PMID-sentid Pub_year Sent_text comp_official_name comp_offset protein_name organism prot_offset 33882688-0 2021 ADAM17 Boosts Cholesterol Efflux and Downstream Effects of High-Density Lipoprotein on Inflammatory Pathways in Macrophages. Cholesterol 14-25 a disintegrin and metallopeptidase domain 17 Mus musculus 0-6 33804608-5 2021 Loss- and gain-of-function studies in murine embryonic fibroblasts showed that constitutive shedding as well as phorbol-ester-induced processing of FGFRs 1, 3, and 4 is mediated by ADAM17. Phorbol Esters 112-125 a disintegrin and metallopeptidase domain 17 Mus musculus 181-187 34896343-0 2022 Simvastatin mitigates streptozotocin-induced type 1 diabetes in mice through downregulation of ADAM10 and ADAM17. Simvastatin 0-11 a disintegrin and metallopeptidase domain 17 Mus musculus 106-112 34896343-0 2022 Simvastatin mitigates streptozotocin-induced type 1 diabetes in mice through downregulation of ADAM10 and ADAM17. Streptozocin 22-36 a disintegrin and metallopeptidase domain 17 Mus musculus 106-112 34896343-12 2022 KEY FINDINGS: Significant increase in biochemical, inflammatory, apoptotic parameters, expression of ADAM10, ADAM17, CXCL16, NF-kappaB, and infiltrated T-cells to the pancreatic islets were found in STZ group. Streptozocin 199-202 a disintegrin and metallopeptidase domain 17 Mus musculus 109-115 34896343-13 2022 SIM treatment in the presence of STZ improved biochemical and inflammatory parameters as well as it reduced the expression of CXCL16, ADAM10, ADAM17, NF-kappaBeta, T-cells migration and apoptosis in the pancreatic islets. Simvastatin 0-3 a disintegrin and metallopeptidase domain 17 Mus musculus 142-148 34896343-13 2022 SIM treatment in the presence of STZ improved biochemical and inflammatory parameters as well as it reduced the expression of CXCL16, ADAM10, ADAM17, NF-kappaBeta, T-cells migration and apoptosis in the pancreatic islets. Streptozocin 33-36 a disintegrin and metallopeptidase domain 17 Mus musculus 142-148 34896343-14 2022 SIGNIFICANCE: SIM mitigated pancreatic beta-cell death induced by STZ through down regulation of ADAM10, ADAM17and CXCL16. Simvastatin 14-17 a disintegrin and metallopeptidase domain 17 Mus musculus 105-111 34896343-14 2022 SIGNIFICANCE: SIM mitigated pancreatic beta-cell death induced by STZ through down regulation of ADAM10, ADAM17and CXCL16. Streptozocin 66-69 a disintegrin and metallopeptidase domain 17 Mus musculus 105-111 34884897-7 2021 Adam17 tubular deletion improved glucose tolerance and protected animals against glomerular injury and prevented podocyte loss in HFD mice. Glucose 33-40 a disintegrin and metallopeptidase domain 17 Mus musculus 0-6 34884897-10 2021 In conclusion, Adam17 in proximal tubules influences glucose tolerance and participates in the kidney injury in an obese pre-diabetic murine model. Glucose 53-60 a disintegrin and metallopeptidase domain 17 Mus musculus 15-21 34545369-7 2021 Lung mRNA abundance of ADAM17 and TMPRSS2, enzymes that shed cell surface ACE2 and facilitate viral cell entry, was reduced by GDX in male but not female mice. GDP-alpha-D-mannuronic acid 127-130 a disintegrin and metallopeptidase domain 17 Mus musculus 23-29 34075077-5 2021 In contrast, antagonistic effects of ADAM10 and ADAM17 were observed in the model of chronic CCl4 intoxication. Carbon Tetrachloride 93-97 a disintegrin and metallopeptidase domain 17 Mus musculus 48-54 35079379-0 2022 TGF-beta-activated kinase-1 inhibitor LL-Z1640-2 reduces joint inflammation and bone destruction in mouse models of rheumatoid arthritis by inhibiting NLRP3 inflammasome, TACE, TNF-alpha and RANKL expression. LL Z1640-2 38-48 a disintegrin and metallopeptidase domain 17 Mus musculus 171-175 34751824-4 2022 We analyzed OA development in tamoxifen-inducible chondrocyte-specific Adam17 knockout mice of a resection of the medial meniscus and medial collateral ligament (medial) model, destabilization of the medial meniscus (DMM) model, and aging model. Tamoxifen 30-39 a disintegrin and metallopeptidase domain 17 Mus musculus 71-77 34751824-5 2022 We analyzed downstream pathways by in vitro experiments, and further performed intra-articular administration of an Adam17 inhibitor TAPI-0 for surgically induced mouse OA. TAPI-0 133-139 a disintegrin and metallopeptidase domain 17 Mus musculus 116-122 34751824-8 2022 Adam17 knockout decreased matrix metallopeptidase 13 (Mmp13) expression in both in vivo and in vitro experiments, whereas Adam17 activation by phorbol-12-myristate-13-acetate (PMA) increased Mmp13 and decreased aggrecan in mouse primary chondrocytes. Tetradecanoylphorbol Acetate 143-174 a disintegrin and metallopeptidase domain 17 Mus musculus 122-128 34751824-8 2022 Adam17 knockout decreased matrix metallopeptidase 13 (Mmp13) expression in both in vivo and in vitro experiments, whereas Adam17 activation by phorbol-12-myristate-13-acetate (PMA) increased Mmp13 and decreased aggrecan in mouse primary chondrocytes. Tetradecanoylphorbol Acetate 176-179 a disintegrin and metallopeptidase domain 17 Mus musculus 122-128 34571815-5 2021 Specifically, idebenone reduced the RAGE/caspase-3 signaling pathway and increased levels of the Abeta degradation enzyme NEP and alpha-secretase ADAM17 in 5xFAD mice. idebenone 14-23 a disintegrin and metallopeptidase domain 17 Mus musculus 146-152 34575910-6 2021 In the heart, DHT upregulated AR protein in both LFD and HFD, ACE2 in HFD, and ADAM17 in LFD. Dihydrotestosterone 14-17 a disintegrin and metallopeptidase domain 17 Mus musculus 79-85 34575910-8 2021 Moreover, ACE2 and ADAM17 were upregulated by DHT in both diets. Dihydrotestosterone 46-49 a disintegrin and metallopeptidase domain 17 Mus musculus 19-25 34130299-10 2021 Compared to mice treated with HNE alone, in HNE + TAPI-2-treated mice, the levels of TACE, EGFR, and MUC5AC mRNA and protein as well as p-EGFR protein were significantly reduced (p < 0.01). TAPI-2 50-56 a disintegrin and metallopeptidase domain 17 Mus musculus 85-89 34130299-11 2021 In HNE + AG1478-treated mice, EGFR and MUC5AC mRNA and protein levels and p-EGFR protein expression were reduced significantly (p < 0.01), but the difference in TACE mRNA and protein expression between the HNE + AG1478 and HNE groups was not significant (p > 0.05). RTKI cpd 9-15 a disintegrin and metallopeptidase domain 17 Mus musculus 161-165 35095853-5 2021 Moreover, inhibition of ADAM17 bioactivity with the specific inhibitor DPC 333 significantly improved both biochemical and histological evidence of liver damage in BDL mice. BMS561392 71-78 a disintegrin and metallopeptidase domain 17 Mus musculus 24-30 33882688-5 2021 Furthermore, ADAM17-deficient macrophages exhibited reduced expression of ABCA1 (ATP-binding cassette A1) and reduced cholesterol efflux and were cholesterol loaded. Cholesterol 118-129 a disintegrin and metallopeptidase domain 17 Mus musculus 13-19 33882688-5 2021 Furthermore, ADAM17-deficient macrophages exhibited reduced expression of ABCA1 (ATP-binding cassette A1) and reduced cholesterol efflux and were cholesterol loaded. Cholesterol 146-157 a disintegrin and metallopeptidase domain 17 Mus musculus 13-19 33882688-9 2021 CONCLUSIONS: The increased cholesterol loading of ADAM17-deficient macrophages prevents both anti-inflammatory and proinflammatory responses of HDL. Cholesterol 27-38 a disintegrin and metallopeptidase domain 17 Mus musculus 50-56 33882688-10 2021 Our findings demonstrate a novel role for ADAM17 in maintaining cholesterol efflux in macrophages, thereby regulating the immune functions of these cells. Cholesterol 64-75 a disintegrin and