lipocalin (NGAL), a marker of tubu
100 lates epithelial cells to express neutrophil gelatinase-associated lipocalin (Ngal), a member of the
101 ss the prognostic value of plasma neutrophil gelatinase-associated lipocalin (NGAL), a novel marker o
102                                   Neutrophil gelatinase-associated lipocalin (Ngal), also known as si
103 bodies induced high expression of neutrophil gelatinase-associated lipocalin (NGAL), an iron-binding
104 sferrin (TF), ceruloplasmin (CP), neutrophil gelatinase-associated lipocalin (NGAL), and monocyte che
105 lant patients to evaluate urinary neutrophil gelatinase-associated lipocalin (NGAL), IL-18, and kidne
106                 Median values for neutrophil gelatinase-associated lipocalin (NGAL), interleukin-18 (
107 e novel AKI biomarkers, including neutrophil gelatinase-associated lipocalin (NGAL), kidney injury mo
108                             Urine neutrophil gelatinase-associated lipocalin (NGAL), kidney injury mo
109 y concentrations of microalbumin, neutrophil gelatinase-associated lipocalin (NGAL), kidney injury mo
110 with urinary interleukin (IL)-18, neutrophil gelatinase-associated lipocalin (NGAL), kidney injury mo
111     This study measured levels of neutrophil gelatinase-associated lipocalin (NGAL), kidney injury mo
112 ve measures of urine IL-18, urine neutrophil gelatinase-associated lipocalin (NGAL), or plasma NGAL c
113 ve measures of urine IL-18, urine neutrophil gelatinase-associated lipocalin (NGAL), or plasma NGAL c
114 ased immunoassay for detection of neutrophil gelatinase-associated lipocalin (NGAL), which is a new d
115 pecific for human MMP-9 and human neutrophil gelatinase-associated lipocalin (NGAL).
116 from human neutrophils and termed neutrophil gelatinase-associated lipocalin (NGAL).
117 tio (ACR), and urinary and plasma neutrophil gelatinase-associated lipocalin (NGAL); each measurement
118                               The neutrophil gelatinase-associated lipocalin (NGAL, also known as LCN
119 uating the cut-off level of urine neutrophil gelatinase-associated lipocalin (uNGAL) for diagnosing A
120                           Urinary neutrophil gelatinase-associated lipocalin (uNGAL) has been identif
121                             Urine neutrophil gelatinase-associated lipocalin (uNGAL) has shown promis
122  0.0004), and was noninferior for neutrophil gelatinase-associated lipocalin [14.7 mug/L (interquarti
123              (Acute Kidney Injury Neutrophil Gelatinase-Associated Lipocalin [N-GAL] Evaluation of Sy
124          Lipocalin 2 (Lcn2; 24p3; neutrophil gelatinase-associated lipocalin [NGAL]) is an antimicrob
125 ination) of 4 urinary biomarkers (neutrophil gelatinase-associated lipocalin [NGAL], interleukin [IL]
126 a tubular damage biomarker (urine neutrophil gelatinase-associated lipocalin [uNGAL]), forming a comp
127 ie2 receptor and in urinary MMP-9/neutrophil gelatinase-associated lipocalin activity after cediranib
128 ence in concentrations of urinary neutrophil gelatinase-associated lipocalin after the 2 infusions (P
129 ermined the prognostic utility of neutrophil gelatinase-associated lipocalin and creatinine, alone an
130     These include a plasma panel (neutrophil gelatinase-associated lipocalin and cystatin C) and a ur
131 ciated with AKI severity, and for neutrophil gelatinase-associated lipocalin and cystatin C, with poo
132                                   Neutrophil gelatinase-associated lipocalin and liver fatty acid-bin
133                             Serum neutrophil gelatinase-associated lipocalin and serum interleukin-18
134                           Urinary neutrophil gelatinase-associated lipocalin and urinary kidney injur
135 rognostic utility of both urinary neutrophil gelatinase-associated lipocalin and varying creatinine-b
136                             Serum neutrophil gelatinase-associated lipocalin at day 3 was lower in th
137     The upper quartile of urinary neutrophil gelatinase-associated lipocalin best predicted the prima
138 um creatinine, interleukin-6, and neutrophil gelatinase-associated lipocalin concentrations.
