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1 the conformational design of antimetastatic disintegrins.
4 a causes upregulation of the metalloprotease-disintegrin ADAM8 (A8) in affected brain regions, spinal
5 sess the contribution of the metalloprotease-disintegrin ADAM9 to ocular neovascularization in mice.
8 talloproteinase with thrombospondin motif, a disintegrin and a metalloprotease, interleukin (IL)-1bet
11 Since PrP(C) is cleaved by members of the disintegrin and matrix-metalloprotease family that are i
12 d generation of the soluble IL-6R by ADAM (a disintegrin and metallo) proteases enables IL-6 trans-si
13 creted proteases, ovochymase 2 (OVCH2) and A disintegrin and metallopeptidase 28 (ADAM28), were expre
16 dding of HEPCAM at two alpha-sites through a disintegrin and metalloprotease (ADAM) and at one beta-s
18 metalloproteases, especially those of the A disintegrin and metalloprotease (ADAM) family, can media
20 embrane-bound precursors by one of several a disintegrin and metalloprotease (ADAM) metalloproteases,
23 ion of matrix metalloproteinase (MMP)- and a disintegrin and metalloprotease (ADAM)-family zinc metal
24 e evidence that human Tim-3 is a target of A disintegrin and metalloprotease (ADAM)-mediated ectodoma
26 with a TLR3 or TLR4 ligand, we identified a disintegrin and metalloprotease (ADAM)15 as a novel TRIF
28 endogenous AXL was dependent on the sheddase disintegrin and metalloprotease 10 (ADAM10) and the gamm
33 The membrane-anchored metalloproteinase a disintegrin and metalloprotease 10 (ADAM10) is required
34 he alpha-hemolysin binding to its receptor A-disintegrin and metalloprotease 10 (ADAM10) upregulates
37 esis or inhibition of mCD23 cleavage by an a disintegrin and metalloprotease 10 inhibitor, GI254023X,
40 on its shedding and binding activities, the disintegrin and metalloprotease 12 (ADAM12) has been imp
41 was significantly correlated with ADAM12 (A Disintegrin And Metalloprotease 12) expression in these
42 ng enzyme type 2 (ACE2) and an increase in a disintegrin and metalloprotease 17 (ADAM17) activity in
46 HER2 trans-activation by IL-1beta required a disintegrin and metalloprotease 17 (ADAM17)-dependent sh
47 (iRhom2) is required for the maturation of A disintegrin and metalloprotease 17 (ADAM17, also called
54 Protein ectodomain shedding by ADAM17 (a disintegrin and metalloprotease 17), a principal regulat
55 vascular epithelial growth factor (VEGF), a disintegrin and metalloprotease 33 (ADAM33), and periost
56 dding is largely attributed to a family of a disintegrin and metalloprotease domain (ADAM) metallopro
57 n of collagen I, CD45, and CD34 or EGFR or a disintegrin and metalloprotease domain 17 and placed in
58 with glutamate and GABA neurotransmission: a disintegrin and metalloprotease domain 22 (Adam22) and h
59 ivation of the sheddase molecule, ADAM 10 (A disintegrin and metalloprotease domain-containing protei
61 nuclear factor of activated T-cells; ADAM, a disintegrin and metalloprotease domain; OTM, orthodontic
65 ed from the cell surface by proteinases of a disintegrin and metalloprotease family; however, the mec
66 ecent studies suggest that serum levels of a disintegrin and metalloprotease protein-12 (ADAM-12) can
67 he length of VWF is regulated by ADAMTS13 (a disintegrin and metalloprotease with a thrombospondin ty
70 rly active 29/31-kDa form of VEGF-C by the A disintegrin and metalloprotease with thrombospondin moti
73 tablished in a pilot approach, identifying a disintegrin and metalloprotease with thrombospondin moti
74 pericytes rapidly activated expression of a disintegrin and metalloprotease with thrombospondin moti
75 t out to investigate the role of ADAMTS-5 (a disintegrin and metalloprotease with thrombospondin moti
76 -21 encodes ADT-2, a member of the ADAMTS (a disintegrin and metalloprotease with thrombospondin moti
78 dothelial cell (HUVEC)-released ADAMTS-13 (a disintegrin and metalloprotease with thrombospondin repe
79 from the endothelial surface by ADAMTS13 (a disintegrin and metalloprotease with thrombospondin type
80 (2) serum creatinine >2.25 mg/dL, and (3) a disintegrin and metalloprotease with thrombospondin type
81 a (TTP) by identifying naturally processed A Disintegrin And Metalloprotease with ThromboSpondin type
82 patients with diabetes, impaired ADAMTS13 (a disintegrin and metalloprotease with thrombospondin type
83 unoglobulin G (IgG) autoantibodies against A Disintegrin And Metalloprotease with ThromboSpondin type
85 ulman syndrome [USS]) severe deficiency of a disintegrin and metalloprotease with thrombospondin type
86 cleavage of von Willebrand factor (VWF) by A disintegrin and metalloprotease with thrombospondin type
88 elated to a severe deficiency in ADAMTS13 (a disintegrin and metalloprotease with thrombospondin type
89 in protein C, protein S, antithrombin and A Disintegrin and Metalloprotease with Thrombospondin type
90 encodes a metalloprotease similar to the "a disintegrin and metalloprotease with thrombospondin" (AD
91 induced shedding was abrogated by an ADAM (A disintegrin and metalloprotease) 10 and 17 selective inh
92 scular smooth muscles, KK stimulates ADAM (a disintegrin and metalloprotease) 17 activity via a PAR1/
94 disintegrin-like domain found in the ADAM (a disintegrin and metalloprotease) family of proteins.