metallopeptidase domain 17 Mus musculus 42-48 33957124-8 2021 Nevertheless, ADAM17Deltacyto could be stimulated by PMA, a well-characterized post-translational activator of ADAM17, corroborating that the cytoplasmic domain of endogenous ADAM17 is not required for its rapid response to PMA. Tetradecanoylphorbol Acetate 53-56 a disintegrin and metallopeptidase domain 17 Mus musculus 14-20 34035876-9 2021 In vivo, we used a mouse model of cardiac fibrosis established by left anterior descending artery ligation; the mice were administered oral gavage with a selective ADAM17 inhibitor (TMI-005) for 4 weeks after the operation. apratastat 182-189 a disintegrin and metallopeptidase domain 17 Mus musculus 164-170 33953303-3 2021 Here we report for the first time, a family with NISBD1 caused by functionally confirmed compound heterozygous missense variants of ADAM17, namely c.1699T>C (p.Cys567Arg) and c.1799G>A (p.Cys600Tyr). cys567arg 160-169 a disintegrin and metallopeptidase domain 17 Mus musculus 132-138 33953303-3 2021 Here we report for the first time, a family with NISBD1 caused by functionally confirmed compound heterozygous missense variants of ADAM17, namely c.1699T>C (p.Cys567Arg) and c.1799G>A (p.Cys600Tyr). cys600tyr 188-197 a disintegrin and metallopeptidase domain 17 Mus musculus 132-138 33953303-5 2021 In a cell-based assay using Adam10/17 double-knockout mouse embryonic fibroblasts (Adam10/17-/- mEFs) exogenously expressing each of these mutants, phorbol 12-myristate 13-acetate-stimulated shedding was strongly reduced compared with wild-type ADAM17. Tetradecanoylphorbol Acetate 148-179 a disintegrin and metallopeptidase domain 17 Mus musculus 245-251 33957124-8 2021 Nevertheless, ADAM17Deltacyto could be stimulated by PMA, a well-characterized post-translational activator of ADAM17, corroborating that the cytoplasmic domain of endogenous ADAM17 is not required for its rapid response to PMA. Tetradecanoylphorbol Acetate 53-56 a disintegrin and metallopeptidase domain 17 Mus musculus 111-117 33957124-8 2021 Nevertheless, ADAM17Deltacyto could be stimulated by PMA, a well-characterized post-translational activator of ADAM17, corroborating that the cytoplasmic domain of endogenous ADAM17 is not required for its rapid response to PMA. Tetradecanoylphorbol Acetate 53-56 a disintegrin and metallopeptidase domain 17 Mus musculus 111-117 33922918-14 2021 ACE2 sheddase Adam17 mRNA was upregulated by DHT in the kidney, which corresponded with increased urinary ACE2 in DHT treated mice. Dihydrotestosterone 45-48 a disintegrin and metallopeptidase domain 17 Mus musculus 14-20 33922918-14 2021 ACE2 sheddase Adam17 mRNA was upregulated by DHT in the kidney, which corresponded with increased urinary ACE2 in DHT treated mice. Dihydrotestosterone 114-117 a disintegrin and metallopeptidase domain 17 Mus musculus 14-20 33303781-5 2020 The cleavage occurs between Pro-355 and Val-356, which is the same cleavage site that the metalloprotease ADAM17 uses in vitro. Proline 28-31 a disintegrin and metallopeptidase domain 17 Mus musculus 106-112 33673337-8 2021 The selectivity of ADAM17 for EDTA-induced Notch1 processing can most likely be explained by a preference for ADAM17 over ADAM10 for the Notch1 cleavage site and by the stronger inhibition of ADAM10 by EDTA. Edetic Acid 30-34 a disintegrin and metallopeptidase domain 17 Mus musculus 19-25 33673337-8 2021 The selectivity of ADAM17 for EDTA-induced Notch1 processing can most likely be explained by a preference for ADAM17 over ADAM10 for the Notch1 cleavage site and by the stronger inhibition of ADAM10 by EDTA. Edetic Acid 30-34 a disintegrin and metallopeptidase domain 17 Mus musculus 110-116 33673337-8 2021 The selectivity of ADAM17 for EDTA-induced Notch1 processing can most likely be explained by a preference for ADAM17 over ADAM10 for the Notch1 cleavage site and by the stronger inhibition of ADAM10 by EDTA. Edetic Acid 202-206 a disintegrin and metallopeptidase domain 17 Mus musculus 19-25 33181031-10 2021 In addition, genetic blockade of ADAM17 protected mice from CS-induced pulmonary inflammation and alveolar cell apoptosis. Cesium 60-62 a disintegrin and metallopeptidase domain 17 Mus musculus 33-39 33375653-11 2020 In addition, stimulation with high concentration of glutamate significantly increased B1R gene and protein expression, along with increased ADAM17 and decreased ACE2 activities in wild-type neurons. Glutamic Acid 52-61 a disintegrin and metallopeptidase domain 17 Mus musculus 140-146 33375653-12 2020 Pretreatment with B1R-specific antagonist R715 reversed these glutamate-induced effects suggesting that indeed B1R is involved in glutamate-mediated upregulation of ADAM17 activity and ACE2 shedding. Glutamic Acid 62-71 a disintegrin and metallopeptidase domain 17 Mus musculus 165-171 33375653-12 2020 Pretreatment with B1R-specific antagonist R715 reversed these glutamate-induced effects suggesting that indeed B1R is involved in glutamate-mediated upregulation of ADAM17 activity and ACE2 shedding. Glutamic Acid 130-139 a disintegrin and metallopeptidase domain 17 Mus musculus 165-171 33298044-2 2020 We previously reported that 4-HIL potentiates anti-inflammatory and anti-insulin resistance effects through down-regulation of TNF-alpha and TNF-alpha converting enzyme (TACE) in 3 T3-L1 adipocytes and HepG2 cells. 4-hydroxyisoleucine 28-33 a disintegrin and metallopeptidase domain 17 Mus musculus 141-168 33298044-2 2020 We previously reported that 4-HIL potentiates anti-inflammatory and anti-insulin resistance effects through down-regulation of TNF-alpha and TNF-alpha converting enzyme (TACE) in 3 T3-L1 adipocytes and HepG2 cells. 4-hydroxyisoleucine 28-33 a disintegrin and metallopeptidase domain 17 Mus musculus 170-174 33303781-5 2020 The cleavage occurs between Pro-355 and Val-356, which is the same cleavage site that the metalloprotease ADAM17 uses in vitro. Valine 40-43 a disintegrin and metallopeptidase domain 17 Mus musculus 106-112 32932701-7 2020 Mice treated with the ADAM17 mAb MEDI3622 prior to sepsis induction exhibited significantly decreased mortality. medi3622 33-41 a disintegrin and metallopeptidase domain 17 Mus musculus 22-28 33005106-0 2020 Long non-coding RNA MALAT1 regulates oxaliplatin-resistance via miR-324-3p/ADAM17 axis in colorectal cancer cells. Oxaliplatin 37-48 a disintegrin and metallopeptidase domain 17 Mus musculus 75-81 33005106-13 2020 Conclusion: MALAT1 modulated the sensitivity of Ox through ADAM17 in Ox-resistant CRC cells by sponging miR-324-3p, thus MALAT1 might serve as a novel insight for the therapy of CRC. mir-324-3p 104-114 a disintegrin and metallopeptidase domain 17 Mus musculus 59-65 32866465-3 2020 By using immunohistochemical and ELISA techniques, it was found that CsA administration causes a rapid activation of a disintegrin and metalloproteases-17 (ADAM-17), epidermal growth factor receptor (EGFR) and subsequent ERK1/2 phosphorylation in the liver and kidney of albino mice. Cyclosporine 69-72 a disintegrin and metallopeptidase domain 17 Mus musculus 156-163 32866465-4 2020 Furthermore, this study presents mechanistic relevance of this signaling cascade involving reactive oxygen species (ROS)-mediated ADAM-17/EGFR/ERK1/2 activation as indicated by a clear reduction in ADAM-17 and EGFR activities as well as ERK1/2 phosphorylation when the animals pretreated with Polyethylene glycol-superoxide dismutase (PEG-SOD) before CsA administration. Reactive Oxygen Species 91-114 a disintegrin and metallopeptidase domain 17 Mus musculus 130-137 32866465-4 2020 Furthermore, this study presents