139 /kg/h for >/=12 hours) and plasma neutrophil gelatinase-associated lipocalin level higher than 150 ng
140 n our adjusted models, enrollment neutrophil gelatinase-associated lipocalin level was independently
141 iscriminatory power of enrollment neutrophil gelatinase-associated lipocalin level was the greatest (
142                             Serum neutrophil gelatinase-associated lipocalin levels are strongly pred
143 mbining both DeltaSCr-initial and neutrophil gelatinase-associated lipocalin measured 3 hours after c
144 come was noninferiority for urine neutrophil gelatinase-associated lipocalin on the day after surgery
145                             Urine neutrophil gelatinase-associated lipocalin remained independently a
146 ylcarnitine linked with levels of neutrophil gelatinase-associated lipocalin representing acute tubul
147 ve iron, interleukin (IL)-18, and neutrophil gelatinase-associated lipocalin to predict PNF and DGF i
148 in, redox-active iron, IL-18, and neutrophil gelatinase-associated lipocalin to predict viability of
149 otic pathways, and no increase in neutrophil gelatinase-associated lipocalin to suggest tubular injur
150                           Urinary neutrophil gelatinase-associated lipocalin was measured at baseline
151 ted in intrinsic AKI, but urinary neutrophil gelatinase-associated lipocalin was most useful (81% spe
152                             Urine neutrophil gelatinase-associated lipocalin was the most sensitive m
153                 Combining urinary neutrophil gelatinase-associated lipocalin with a novel creatinine-
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 T components (elastase, histones, neutrophil gelatinase-associated lipocalin, and proteinase-3) were
161 f high-mobility group protein B1, neutrophil gelatinase-associated lipocalin, and S100B were higher i
162 arkers of renal injury, including neutrophil gelatinase-associated lipocalin, CXCL1, and CXCL2.
163 jury proteins (osteopontin [OPN], neutrophil gelatinase-associated lipocalin, cystatin C, trefoil fac
164 els of the iron acceptor proteins neutrophil gelatinase-associated lipocalin, hemopexin, and transfer
165 ls of novel biomarkers, including neutrophil gelatinase-associated lipocalin, high-mobility group pro
166   Kidney injury biomarker levels (neutrophil gelatinase-associated lipocalin, IL-18, and kidney injur
167 ollowing five urinary biomarkers: neutrophil gelatinase-associated lipocalin, IL-18, kidney injury mo
168  highest tertiles of peak urinary neutrophil gelatinase-associated lipocalin, IL-18, KIM-1, liver fat
169 nd cystatin C) and a urine panel (neutrophil gelatinase-associated lipocalin, interleukin 18, and kid
170              A biomarker panel of neutrophil gelatinase-associated lipocalin, interleukin-1ra, and Pr
171 er surgery) urine interleukin 18, neutrophil gelatinase-associated lipocalin, kidney injury molecule
172 dy, 5 urinary biomarkers (urinary neutrophil gelatinase-associated lipocalin, kidney injury molecule-
173 tamyl transpeptidase, cystatin C, neutrophil gelatinase-associated lipocalin, kidney injury molecule-
174 ge markers of renal injury (urine neutrophil gelatinase-associated lipocalin, kidney injury molecule-
175 n and blood flow, whereas GFR and neutrophil gelatinase-associated lipocalin, monocyte chemoattractan
176  we measured renal vein levels of neutrophil gelatinase-associated lipocalin, monocyte chemoattractan
177                                   Neutrophil gelatinase-associated lipocalin, myeloperoxidase, and in
178 dney injury molecule-1, KIM-1 and neutrophil gelatinase-associated lipocalin, NGAL), kidney growth, a
179 gen activator receptor, suPAR and neutrophil gelatinase-associated lipocalin, NGAL.
180  (SCN; also known as lipocalin-2, neutrophil gelatinase-associated lipocalin, or 24p3) into the urina
181 d, the optimal 3-marker panel was neutrophil gelatinase-associated lipocalin, protein C, and interleu
182 nd human homologues 24p3/lcn2 and neutrophil gelatinase-associated lipocalin, show great functional d
183                        Renal vein neutrophil gelatinase-associated lipocalin, tumor necrosis factor-a
184 of recombinant wild-type sequence neutrophil gelatinase-associated lipocalin, wild-type cys(98)-24p3/
185 n of kidney injury molecule-1 and neutrophil gelatinase-associated lipocalin.
186 ted induction of c-fos, junb, and neutrophil gelatinase-associated lipocalin.
187 ated the expression of NGAL/LCN2 (neutrophil gelatinase-associated lipocalin/lipocalin 2), a secreted
188  (SCN; also known as lipocalin 2, neutrophil gelatinase-associated lipocalin/NGAL, or 24p3).
189 adhesion molecule, periostin, and neutrophil gelatinase-associated lipocalin; and a two-fold decrease
190                       By introducing chicken gelatinase B (chMMP-9) as a specific marker for heteroph
191 e elastase (matrix metalloproteinase-12) and gelatinase B (matrix metalloproteinase-9).
192  metalloproteinases gelatinase A (MMP-2) and gelatinase B (MMP-9) after partial hepatectomy.
193               The effect of Brij-35 on human gelatinase B (MMP-9), matrilysin (MMP-7), and membrane-t
194 ate that a Plg cascade synergizes with MMP-9/gelatinase B in vivo during dermal-epidermal separation
195 urvival can be improved by inhibiting MMP-9 (gelatinase B) activity.