95 re we show that receptor cleavage by ADAM (A Disintegrin And Metalloprotease) metalloproteases promot
96 ADAMDEC1 (Decysin-1) is a putative ADAM (a disintegrin and metalloprotease)-like metalloprotease wi
100 ransmembrane cell-surface metalloprotease, a disintegrin and metalloprotease-17 (ADAM17), and into AD
101 tream matrix metalloproteinases (MMPs) and a disintegrin and metalloproteases (ADAMs) and stimulate p
102 ng mediated by the cell surface proteases "a disintegrin and metalloproteases" (ADAM)-10 and ADAM-17,
104 le of TSPAN33, a tetraspanin implicated in a disintegrin and metalloproteinase (ADAM) 10 maturation,
105 in-22alpha promotor-driven deficiency of the disintegrin and metalloproteinase (ADAM) 17 (SM22-Adam17
108 med a PCR screen for proteolyticlly active A Disintegrin And Metalloproteinase (ADAM) family members.
112 gulate ectodomain shedding mediated by the A Disintegrin And Metalloproteinase (ADAM) subfamily of pr
115 downregulation of metalloproteases mainly a disintegrin and metalloproteinase (ADAM)10, ADAM17, ADAM
116 primed B cell increased gene expression of a disintegrin and metalloproteinase (ADAM)10, which is the
117 wo major transmembrane metalloproteinases, a disintegrin and metalloproteinase (ADAM)17 and ADAM10, a
118 ch as matrix metalloproteinases (MMPs) and a disintegrin and metalloproteinase (ADAMs), are critical
123 ected from skin and lung fibrosis and that a disintegrin and metalloproteinase 10 (ADAM10) is the maj
126 viously described mice lacking endothelial a disintegrin and metalloproteinase 10 (ADAM10), a key reg
128 how that TACI is sequentially processed by a disintegrin and metalloproteinase 10 and gamma-secretase
130 estingly, the drug-induced upregulation of a disintegrin and metalloproteinase 10 on MM cells is asso
131 TACI proteolysis involved shedding by a disintegrin and metalloproteinase 10 releasing sTACI fro
132 by the alpha- and beta-secretases ADAM10 (a disintegrin and metalloproteinase 10) and BACE1 (beta-si
134 sintegrin and metalloproteinase 17 but not a disintegrin and metalloproteinase 10, respectively, whic
135 d high levels of the FcepsilonRII sheddase a disintegrin and metalloproteinase 10, which implies that
136 phiregulin, independent of metalloprotease a disintegrin and metalloproteinase 17 (ADAM17) activity.
138 els of senescence that the metalloprotease A disintegrin and metalloproteinase 17 (ADAM17) is activat
139 f integrin ligation, the metalloproteinase A disintegrin and metalloproteinase 17 (ADAM17) sheds L-se
140 evious studies showed that inactivation of A disintegrin and metalloproteinase 17 (ADAM17), a membran
141 viously shown that epidermal deficiency of a disintegrin and metalloproteinase 17 (ADAM17), the princ
144 Indeed, inhibition of gamma-secretase and a disintegrin and metalloproteinase 17 but not a disintegr
145 embrane-anchored metalloproteinase ADAM17 (a disintegrin and metalloproteinase 17) in endothelial cel
153 ng of HB-EGF by TNFalpha-converting enzyme/a disintegrin and metalloproteinase 9 (ADAM9) and ADAM17.