mechanistic relevance of this signaling cascade involving reactive oxygen species (ROS)-mediated ADAM-17/EGFR/ERK1/2 activation as indicated by a clear reduction in ADAM-17 and EGFR activities as well as ERK1/2 phosphorylation when the animals pretreated with Polyethylene glycol-superoxide dismutase (PEG-SOD) before CsA administration. Reactive Oxygen Species 91-114 a disintegrin and metallopeptidase domain 17 Mus musculus 198-205 32866465-4 2020 Furthermore, this study presents mechanistic relevance of this signaling cascade involving reactive oxygen species (ROS)-mediated ADAM-17/EGFR/ERK1/2 activation as indicated by a clear reduction in ADAM-17 and EGFR activities as well as ERK1/2 phosphorylation when the animals pretreated with Polyethylene glycol-superoxide dismutase (PEG-SOD) before CsA administration. Reactive Oxygen Species 116-119 a disintegrin and metallopeptidase domain 17 Mus musculus 130-137 32866465-4 2020 Furthermore, this study presents mechanistic relevance of this signaling cascade involving reactive oxygen species (ROS)-mediated ADAM-17/EGFR/ERK1/2 activation as indicated by a clear reduction in ADAM-17 and EGFR activities as well as ERK1/2 phosphorylation when the animals pretreated with Polyethylene glycol-superoxide dismutase (PEG-SOD) before CsA administration. Reactive Oxygen Species 116-119 a disintegrin and metallopeptidase domain 17 Mus musculus 198-205 32866465-4 2020 Furthermore, this study presents mechanistic relevance of this signaling cascade involving reactive oxygen species (ROS)-mediated ADAM-17/EGFR/ERK1/2 activation as indicated by a clear reduction in ADAM-17 and EGFR activities as well as ERK1/2 phosphorylation when the animals pretreated with Polyethylene glycol-superoxide dismutase (PEG-SOD) before CsA administration. Cyclosporine 351-354 a disintegrin and metallopeptidase domain 17 Mus musculus 130-137 32866465-5 2020 Collectively, our findings demonstrate that CsA has the ability to activate ADAM-17-mediated EGFR/ERK1/2 phosphorylation in the liver and kidney of albino mice in ROS-dependent manner. Cyclosporine 44-47 a disintegrin and metallopeptidase domain 17 Mus musculus 76-83 32866465-5 2020 Collectively, our findings demonstrate that CsA has the ability to activate ADAM-17-mediated EGFR/ERK1/2 phosphorylation in the liver and kidney of albino mice in ROS-dependent manner. Reactive Oxygen Species 163-166 a disintegrin and metallopeptidase domain 17 Mus musculus 76-83 31951006-7 2020 From these results, it is thought that the increase in heparan sulfate is due to insufficient cleavage of the core protein by ADAM17. Sulfates 63-70 a disintegrin and metallopeptidase domain 17 Mus musculus 126-132 32453025-6 2020 Tea polyphenols, major active compounds in green tea, suppressed TNFalpha production through downregulating TNFalpha converting enzyme (TACE) level. Polyphenols 4-15 a disintegrin and metallopeptidase domain 17 Mus musculus 108-134 32453025-6 2020 Tea polyphenols, major active compounds in green tea, suppressed TNFalpha production through downregulating TNFalpha converting enzyme (TACE) level. Polyphenols 4-15 a disintegrin and metallopeptidase domain 17 Mus musculus 136-140 32453025-8 2020 The aforementioned results demonstrate cognition protective effects of tea polyphenols in S-DEP mice model, which provide a theoretical basis for the treatments of S-DEP-induced cognition impairment by targeting the TACE/TNFalpha/AMPA pathway. Polyphenols 75-86 a disintegrin and metallopeptidase domain 17 Mus musculus 216-220 31883180-13 2020 The present results provide in vivo and in vitro evidence that microglial glutamate release in SALS spinal cords is enhanced by intracellular soluble iron accumulation-induced activation of ACO1 and TACE and by increased extracellular TNFalpha-stimulated GLS-C upregulation, and suggest a positive feedback mechanism to maintain increased intracellular soluble iron levels, involving TNFalpha, hepcidin, and FPN. Glutamic Acid 74-83 a disintegrin and metallopeptidase domain 17 Mus musculus 199-203 31883180-13 2020 The present results provide in vivo and in vitro evidence that microglial glutamate release in SALS spinal cords is enhanced by intracellular soluble iron accumulation-induced activation of ACO1 and TACE and by increased extracellular TNFalpha-stimulated GLS-C upregulation, and suggest a positive feedback mechanism to maintain increased intracellular soluble iron levels, involving TNFalpha, hepcidin, and FPN. Iron 150-154 a disintegrin and metallopeptidase domain 17 Mus musculus 199-203 31442576-0 2019 Novel ADAM-17 inhibitor ZLDI-8 inhibits the proliferation and metastasis of chemo-resistant non-small-cell lung cancer by reversing Notch and epithelial mesenchymal transition in vitro and in vivo. ZLDI-8 24-30 a disintegrin and metallopeptidase domain 17 Mus musculus 6-13 32024241-6 2020 Loss of ADAM17 in endothelial cells markedly reduced oxidative stress evidenced by decreased levels of superoxide, 3-nitrotyrosine, and 4-hydroxynonenal and decreased leukocyte-endothelium adhesive interactions in vivo and in vitro. Superoxides 103-113 a disintegrin and metallopeptidase domain 17 Mus musculus 8-14 32024241-6 2020 Loss of ADAM17 in endothelial cells markedly reduced oxidative stress evidenced by decreased levels of superoxide, 3-nitrotyrosine, and 4-hydroxynonenal and decreased leukocyte-endothelium adhesive interactions in vivo and in vitro. 3-nitrotyrosine 115-130 a disintegrin and metallopeptidase domain 17 Mus musculus 8-14 32024241-6 2020 Loss of ADAM17 in endothelial cells markedly reduced oxidative stress evidenced by decreased levels of superoxide, 3-nitrotyrosine, and 4-hydroxynonenal and decreased leukocyte-endothelium adhesive interactions in vivo and in vitro. 4-hydroxy-2-nonenal 136-152 a disintegrin and metallopeptidase domain 17 Mus musculus 8-14 31442576-3 2019 ZLDI-8 is an inhibitor of Notch activating/cleaving enzyme ADAM-17 we found before. ZLDI-8 0-6 a disintegrin and metallopeptidase domain 17 Mus musculus 59-66 30746765-7 2019 Proteinases known to mediate LRP1 shedding, including ADAM10 and ADAM17, were expressed at increased levels in the SDH after PNL. sdh 115-118 a disintegrin and metallopeptidase domain 17 Mus musculus 65-71 31153974-6 2019 Moreover, 4-PBA blunted the expression of iRhom2, TACE, TNFR2 and phosphorylated NF-kappaB to prevent HFD-induced expression of inflammatory factors. 4-phenylbutylamine 10-15 a disintegrin and metallopeptidase domain 17 Mus musculus 50-54 29956475-7 2018 ADAM-17/EGFR signalling axis was also activated in intestinal tumours of DCA-treated Apcmin/+ mice, whereas no significant change occurred in tumour adjacent tissues after DCA exposure. Deoxycholic Acid 73-76 a disintegrin and metallopeptidase domain 17 Mus musculus 0-7 31006330-4 2019 The aim of this study was to determine whether ADAM17 modulates presympathetic neuronal activity to promote autonomic dysregulation in salt-sensitive hypertension. Salts 135-139 a disintegrin and metallopeptidase domain 17 Mus musculus 47-53 31006330-6 2019 In mice lacking ADAM17 in glutamatergic neurons, the blood pressure increase induced by deoxycorticosterone acetate-salt treatment was blunted. Desoxycorticosterone Acetate 88-115 a disintegrin and metallopeptidase domain 17 Mus musculus 16-22 31006330-6 2019 In mice lacking ADAM17 in glutamatergic neurons, the blood pressure increase induced by deoxycorticosterone acetate-salt treatment was blunted. Salts 116-120 a disintegrin and metallopeptidase domain 17 Mus musculus 16-22 31006330-7 2019 Deoxycorticosterone acetate-salt significantly elevated