196 nd activation of metalloproteinase-9 (MMP-9, gelatinase B) in a well-established steatotic rat liver
197 gated the role of metalloproteinase-9 (MMP-9/gelatinase B) in liver ischemia/reperfusion (I/R) injury
198 d cord and matrix metalloproteinase-9 (MMP-9/gelatinase B), expressed by infiltrating monocytes.
199 lloproteinases, MMP-2/gelatinase A and MMP-9/gelatinase B, which are known to have critical roles in
200 of the extracellular matrix-degrading enzyme gelatinase B/matrix metalloproteinase-9 (Mmp-9) on islet
201 kage within 30-60 min, likely independent of gelatinase B/MMP-9 activities.
202                               Although MMP-9/gelatinase-B is an important component of these TGF-beta
203 or gelatinases (MMP-2/gelatinase-A and MMP-9/gelatinase-B) in apolipoprotein E-deficient (apoE-/-) mi
204 expression of matrix metalloproteinase MMP-9/gelatinase-B.
205 If the plasmid-containing host also produces gelatinase, bacteriocin cannot be detected.
206 opment of a sensor platform for detection of gelatinases based on porous silicon photonic films.
207                                              Gelatinase belongs to the M4 family of bacterial zinc me
208 sor histidine kinase, upon activation by the gelatinase biosynthesis-activating pheromone (GBAP) pept
209     GFP reporter assays confirmed that GBAP (gelatinase biosynthesis-activating pheromone) quorum non
210 -MMP-9 complex was reconstituted in vitro in gelatinase buffer.
211  biofilm formation through the production of gelatinase, but the mechanism has been hitherto unknown.
212 ce of the initial, transient upregulation of gelatinase by AA injection is unknown, and further studi
213 teinase (MMP)-2 and MMP-9, are extracellular gelatinases capable of degrading another amyloidogenic p
214 provide the first evidence for inhibition of gelatinase catalytic activity by anacardic acid, providi
215 rix metalloproteinase-2 (MMP-2)-an important gelatinase closely associated with tumor aggressiveness
216 ival tissue of the untreated arthritic rats, gelatinase, collagenase, TNF-alpha, and IL-1beta were al
217 little or no translocation and no detectable gelatinase, confirming the importance of both fsr and ge
218 lated targets include other factors, besides gelatinase, described as important for biofilms (BopD),
219 gest that a critical balance between the two gelatinases determines the outcome of inflammatory respo
220  gradients established through the action of gelatinases (eg, matrix metalloproteinase 9), which degr
221                      Eyes were evaluated for gelatinase expression and activity by gel and in situ zy
222 u zymography of retinal tumors showed strong gelatinase expression and activity within transgenic RB
223  rat thermal injury model is associated with gelatinase expression and activity.
224                 Here we show that glomerular gelatinase expression, specifically matrix metalloprotei
225 x metalloproteinase (MMP)-9, a member of the gelatinase family of MMPs, mediates leukocyte migration
226 e, confirming the importance of both fsr and gelatinase for E. faecalis translocation.
227                       Here we show that both gelatinase (GelE) and serine protease (SprE) contribute
228 ion by E. faecalis OG1RF; these mutants lost gelatinase (GelE) and serine protease (SprE) production
229 tion mutant (TX5128), which produces neither gelatinase (GelE) nor the cotranscribed (in the wild typ
230                                              Gelatinase (GelE) purified from E. faecalis V583 was use
231             The endocarditis antigen (efaA), gelatinase (gelE), collagen-binding protein (ace), and a
232 fratricide as the governing principle behind gelatinase (GelE)-mediated cell death and eDNA release.
233 duction of an extracellular metalloprotease, gelatinase (GelE).
234 E. faecalis V583 and E. faecalis lacking the gelatinase gene (gelE).
235 d with plasma membrane/secretory vesicle and gelatinase granule fractions increased after fMLP stimul
236 eriodontal bone loss with the expressions of gelatinases (i.e., matrix metalloproteinase [MMP]-2 and
237     Zymographic analysis showed that the HMW gelatinase in OA SF comigrated with a purified NGAL-MMP-
238    We therefore investigated the role of the gelatinases in neuronal addition to the HVC of adult fem
239 s study, we first examined the expression of gelatinases in vivo using a collagenase-induced mouse mo
240 ed by a compartmental redistribution of this gelatinase, in which intracellular retention resulted in
241                                    Moreover, gelatinase inhibition resulted in a significant increase
242   Carbamate 5b was metabolized to the potent gelatinase inhibitor 2, which was present at therapeutic
243 -MMP-9 neutralizing antibody or with a broad gelatinase inhibitor for both MMP-9 and metalloproteinas
244 tudy was to identify and develop a selective gelatinase inhibitor for imaging active MMP2/MMP9 in viv
245 determined that the highly specific thiirane gelatinase inhibitor SB-3CT blocks MMP-9 activity, inclu
246 ated testosterone-implanted females with the gelatinase inhibitor SB-3CT.