154 PS/TLR4-mediated generation of sMER required disintegrin and metalloproteinase ADAM17 and was indepen
155 proteinases (MMPs) and proteins containing a disintegrin and metalloproteinase domain (ADAM) are impo
158 heir plasma membrane expression of ADAM17 (a disintegrin and metalloproteinase domain 17), an enzyme
160 Palpha during inflammation is regulated by a disintegrin and metalloproteinase domain-containing prot
161 eases responsible for ectodomain shedding is disintegrin and metalloproteinase domain-containing prot
164 eucine-rich, glioma-inactivated 1 (LGI1) and disintegrin and metalloproteinase domain-containing prot
166 iotensin-converting enzyme-sheddase ADAM9 (a disintegrin and metalloproteinase domain-containing prot
167 ress or a chemical agonist Yoda1 activated a disintegrin and metalloproteinase domain-containing prot
168 anded from a single, deeply conserved adam28 disintegrin and metalloproteinase gene, to as many as 31
169 Genetic truncation of the transmembrane disintegrin and metalloproteinase protein ADAM11 resulte
170 tudies have elucidated the significance of a disintegrin and metalloproteinase proteins (ADAMs) in PN
171 ntegrin and metalloproteinase 10 (ADAM10), a disintegrin and metalloproteinase that resides in the po
173 hrough continuous proteolysis by ADAMTS13 (a disintegrin and metalloproteinase with a thrombospondin
174 adults and mice have implicated ADAMTS13 (a disintegrin and metalloproteinase with a thrombospondin
175 lecular-weight rVWF multimers by ADAMTS13 (a disintegrin and metalloproteinase with a thrombospondin
176 pathy caused by an inherited deficiency of a disintegrin and metalloproteinase with a thrombospondin
178 ly in patients with nondeficient ADAMTS13 (a disintegrin and metalloproteinase with a thrombospondin
179 opment of autoantibodies against ADAMTS13 (a disintegrin and metalloproteinase with a thrombospondin
180 family of extracellular proteases (called a disintegrin and metalloproteinase with thrombospondin mo
182 in the development of osteoarthritis, and a disintegrin and metalloproteinase with thrombospondin mo
184 ggrecan, matrix metalloproteinases (MMPs), a disintegrin and metalloproteinase with thrombospondin mo
185 a-inducible factor-2alpha, syndecan-4, and a disintegrin and metalloproteinase with thrombospondin mo
188 lly, fewer beta-catenin, pSMAD2-, pSMAD3-, a disintegrin and metalloproteinase with thrombospondin mo
189 oproteinase family that cleaves lecticans, a disintegrin and metalloproteinase with thrombospondin mo
190 f1), an endosulfatase gene, and CG4096, an A Disintegrin And Metalloproteinase with ThromboSpondin mo
192 osteoarthritis include metalloproteinases, a disintegrin and metalloproteinase with thrombospondin mo
193 m whereby two distinct metalloproteinases, a disintegrin and metalloproteinase with thrombospondin mo
194 agens by metalloproteinases of the ADAMTS (a disintegrin and metalloproteinase with thrombospondin mo
196 y microenvironment release factors such as a disintegrin and metalloproteinase with thrombospondin mo
197 ecent studies have implicated the protease a disintegrin and metalloproteinase with thrombospondin mo
199 ch as matrix metalloproteinases (MMPs) and a disintegrin and metalloproteinase with thrombospondin mo
201 e Yeast Two-Hybrid approach, we identified a disintegrin and metalloproteinase with thrombospondin re
202 MAs often associated with severe ADAMTS13 (a disintegrin and metalloproteinase with thrombospondin ty
203 strings are naturally cleaved by ADAMTS13 (a disintegrin and metalloproteinase with thrombospondin ty
204 helial activation and dysfunction, whereas a disintegrin and metalloproteinase with thrombospondin ty
205 to the structure and function of ADAMTS13 (a disintegrin and metalloproteinase with thrombospondin-1
206 g for 9 months and correlating with higher a disintegrin and metalloproteinase with thrombospondin-13
207 thrombospondin-13 activity and lower anti-a disintegrin and metalloproteinase with thrombospondin-13
210 age of membrane-anchored proteins by ADAM (a disintegrin and metalloproteinase) endopeptidases plays
211 idate the role of key members of the ADAM (a disintegrin and metalloproteinase) enzyme family, as wel
212 similar to proteins belonging to the ADAM (a disintegrin and metalloproteinase) family, known to proc
219 nd factor (VWF) cleaving enzyme, ADAMTS13 (a disintegrin and metalloproteinase, with a thrombospondin
220 s of matrix metalloproteinase-7 (MMP7) and a disintegrin and metalloproteinase-12 (ADAM12) in alpha(1
222 lls that is cleaved by the metalloprotease a disintegrin and metalloproteinase-17 upon stimulation.