cardiac and vascular sympathetic drive in control mice, while such effects were reduced in mice with ADAM17 knockdown. Desoxycorticosterone Acetate 0-28 a disintegrin and metallopeptidase domain 17 Mus musculus 157-163 31006330-10 2019 Overall, our data highlight the pivotal role of neuronal ADAM17 in regulating sympathetic activity and demonstrate that activation of ADAM17 in glutamatergic neurons leads to a selective increase of sympathetic output, but not vagal tone, to specific organs, ultimately contributing to dysautonomia and salt-sensitive hypertension. Salts 303-307 a disintegrin and metallopeptidase domain 17 Mus musculus 134-140 31685773-0 2019 A Novel TNF-alpha Converting Enzyme (TACE) Selective Inhibitor JTP-96193 Prevents Insulin Resistance in KK-Ay Type 2 Diabetic Mice and Diabetic Peripheral Neuropathy in Type 1 Diabetic Mice. jtp-96193 63-72 a disintegrin and metallopeptidase domain 17 Mus musculus 8-35 31685773-0 2019 A Novel TNF-alpha Converting Enzyme (TACE) Selective Inhibitor JTP-96193 Prevents Insulin Resistance in KK-Ay Type 2 Diabetic Mice and Diabetic Peripheral Neuropathy in Type 1 Diabetic Mice. jtp-96193 63-72 a disintegrin and metallopeptidase domain 17 Mus musculus 37-41 31685773-2 2019 In the present study, pharmacological effects of a novel TACE selective inhibitor, JTP-96193, on type 2 diabetes and diabetic peripheral neuropathy (DPN) as its major complication was examined. jtp-96193 83-92 a disintegrin and metallopeptidase domain 17 Mus musculus 57-61 31685773-3 2019 Enzyme inhibitory activity of JTP-96193 on TACE and other ADAMs was measured in in vitro. jtp-96193 30-39 a disintegrin and metallopeptidase domain 17 Mus musculus 43-47 29215702-0 2018 ADAM17 participates in the protective effect of paeoniflorin on mouse brain microvascular endothelial cells. peoniflorin 48-60 a disintegrin and metallopeptidase domain 17 Mus musculus 0-6 29215702-4 2018 Next, by detecting the phosphorylation of a disintegrin and metalloprotease 17 (ADAM17) at Thr 735 and performing loss-of-function experiments with the ADAM17 inhibitor and ADAM 17-siRNA, we showed that PF-induced transactivation of EGFR and downstream ERKs and AKT signaling pathways were dependent on ADAM17. Threonine 91-94 a disintegrin and metallopeptidase domain 17 Mus musculus 80-86 29215702-5 2018 Furthermore, PF-induced phosphorylation of ADAM17 and the EGFR transactivation were inhibited by the inhibitors of adenosine A1 receptor (A1R) or Src kinase that were applied to cells prior to PF treatment, implying the involvement of A1R, and Src in the activation of ADAM17. peoniflorin 13-15 a disintegrin and metallopeptidase domain 17 Mus musculus 43-49 29215702-5 2018 Furthermore, PF-induced phosphorylation of ADAM17 and the EGFR transactivation were inhibited by the inhibitors of adenosine A1 receptor (A1R) or Src kinase that were applied to cells prior to PF treatment, implying the involvement of A1R, and Src in the activation of ADAM17. peoniflorin 13-15 a disintegrin and metallopeptidase domain 17 Mus musculus 269-275 29215702-5 2018 Furthermore, PF-induced phosphorylation of ADAM17 and the EGFR transactivation were inhibited by the inhibitors of adenosine A1 receptor (A1R) or Src kinase that were applied to cells prior to PF treatment, implying the involvement of A1R, and Src in the activation of ADAM17. peoniflorin 193-195 a disintegrin and metallopeptidase domain 17 Mus musculus 43-49 30588188-2 2018 Pirarubicin and pirarubicin-based combination therapies have been demonstrated to be effective against HCC in TACE. pirarubicin 0-11 a disintegrin and metallopeptidase domain 17 Mus musculus 110-114 30297396-6 2018 iNOS/NO led to Notch1 signaling through a pathway involving the soluble guanylyl cyclase/cGMP/PKG-dependent activation of TACE/ADAM17 and up-regulation of iRhom2 in LCSCs. Cyclic GMP 89-93 a disintegrin and metallopeptidase domain 17 Mus musculus 122-126 30297396-6 2018 iNOS/NO led to Notch1 signaling through a pathway involving the soluble guanylyl cyclase/cGMP/PKG-dependent activation of TACE/ADAM17 and up-regulation of iRhom2 in LCSCs. Cyclic GMP 89-93 a disintegrin and metallopeptidase domain 17 Mus musculus 127-133 29956475-0 2018 Deoxycholic acid activates epidermal growth factor receptor and promotes intestinal carcinogenesis by ADAM17-dependent ligand release. Deoxycholic Acid 0-16 a disintegrin and metallopeptidase domain 17 Mus musculus 102-108 29956475-5 2018 Moreover, ADAM-17 was required in DCA-induced promotion of shedding of AREG and activation of EGFR/Akt signalling pathway. Deoxycholic Acid 34-37 a disintegrin and metallopeptidase domain 17 Mus musculus 10-17 30709842-6 2019 The transient increase in Adam17 mRNA in response to PMA was strongly reduced by an inhibitor of ERK1/2 phosphorylation, U0126. U 0126 121-126 a disintegrin and metallopeptidase domain 17 Mus musculus 26-32 30395261-5 2019 TACE was identified as the protease responsible for phorbol 12-myristate 13-acetate (PMA)-induced VCAM-1 release in murine endothelial cells. Tetradecanoylphorbol Acetate 52-83 a disintegrin and metallopeptidase domain 17 Mus musculus 0-4 30395261-5 2019 TACE was identified as the protease responsible for phorbol 12-myristate 13-acetate (PMA)-induced VCAM-1 release in murine endothelial cells. Tetradecanoylphorbol Acetate 85-88 a disintegrin and metallopeptidase domain 17 Mus musculus 0-4 30588188-2 2018 Pirarubicin and pirarubicin-based combination therapies have been demonstrated to be effective against HCC in TACE. pirarubicin 16-27 a disintegrin and metallopeptidase domain 17 Mus musculus 110-114 29499360-2 2018 However, it remains unclear whether ursolic acid (UA), a natural pentacyclic triterpenoid carboxylic acid, can have an impact on STAT3 and ADAM17 and hence influence the formation of AAA. ursolic acid 36-48 a disintegrin and metallopeptidase domain 17 Mus musculus 139-145 29499360-2 2018 However, it remains unclear whether ursolic acid (UA), a natural pentacyclic triterpenoid carboxylic acid, can have an impact on STAT3 and ADAM17 and hence influence the formation of AAA. ursolic acid 50-52 a disintegrin and metallopeptidase domain 17 Mus musculus 139-145 29499360-8 2018 UA alleviated the degradation of elastin fibers and inflammation and decreased the expression of MMP2, MMP9, ADAM17 and phospho-STAT3 (pSTAT3) in aorta of mice induced with AngII. ursolic acid 0-2 a disintegrin and metallopeptidase domain 17 Mus musculus 109-115 29499360-9 2018 UA inhibited the constitutive and stimuli-induced (AngII and tumor necrosis factor-alpha) expression of MMP2, MMP9, ADAM17 and pSTAT3 in vascular smooth muscle cells (VSMCs). ursolic acid 0-2 a disintegrin and metallopeptidase domain 17 Mus musculus 116-122 29499360-11 2018 CONCLUSIONS: We demonstrated that UA ameliorated the severity of AAA and exhibited an inhibitory effect on the expression of pSTAT3 and ADAM17. ursolic acid 34-36 a disintegrin and metallopeptidase domain 17 Mus musculus 136-142 29560122-0 2018 The enhanced susceptibility of ADAM-17 hypomorphic mice to DSS-induced colitis is not ameliorated by loss of RIPK3, revealing an unexpected function of ADAM-17 in necroptosis. Dextran Sulfate 59-62 a disintegrin and metallopeptidase domain 17 Mus musculus 31-38 29560122-1 2018 The disintegrin metalloprotease ADAM17 has a critical role in intestinal inflammation and regeneration in mice, as illustrated by the dramatically increased susceptibility of ADAM17 hypomorphic (ADAM17ex/ex) mice to dextran sulfate sodium (DSS)-induced colitis. Dextran Sulfate 216-238 a disintegrin and metallopeptidase domain 17 Mus musculus 