247       In contrast, mice treated with a broad gelatinase inhibitor showed rather inferior protection a
248                                              Gelatinase inhibitor treatment abolished NIRF signals in
249 erivatives of SB-3CT, a selective and potent gelatinase inhibitor, were synthesized and evaluated.
250 tinase and translocation, demonstrating that gelatinase is important for E. faecalis translocation.
251                  These results indicate that gelatinase is important for the successful in vitro tran
252                                              Gelatinase is synthesized as a preproenzyme consisting o
253 gest that of the two enterococcal proteases, gelatinase is the principal mediator of pathogenesis in
254 ve also been described for elastase, MMP-13, gelatinases, mast cell proteases and proteases derived f
255 studies suggested a detrimental role for the gelatinase matrix metalloproteinase (MMP)-9 in ICH, the
256 an also modulate the extracellular levels of gelatinases (matrix metalloproteases, MMPs) and potentia
257                                              Gelatinases, matrix metalloproteinase (MMP)-2, and MMP-9
258  have demonstrated detrimental roles for the gelatinase MMP-9 in focal cerebral ischemia, how dysregu
259 veral MMPs, including collagenase MMP-13 and gelatinase MMP-9.
260 uraged us to investigate the activity of the gelatinases MMP-2 and MMP-9 in both cell lines.
261          Gel zymography showed elevations in gelatinase (MMP-2 and MMP-9) activity.
262                      ROS, nitrotyrosine, and gelatinase (MMP-2 and MMP-9) zymogen activity markedly i
263                                   The 92-kDa gelatinase (MMP-9) expression is prerequisite for tissue
264                           Because the 92-kDa gelatinase (MMP-9) is a known mediator of tumor cell inv
265                                         Both gelatinases (MMP-2 and -9) and membrane-type 1 MMP (MMP-
266                                              Gelatinases (MMP-2 and MMP-9(Delta444-707)) appear incap
267 D-336, a novel highly selective inhibitor of gelatinases (MMP-2 and MMP-9) and MMP-14, accelerates di
268 ue has high affinity and selectivity for the gelatinases (MMP-2 and MMP-9) and represents a new class
269 erotic plaques, we used a NIRF substrate for gelatinases (MMP-2/gelatinase-A and MMP-9/gelatinase-B)
270 iovascular remodeling, and MMPs, such as the gelatinases (MMP-9 and MMP-2), have been identified in t
271                                    The other gelatinase, MMP-2, is not involved in morphine dependenc
272     Here, we expand our study toward another gelatinase, MMP-2, using molecular dynamics simulations.
273 e interstitial collagenase MMP-1 and the two gelatinases, MMP-2 and MMP-9, but not the membrane-tethe
274                                          The gelatinases, MMP-2 and MMP-9, digest the endothelial bas
275                                              Gelatinases MMP2 and MMP9 are of particular interest bec
276 w that nCol is a true collagenase, MMP9 is a gelatinase, MMP3/10a is a stromelysin, and MMP3/10b has
277             CsA inhibited the expressions of gelatinase MMPs and EMMPRIN and partially prevented the
278 d@C82(OH)22 is distinguished between the two gelatinase MMPs with atomic details, but also shed light
279                       To assess the possible gelatinase modulation after AA treatment, a single subco
280 of which have gelE but not fsrA or fsrB, are gelatinase negative, and do not translocate), resulted i
281                              The majority of gelatinase-negative isolates, including 14 endocarditis
282  isolates but little to no translocation for gelatinase nonproducers.
283 spin-coating gelatin, a substrate protein to gelatinases, onto the porous silicon, which forms a thin
284 isolates), which showed translocation by all gelatinase-positive isolates but little to no translocat
285  digestion products of gelatin by the active gelatinase present in the sample are able to enter the p
286 tin zymography studies on these two secreted gelatinases, present in the conditioned media from 3T3-L
287 proteinases (TIMPs) and did not activate pro-gelatinases (pro-MMP-2 and pro-MMP-9) even in the presen
288 more, introduction of fsr genes into two non-gelatinase-producing E. faecalis isolates, the well-char
289 gative, and do not translocate), resulted in gelatinase production by these strains and restored tran
290                            The importance of gelatinase production was also corroborated among 20 E.
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  gene gelE encoding the zinc-metalloprotease gelatinase was found to prevent biofilm formation, sugge
298 lis is a secreted bacterial protease, termed gelatinase, which has been shown to contribute to the pr
299 -130-kd band for high molecular weight (HMW) gelatinase, which has not been characterized.
300                             In addition, our gelatinase zymography and fluorescence data confirmed th

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