223 ates the TNF-alpha convertase enzyme (TACE/a disintegrin and metalloproteinase-17), leading to activa
226 matrix-specific manner and is required for a disintegrin and metalloproteinase-mediated shedding of t
228 t proteases with Cad6B in vitro shows that a disintegrin and metalloproteinases (ADAMs) ADAM10 and AD
231 omain cleavage of cell-surface proteins by A disintegrin and metalloproteinases (ADAMs) is highly reg
232 beta-site amyloid cleaving enzyme (Bace1), A disintegrin and metalloproteinases (Adams), and presenil
236 atrix metalloproteinases) and the related "a disintegrin and metalloproteinases" (ADAMs) promote tumo
238 fect on matrix metalloproteinase (MMP)-13, a disintegrin and MMP with thrombospondin motifs (ADAMTS)-
240 his investigation addressed the paradox that disintegrins and small RGD-ligands readily bind to the r
243 ife-essential molecules from precursors by a-disintegrin-and-metalloproteases (ADAMs) is regulated wi
245 Knockdown of MMP8 or incubation with the a-disintegrin-and-metalloproteinase-domain-10 inhibitor GI
246 10 and that MMP8 deficiency reduced mature a-disintegrin-and-metalloproteinase-domain-10 on SPCs.
247 xpression levels of ADAM8, a metalloprotease disintegrin, are correlated with poor clinical outcome.
248 a non-protease member of the ADAM family of disintegrins, as a direct estrogen receptor (ER)-indepen
249 analysis of ADAM17 revealed that within its disintegrin/cysteine-rich region are two highly conserve
251 matrix metalloproteinase (MT1-MMP), ADAMs (a disintegrin domain and metalloproteinases), and gamma-se
253 egrins alpha6 and beta1 bind to TACE via the disintegrin domain but also that mechanical strain enhan
254 DAM) proteins inhibit reprogramming, and the disintegrin domain of ADAM29 is necessary and sufficient
255 mpetitive inhibitor of human ADAM9 catalytic/disintegrin domain with an overall inhibition constant o
256 nsists of a prodomain, a catalytic domain, a disintegrin domain, and a membrane-proximal domain as we
257 361, designed by structural modelling of the disintegrin domain, prevents ADAM8 multimerization.
260 membrane-proximal stalk, cysteine-rich, and disintegrin domains of ADAM10 mediated its co-immunoprec
264 ow that ADAM11, a transmembrane noncatalytic disintegrin, is the first reported Kv1-interacting prote
266 ultidomain protein with metalloprotease (M), disintegrin-like (D), thrombospondin-1 (T), Cys-rich (C)
267 has a short propeptide, metalloprotease (M), disintegrin-like (D), thrombospondin-1 (T), Cys-rich (C)
268 lthough UL-VWF is proteolysed by ADAMTS13 (a disintegrin-like and metalloprotease domain with thrombo
269 etermined that mice deficient in ADAMTS5, (A Disintegrin-like And Metalloprotease domain with Thrombo
270 cluding matrix metalloproteases (MMPs) and a disintegrin-like and metalloprotease with thrombospondin
271 -1beta and a resultant increase in ADAMTS (a disintegrin-like and metalloprotease with thrombospondin
272 activity of VWF is modulated by ADAMTS13 (a disintegrin-like and metalloprotease with thrombospondin
273 tly, we reported a gene network of ADAMTS (A Disintegrin-like and Metalloprotease with Thrombospondin
274 ealed that a significant number of ADAMTS (a disintegrin-like and metalloproteinase (reprolysin type)
275 beta domain of the versican-V1 variant by a disintegrin-like and metalloproteinase domain with throm
279 LOC306664 is predicted to translate into A Disintegrin-like and Metalloproteinase with Thrombospond
283 CM enzyme ADAMTS5, a member of the ADAMTS (A Disintegrin-like and Metalloproteinase with Thrombospond
284 tivity and protein expression of ADAMTS13 (a disintegrin-like and metalloproteinase with thrombospond
288 sequence similarity to the integrin-binding disintegrin-like domain found in the ADAM (a disintegrin
289 fy the surface provided by the catalytic and disintegrin-like domains of ADAMTS-5 as a legitimate tar
290 interact, and showed that the catalytic and disintegrin-like domains support these intermolecular in
291 Here, we report that melittin activates disintegrin-like metalloproteases (ADAMs) and that downs
293 loy some combination of ancillary C-terminal disintegrin-like, thrombospondin-1, cysteine-rich, and s
294 and cellular prion (PrP(c)) undergo similar disintegrin-mediated alpha-secretase cleavage yielding N
296 etalloproteinase inhibitors or antibodies to disintegrin metalloproteinase 8 (ADAM8), a major eosinop
297 inal 385-amino acid fragment of ADAMTS-18 (a disintegrin metalloproteinase with thrombospondin motifs
298 n of the disulfide-isomerase ERp5 and of the disintegrin-metalloproteinase ADAM10, able to shed the l
299 oteinases (MMPs) and the related families of disintegrin metalloproteinases (ADAMs) and ADAMs with th
300 tion across the four most abundant proteins (disintegrins, phospholipase A(2)'s, serine proteinases,