32-38 29560122-1 2018 The disintegrin metalloprotease ADAM17 has a critical role in intestinal inflammation and regeneration in mice, as illustrated by the dramatically increased susceptibility of ADAM17 hypomorphic (ADAM17ex/ex) mice to dextran sulfate sodium (DSS)-induced colitis. Dextran Sulfate 216-238 a disintegrin and metallopeptidase domain 17 Mus musculus 175-181 29560122-1 2018 The disintegrin metalloprotease ADAM17 has a critical role in intestinal inflammation and regeneration in mice, as illustrated by the dramatically increased susceptibility of ADAM17 hypomorphic (ADAM17ex/ex) mice to dextran sulfate sodium (DSS)-induced colitis. Dextran Sulfate 216-238 a disintegrin and metallopeptidase domain 17 Mus musculus 175-181 29962345-11 2018 The levels of sAPPalpha, ADAM10 and ADAM17 in the hippocampus of BBR-treated mice significantly increased, compared with the control ones (P<0.05). Berberine 65-68 a disintegrin and metallopeptidase domain 17 Mus musculus 36-42 29560122-1 2018 The disintegrin metalloprotease ADAM17 has a critical role in intestinal inflammation and regeneration in mice, as illustrated by the dramatically increased susceptibility of ADAM17 hypomorphic (ADAM17ex/ex) mice to dextran sulfate sodium (DSS)-induced colitis. Dextran Sulfate 240-243 a disintegrin and metallopeptidase domain 17 Mus musculus 32-38 29560122-4 2018 Despite the loss of RIPK3, ADAM17ex/ex/RIPK3-/- mice showed the same increased susceptibility as ADAM17ex/ex mice in both acute and chronic models of DSS-induced colitis. Dextran Sulfate 150-153 a disintegrin and metallopeptidase domain 17 Mus musculus 27-33 28554668-0 2017 Anti-tumor effects of a "human & mouse cross-reactive" anti-ADAM17 antibody in a pancreatic cancer model in vivo. Adenosine Monophosphate 32-35 a disintegrin and metallopeptidase domain 17 Mus musculus 64-70 28671983-0 2017 Isoflurane promotes phagocytosis of apoptotic neutrophils through AMPK-mediated ADAM17/Mer signaling. Isoflurane 0-10 a disintegrin and metallopeptidase domain 17 Mus musculus 80-86 28947615-0 2017 Vascular ADAM17 (a Disintegrin and Metalloproteinase Domain 17) Is Required for Angiotensin II/beta-Aminopropionitrile-Induced Abdominal Aortic Aneurysm. Aminopropionitrile 95-118 a disintegrin and metallopeptidase domain 17 Mus musculus 9-15 28947615-0 2017 Vascular ADAM17 (a Disintegrin and Metalloproteinase Domain 17) Is Required for Angiotensin II/beta-Aminopropionitrile-Induced Abdominal Aortic Aneurysm. Aminopropionitrile 95-118 a disintegrin and metallopeptidase domain 17 Mus musculus 17-62 28947615-7 2017 In contrast, all AngII and beta-aminopropionitrile-treated VSMC ADAM17-deficient mice survived and showed reduction in external/internal diameters (51%/28%, respectively). Aminopropionitrile 27-50 a disintegrin and metallopeptidase domain 17 Mus musculus 64-70 28947615-9 2017 However, both VSMC ADAM17-deficient and control mice treated with AngII and beta-aminopropionitrile developed comparable levels of hypertension. Aminopropionitrile 76-99 a disintegrin and metallopeptidase domain 17 Mus musculus 19-25 28537905-5 2017 Here we explore the mechanism of LPS-induced TNF-alpha secretion and reveal p38 MAPK signaling as a target of Dex that is involved in control of tumor necrosis factor-alpha (TNF-alpha)-converting enzyme (TACE) activity; that later mediates the shedding of TNF-alpha that allows its secretion. Dexamethasone 110-113 a disintegrin and metallopeptidase domain 17 Mus musculus 204-208 28671983-5 2017 Isoflurane treatment also caused a decrease in a disintegrin and metalloproteinase 17 (ADAM17) on the cell surface and a concomitant increase in its cytoplasmic fraction. Isoflurane 0-10 a disintegrin and metallopeptidase domain 17 Mus musculus 87-93 28671983-10 2017 Increased macrophage efferocytosis following isoflurane treatment correlates with upregulation of Mer surface expression through AMPK-mediated blockade of ADAM17 trafficking to the cell membrane. Isoflurane 45-55 a disintegrin and metallopeptidase domain 17 Mus musculus 155-161 28004780-5 2016 Restored TG1 expression of EGF-stimulated differentiated Adam17-/- keratinocytes was strongly repressed by inhibitors for PLCgamma1 or protein kinase C (PKC) pathways, while treatment with the PKC stimulator 12-O-tetradecanoylphorbol-13-acetate restored TG activity in the epidermis of keratinocyte-specific Adam17-/- (AD17DeltaKC) mice. Tetradecanoylphorbol Acetate 208-244 a disintegrin and metallopeptidase domain 17 Mus musculus 57-63 29082234-4 2017 We hypothesized that alcohol impairs HDE-induced TNFalpha, ICAM-1 expression and neutrophil adhesion by directly inhibiting TNFalpha converting enzyme (TACE) activity. Alcohols 21-28 a disintegrin and metallopeptidase domain 17 Mus musculus 124-150 29082234-4 2017 We hypothesized that alcohol impairs HDE-induced TNFalpha, ICAM-1 expression and neutrophil adhesion by directly inhibiting TNFalpha converting enzyme (TACE) activity. Alcohols 21-28 a disintegrin and metallopeptidase domain 17 Mus musculus 152-156 29082234-12 2017 TACE activity increased following HDE exposure, but TACE activity was inhibited following alcohol pretreatment. Alcohols 90-97 a disintegrin and metallopeptidase domain 17 Mus musculus 52-56 29082234-14 2017 CONCLUSIONS: Alcohol diminishes HDE-induced ICAM-1 expression, TNFalpha release, and neutrophil adhesion via inhibition of TACE activity. Alcohols 13-20 a disintegrin and metallopeptidase domain 17 Mus musculus 123-127 27909955-7 2017 DAB also inhibited the expression and activity of PMA-induced TACE in HUVECs suggesting that p38, ERK1/2, and JNK could be molecular targets of DAB. dabrafenib 0-3 a disintegrin and metallopeptidase domain 17 Mus musculus 62-66 27909955-7 2017 DAB also inhibited the expression and activity of PMA-induced TACE in HUVECs suggesting that p38, ERK1/2, and JNK could be molecular targets of DAB. dabrafenib 144-147 a disintegrin and metallopeptidase domain 17 Mus musculus 62-66 27623510-6 2017 As for the mechanism of CD62L regulation, we found that ATP, which is released in skin upon hapten-exposure, is inducing the protease ADAM17 in LN-residing T cells via engagement of P2X7 ATP receptors. Adenosine Triphosphate 56-59 a disintegrin and metallopeptidase domain 17 Mus musculus 134-140 27799291-0 2016 Niacin-mediated Tace activation ameliorates CMT neuropathies with focal hypermyelination. Niacin 0-6 a disintegrin and metallopeptidase domain 17 Mus musculus 16-20 27799291-6 2016 Here we show that in vivo delivery of Niaspan, a FDA-approved drug known to enhance TACE activity, efficiently rescues myelination in the Mtmr2-/- mouse, a model of CMT4B1 with myelin outfoldings, and in the Pmp22+/- mouse, which reproduces HNPP (hereditary neuropathy with liability to pressure palsies) with tomacula. Niacin 38-45 a disintegrin and metallopeptidase domain 17 Mus musculus 84-88 27698010-6 2016 Attempts to genetically delete the floxed ADAM17 gene selectively in myeloid cells infiltrating an air pouch cavity upon injection of carrageenan failed because in transgenic mice, LysMcre did not lead to appreciable loss of the ADAM17 protein in these cells. Carrageenan 134-145 a disintegrin and metallopeptidase domain 17 Mus musculus 42-48 26697977-0 2016 Paricalcitol modulates ACE2 shedding and renal ADAM17 in NOD mice beyond proteinuria. paricalcitol 0-12 a disintegrin and metallopeptidase domain 17 Mus musculus 47-53 27372924-4 2016 The aim of the present study is to investigate the neuroprotective mechanisms of H2S involving in the activity of beta-secretase (BACE1), gamma-secretase (PS1) and alpha-secretase (ADAM17). Deuterium 81-84 a disintegrin and metallopeptidase domain 17 Mus musculus 181-187 27372924-10 2016 After intraperitoneal administration of an H2S donor (NaHS) into APP/PS1 mice, the levels of BACE1, PS1 and pp38MAPK were reduced and ADAM17 increased. Deuterium 43-46 a disintegrin and metallopeptidase domain 17 Mus musculus 134-140 27372924-10 2016 After intraperitoneal administration of an H2S donor (NaHS) into APP/PS1 mice, the levels of BACE1, PS1 and pp38MAPK were reduced and ADAM17 increased. sodium bisulfide 54-58 a disintegrin and metallopeptidase domain 17 Mus musculus 134-140 26697977-9 2016 Renal content of ADAM17 was significantly decreased in animals that received a high dose of paricalcitol. paricalcitol 92-104 a disintegrin and metallopeptidase domain 17 Mus musculus 17-23 26697977-12 2016 In NOD mice with type 1 diabetes, paricalcitol modulates ACE2 activity, ADAM17, and oxidative stress renal content independently from the glycemic profile and urinary albumin excretion. paricalcitol 34-46 a disintegrin and metallopeptidase domain 17 Mus musculus 72-78 26842246-0 2016 Alcohol Decreases Organic Dust-Stimulated Airway Epithelial TNF-Alpha Through a Nitric Oxide and Protein Kinase-Mediated Inhibition of TACE. Alcohols 0-7 a disintegrin and metallopeptidase domain 17 Mus musculus 135-139 26842246-9 2016 METHODS: Because we recently demonstrated that PKA activation inhibits the TNF-alpha sheddase, TNF-alpha-converting enzyme (TACE), we hypothesized that an alcohol-mediated PKA pathway blocks TACE activity and prevents the normative inflammatory response to hog barn dust exposure. Alcohols 155-162 a disintegrin and metallopeptidase domain 17 Mus musculus 95-122 26842246-9 2016 METHODS: Because we recently demonstrated that PKA activation inhibits the TNF-alpha sheddase, TNF-alpha-converting enzyme (TACE), we hypothesized that an alcohol-mediated PKA pathway blocks TACE activity and prevents the normative inflammatory response to hog barn dust exposure. Alcohols 155-162 a disintegrin and metallopeptidase domain 17 Mus musculus 124-128 26842246-9 2016 METHODS: Because we recently demonstrated that PKA activation inhibits the TNF-alpha sheddase, TNF-alpha-converting enzyme (TACE), we hypothesized that an alcohol-mediated PKA pathway blocks TACE activity and prevents the normative inflammatory response to hog barn dust exposure. Alcohols 155-162 a disintegrin and metallopeptidase domain 17 Mus musculus 191-195 26842246-16 2016 CONCLUSIONS: These data suggest that alcohol requires a soluble cyclase-generated cAMP-PKA pathway that is dependent upon the action of NO to inhibit TACE and TNF-alpha release. Alcohols 37-44 a disintegrin and metallopeptidase domain 17 Mus musculus 150-154 26842246-16 2016 CONCLUSIONS: These data suggest that alcohol requires a soluble cyclase-generated cAMP-PKA pathway that is dependent upon the action of NO to inhibit TACE and TNF-alpha release. Cyclic AMP 82-86 a disintegrin and metallopeptidase domain 17 Mus musculus 150-154 26002422-0 2015 Iron accumulation promotes TACE-mediated TNF-alpha secretion and neurodegeneration in a mouse model of ALS. Iron 0-4 a disintegrin and metallopeptidase domain 17 Mus musculus 27-31 27077118-3 2016 Mice with systemic deletion of Adam17 developed severe dextran sulfate sodium-induced colitis when compared to mice with myeloid cell Adam17 deletion or control littermates. Dextran Sulfate 55-77 a disintegrin and metallopeptidase domain 17 Mus musculus 31-37 26586620-0 2016 Suppressive effects of polyozellin on endothelial protein C receptor shedding via inhibiting TACE activity and MAP kinases. polyozellin 23-34 a disintegrin and metallopeptidase domain 17 Mus musculus 93-97 26586620-7 2016 Polyozellin also inhibited the expression and activity of PMA-induced TACE in HUVECs suggesting that p38, ERK1/2, and JNK could be the molecular targets of POZ. polyozellin 0-11 a disintegrin and metallopeptidase domain 17 Mus musculus 70-74 26338334-5 2015 EGFR overexpression in TACE deficient OLs in vivo restores OL development and postnatal CNS myelination, but also OL regeneration and CNS remyelination following demyelination. N-biotin-C-Co4(mu3-O)4(Py)4(H2O)4-beta-alanine 38-41 a disintegrin and metallopeptidase domain 17 Mus musculus 23-27 26254330-0 2015 alpha-Lipoic acid reduces neurogenic hypertension by blunting oxidative stress-mediated increase in ADAM17. Thioctic Acid 0-17 a disintegrin and metallopeptidase domain 17 Mus musculus 100-106 26254330-7 2015 In deoxycorticosterone acetate (DOCA)-salt hypertensive mice, a model in which ADAM17 expression and activity are increased, hypertension was blunted by pretreatment with LA (119.0 +- 2.4 vs. 131.4 +- 2.2 mmHg, P < 0.05). Desoxycorticosterone Acetate 32-36 a disintegrin and metallopeptidase domain 17 Mus musculus 79-85 26183206-3 2015 We discuss the relationship between the sphingolipid acyl chain length and TACE activity and the relevance of this data to septic shock. Sphingolipids 40-52 a disintegrin and metallopeptidase domain 17 Mus musculus 75-79 26002422-5 2015 Furthermore, SOD1(G93A)-induced iron accumulation mediated the increase in the enzymatic activity of TNF-alpha converting enzyme (TACE), leading to secretion of TNF-alpha at least in part through iron-dependent oxidative stress. Iron 32-36 a disintegrin and metallopeptidase domain 17 Mus musculus 101-128 26002422-5 2015 Furthermore, SOD1(G93A)-induced iron accumulation mediated the increase in the enzymatic activity of TNF-alpha converting enzyme (TACE), leading to secretion of TNF-alpha at least in part through iron-dependent oxidative stress. Iron 32-36 a disintegrin and metallopeptidase domain 17 Mus musculus 130-134 26002422-5 2015 Furthermore, SOD1(G93A)-induced iron accumulation mediated the increase in the enzymatic activity of TNF-alpha converting enzyme (TACE), leading to secretion of TNF-alpha at least in part through iron-dependent oxidative stress. Iron 196-200 a disintegrin and metallopeptidase domain 17 Mus musculus 101-128 26002422-5 2015 Furthermore, SOD1(G93A)-induced iron accumulation mediated the increase in the enzymatic activity of TNF-alpha converting enzyme (TACE), leading to secretion of TNF-alpha at least in part through iron-dependent oxidative stress. Iron 196-200 a disintegrin and metallopeptidase domain 17 Mus musculus 130-134 25935488-0 2015 Anti-arthritis effect of a novel quinazoline derivative through inhibiting production of TNF-alpha mediated by TNF-alpha converting enzyme in murine collagen-induced arthritis model. Quinazolines 33-44 a disintegrin and metallopeptidase domain 17 Mus musculus 111-138 25935488-9 2015 In conclusion, we discovered a novel quinazoline derivative which ameliorates arthritis through inhibiting production of TNF-alpha mediated by TACE for the first time. Quinazolines 37-48 a disintegrin and metallopeptidase domain 17 Mus musculus 143-147 25628461-2 2015 Using a clinically relevant mouse model of polymicrobial abdominal sepsis, we found that the production of inducible nitric oxide synthase (iNOS) in hepatocytes led to the cyclic guanosine monophosphate (cGMP)-dependent activation of the protease TACE (TNF-converting enzyme) and the shedding of TNFR. Cyclic GMP 172-202 a disintegrin and metallopeptidase domain 17 Mus musculus 247-251 25916723-10 2015 In addition, AngII infusion enhanced ADAM17 expression, EGFR activation, and ER/oxidative stress in the vasculature, which were diminished in both erlotinib-treated and 4-phenylbutyrate-treated mice. Erlotinib Hydrochloride 147-156 a disintegrin and metallopeptidase domain 17 Mus musculus 37-43 25916723-10 2015 In addition, AngII infusion enhanced ADAM17 expression, EGFR activation, and ER/oxidative stress in the vasculature, which were diminished in both erlotinib-treated and 4-phenylbutyrate-treated mice. 4-phenylbutyric acid 169-185 a disintegrin and metallopeptidase domain 17 Mus musculus 37-43 25628461-2 2015 Using a clinically relevant mouse model of polymicrobial abdominal sepsis, we found that the production of inducible nitric oxide synthase (iNOS) in hepatocytes led to the cyclic guanosine monophosphate (cGMP)-dependent activation of the protease TACE (TNF-converting enzyme) and the shedding of TNFR. Cyclic GMP 204-208 a disintegrin and metallopeptidase domain 17 Mus musculus 247-251 25150062-10 2014 In contrast, 8-Br-cAMP decreased HDE-stimulated tumor necrosis factor (TNF)-alpha-converting enzyme (TACE; ADAM-17) activity and subsequent TNF-alpha release (P < 0.001). 8-Bromo Cyclic Adenosine Monophosphate 13-22 a disintegrin and metallopeptidase domain 17 Mus musculus 101-105 25218057-11 2015 Accordingly, ADAM17 overexpression downregulated TSP1 expression, and the TSP1 inhibitor LSKL rescued angiogenesis in the tube formation assay downstream of VEGF in the presence of ADAM17 inhibition. LSKL, Inhibitor of Thrombospondin (TSP-1) 89-93 a disintegrin and metallopeptidase domain 17 Mus musculus 181-187 25350560-5 2014 We further clarified the relationship between two molecules downstream of PKC delta and theta and TACE in COCs: nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX) and its products, reactive oxygen species (ROS). nicotinamide adenine 112-132 a disintegrin and metallopeptidase domain 17 Mus musculus 98-102 25350560-8 2014 Moreover, FSH-induced TACE activity in cumulus cells was decreased markedly by inhibition of NOX and ROS. nicotine 1-N-oxide 93-96 a disintegrin and metallopeptidase domain 17 Mus musculus 22-26 25350560-8 2014 Moreover, FSH-induced TACE activity in cumulus cells was decreased markedly by inhibition of NOX and ROS. Reactive Oxygen Species 101-104 a disintegrin and metallopeptidase domain 17 Mus musculus 22-26 25350560-9 2014 In conclusion, PKC delta and theta possibly mediate FSH-induced meiotic resumption in mouse COCs via NOX-ROS-TACE signaling pathway. nox-ros 101-108 a disintegrin and metallopeptidase domain 17 Mus musculus 109-113 25028693-4 2015 Loss of MCJ in macrophages results in increased mitochondrial respiration and elevated basal levels of reactive oxygen species that cause activation of the JNK/c-Jun pathway, lead to the upregulation of the TACE (also known as ADAM17) inhibitor TIMP-3, and lead to the inhibition of tumor necrosis factor shedding from the plasma membrane. Reactive Oxygen Species 103-126 a disintegrin and metallopeptidase domain 17 Mus musculus 207-211 25028693-4 2015 Loss of MCJ in macrophages results in increased mitochondrial respiration and elevated basal levels of reactive oxygen species that cause activation of the JNK/c-Jun pathway, lead to the upregulation of the TACE (also known as ADAM17) inhibitor TIMP-3, and lead to the inhibition of tumor necrosis factor shedding from the plasma membrane. Reactive Oxygen Species 103-126 a disintegrin and metallopeptidase domain 17 Mus musculus 227-233 25384035-5 2014 In the present study, to assess the possible role of TACE in the pathogenesis of psoriasis, we investigated the involvement of TACE in TPA-induced psoriasis-like lesions in K5.Stat3C mice, which represent a mouse model of psoriasis. Tetradecanoylphorbol Acetate 135-138 a disintegrin and metallopeptidase domain 17 Mus musculus 127-131 25350560-0 2014 PKCdelta and theta possibly mediate FSH-induced mouse oocyte maturation via NOX-ROS-TACE cascade signaling pathway. nox-ros 76-83 a disintegrin and metallopeptidase domain 17 Mus musculus 84-88 25150062-10 2014 In contrast, 8-Br-cAMP decreased HDE-stimulated tumor necrosis factor (TNF)-alpha-converting enzyme (TACE; ADAM-17) activity and subsequent TNF-alpha release (P < 0.001). 8-Bromo Cyclic Adenosine Monophosphate 13-22 a disintegrin and metallopeptidase domain 17 Mus musculus 107-114 25017047-7 2014 The underlying basis involves direct association of activated ERK with a disintegrin and metalloprotease domain 17 (ADAM17, an alpha-secretase candidate) and ERK-dependent threonine phosphorylation of ADAM17. Threonine 172-181 a disintegrin and metallopeptidase domain 17 Mus musculus 201-207 25085885-7 2014 This was corroborated in the isolated perfused mouse lung, where elevated CO2 also inhibited stretch-activated shedding of the ADAM17 substrate TNFR1 from airway epithelial cells. N2,N6-bis(4-(2-aminoethoxy)quinolin-2-yl)-4-((4-fluorobenzyl)oxy)pyridine-2,6-dicarboxamide 74-77 a disintegrin and metallopeptidase domain 17 Mus musculus 127-133 25414771-9 2014 Collectively, the concurrent inhibition of MMP and TACE by NNGH, M8I, or M9I may contribute to their strong anti-inflammatory and neuroprotective effects. m8i 65-68 a disintegrin and metallopeptidase domain 17 Mus musculus 51-55 25108021-6 2014 In this study, we show that that ADAM17 deficiency results in spleen and lymph node enlargement, as well as increased levels of Ag-specific class-switched Ig production following immunization with OVA together with anti-CD40 mAbs and polyinosinic-polycytidylic acid. Poly I-C 234-265 a disintegrin and metallopeptidase domain 17 Mus musculus 33-39 25414771-9 2014 Collectively, the concurrent inhibition of MMP and TACE by NNGH, M8I, or M9I may contribute to their strong anti-inflammatory and neuroprotective effects. NNGH 59-63 a disintegrin and metallopeptidase domain 17 Mus musculus 51-55 24899059-6 2014 PKD cells also displayed increased lactate formation and extracellular acidification indicative of aerobic glycolysis (Warburg effect), which was blocked by ADAM17 inhibition. Lactic Acid 35-42 a disintegrin and metallopeptidase domain 17 Mus musculus 157-163 25049354-3 2014 Subsequent experiments showed that MMP-8 exhibits TNF-alpha-converting enzyme (TACE) activity by cleaving the prodomain of TNF-alpha (A(74)/Q(75), A(76)/V(77) residues) and, furthermore, that M8I inhibits TACE activity more efficiently than TAPI-0, a general TACE inhibitor. m8i 192-195 a disintegrin and metallopeptidase domain 17 Mus musculus 50-77 25049354-3 2014 Subsequent experiments showed that MMP-8 exhibits TNF-alpha-converting enzyme (TACE) activity by cleaving the prodomain of TNF-alpha (A(74)/Q(75), A(76)/V(77) residues) and, furthermore, that M8I inhibits TACE activity more efficiently than TAPI-0, a general TACE inhibitor. m8i 192-195 a disintegrin and metallopeptidase domain 17 Mus musculus 79-83 25049354-3 2014 Subsequent experiments showed that MMP-8 exhibits TNF-alpha-converting enzyme (TACE) activity by cleaving the prodomain of TNF-alpha (A(74)/Q(75), A(76)/V(77) residues) and, furthermore, that M8I inhibits TACE activity more efficiently than TAPI-0, a general TACE inhibitor. TAPI-0 241-247 a disintegrin and metallopeptidase domain 17 Mus musculus 50-77 25049354-3 2014 Subsequent experiments showed that MMP-8 exhibits TNF-alpha-converting enzyme (TACE) activity by cleaving the prodomain of TNF-alpha (A(74)/Q(75), A(76)/V(77) residues) and, furthermore, that M8I inhibits TACE activity more efficiently than TAPI-0, a general TACE inhibitor. TAPI-0 241-247 a disintegrin and metallopeptidase domain 17 Mus musculus 79-83 24946851-0 2014 Chemopreventive effect of a novel, selective TACE inhibitor on DMBA- and TPA-induced skin carcinogenesis. 9,10-Dimethyl-1,2-benzanthracene 63-67 a disintegrin and metallopeptidase domain 17 Mus musculus 45-49 24946851-0 2014 Chemopreventive effect of a novel, selective TACE inhibitor on DMBA- and TPA-induced skin carcinogenesis. Tetradecanoylphorbol Acetate 73-76 a disintegrin and metallopeptidase domain 17 Mus musculus 45-49 24946851-11 2014 DISCUSSION AND CONCLUSION: These findings suggest that selective blockade of TACE suppresses TPA-induced epidermal hyperplasia, inflammatory cell infiltration and cytokine level. Tetradecanoylphorbol Acetate 93-96 a disintegrin and metallopeptidase domain 17 Mus musculus 77-81 24756098-5 2014 The aim of this study was to investigate whether exercise training and/or metformin improve glucose homeostasis and albuminuria and downregulate renal ADAM17 and ACE2 shedding in db/db mice. Metformin 74-83 a disintegrin and metallopeptidase domain 17 Mus musculus 151-157 24769623-10 2014 Collectively, these data suggest that we successfully developed an exosite inhibitor of TACE with sub-nanomolar affinity, which possesses both murine and human immunoreactive properties that can be used for in vivo application in murine pre-clinical cancer models. exosite 67-74 a disintegrin and metallopeptidase domain 17 Mus musculus 88-92 24756098-12 2014 In conclusion, exercise training alone and in combination with metformin prevented shedding of renal ACE2 by decreasing ADAM17 protein. Metformin 63-72 a disintegrin and metallopeptidase domain 17 Mus musculus 120-126 24412510-9 2014 H2S administration also led to significant decrease in extracellular levels of Abeta40 and Abeta42, the expression of BACE1 and PS1, and a significant increase of ADAM17 expression. Hydrogen Sulfide 0-3 a disintegrin and metallopeptidase domain 17 Mus musculus 163-169 24635658-6 2014 We show that the largest difference in the cleavage site specificities of ADAM10 and ADAM17 is at the P1" site: while both enzymes cleave N-terminal of leucine, only ADAM10 shows additional preference toward aromatic amino acids, whereas ADAM17 exhibits the highest preference for valine. Leucine 152-159 a disintegrin and metallopeptidase domain 17 Mus musculus 85-91 24635658-6 2014 We show that the largest difference in the cleavage site specificities of ADAM10 and ADAM17 is at the P1" site: while both enzymes cleave N-terminal of leucine, only ADAM10 shows additional preference toward aromatic amino acids, whereas ADAM17 exhibits the highest preference for valine. Leucine 152-159 a disintegrin and metallopeptidase domain 17 Mus musculus 238-244 24635658-6 2014 We show that the largest difference in the cleavage site specificities of ADAM10 and ADAM17 is at the P1" site: while both enzymes cleave N-terminal of leucine, only ADAM10 shows additional preference toward aromatic amino acids, whereas ADAM17 exhibits the highest preference for valine. Amino Acids, Aromatic 208-228 a disintegrin and metallopeptidase domain 17 Mus musculus 85-91 24635658-6 2014 We show that the largest difference in the cleavage site specificities of ADAM10 and ADAM17 is at the P1" site: while both enzymes cleave N-terminal of leucine, only ADAM10 shows additional preference toward aromatic amino acids, whereas ADAM17 exhibits the highest preference for valine. Amino Acids, Aromatic 208-228 a disintegrin and metallopeptidase domain 17 Mus musculus 238-244 24635658-6 2014 We show that the largest difference in the cleavage site specificities of ADAM10 and ADAM17 is at the P1" site: while both enzymes cleave N-terminal of leucine, only ADAM10 shows additional preference toward aromatic amino acids, whereas ADAM17 exhibits the highest preference for valine. Valine 281-287 a disintegrin and metallopeptidase domain 17 Mus musculus 85-91 24635658-6 2014 We show that the largest difference in the cleavage site specificities of ADAM10 and ADAM17 is at the P1" site: while both enzymes cleave N-terminal of leucine, only ADAM10 shows additional preference toward aromatic amino acids, whereas ADAM17 exhibits the highest preference for valine. Valine 281-287 a disintegrin and metallopeptidase domain 17 Mus musculus 238-244 23777205-8 2013 Regardless of the cell tested, treatment with the TACE inhibitor TAPI-0 led to a significant decrease in sTNFR2 shed (P<0.05). TAPI-0 65-71 a disintegrin and metallopeptidase domain 17 Mus musculus 50-54 24275664-4 2014 In proTNF-alpha the Arg-Ser-Ser-Ser-Arg sequence is situated next to the previously established ADAM17 cleavage site. Arginine 20-23 a disintegrin and metallopeptidase domain 17 Mus musculus 96-102 24275664-4 2014 In proTNF-alpha the Arg-Ser-Ser-Ser-Arg sequence is situated next to the previously established ADAM17 cleavage site. Serine 24-27 a disintegrin and metallopeptidase domain 17 Mus musculus 96-102 24275664-4 2014 In proTNF-alpha the Arg-Ser-Ser-Ser-Arg sequence is situated next to the previously established ADAM17 cleavage site. Serine 28-31 a disintegrin and metallopeptidase domain 17 Mus musculus 96-102 24275664-4 2014 In proTNF-alpha the Arg-Ser-Ser-Ser-Arg sequence is situated next to the previously established ADAM17 cleavage site. Serine 28-31 a disintegrin and metallopeptidase domain 17 Mus musculus 96-102 24275664-4 2014 In proTNF-alpha the Arg-Ser-Ser-Ser-Arg sequence is situated next to the previously established ADAM17 cleavage site. Arginine 36-39 a disintegrin and metallopeptidase domain 17 Mus musculus 96-102 24332999-6 2014 Reactive oxygen species played a key role since p47(phox)KO mice were resistant to Ang II-induced TACE phosphorylation and activation with preservation of myocardial ACE2 which dampened Ang II-induced cardiac dysfunction and hypertrophy. Reactive Oxygen Species 0-23 a disintegrin and metallopeptidase domain 17 Mus musculus 98-102 23942551-6 2013 High glucose stimulated Src, TACE, epidermal growth factor receptor (EGFR), mitogen-activated protein kinases (MAPKs), extracellular signal-regulated kinase (ERK1/2, p38), and collagen IV accumulation in mesangial cells. Glucose 5-12 a disintegrin and metallopeptidase domain 17 Mus musculus 29-33 24454948-10 2014 Incubation of cells in high D-glucose (25 mM) (and to a lesser extent Ang II) for 48-72 h increased ACE2 activity in the media (p<0.001), an effect blocked by inhibition of a disintegrin and metalloproteinase (ADAM)17. Glucose 28-37 a disintegrin and metallopeptidase domain 17 Mus musculus 194-220 24454948-11 2014 High D-glucose increased ADAM17 activity in cell lysates (p<0.05). Glucose 5-14 a disintegrin and metallopeptidase domain 17 Mus musculus 25-31 24454948-13 2014 ACE2 shedding is stimulated by high D-glucose, at least partly via an ADAM17-mediated pathway. Glucose 36-45 a disintegrin and metallopeptidase domain 17 Mus musculus 70-76 23942551-10 2013 These data indicate a role for Src in a high glucose-Src-TACE-heparin-binding epidermal growth factor-EGFR-MAPK-signaling pathway to collagen accumulation. Glucose 45-52 a disintegrin and metallopeptidase domain 17 Mus musculus 57-61 23942551-10 2013 These data indicate a role for Src in a high glucose-Src-TACE-heparin-binding epidermal growth factor-EGFR-MAPK-signaling pathway to collagen accumulation. Heparin 62-69 a disintegrin and metallopeptidase domain 17 Mus musculus 57-61 23816535-5 2013 To investigate this, we studied the effects of a selective TACE inhibitor DPC-333 on murine model of liver injury and fibrosis induced with concanavalin A (Con A). BMS561392 74-81 a disintegrin and metallopeptidase domain 17 Mus musculus 59-63 23678045-6 2013 In cultured mouse proximal tubular epithelial cells (MCTs), high glucose increases ADAM17 activity, Nox4 and fibronectin expression, cellular collagen content, and NADPH oxidase activity. Glucose 65-72 a disintegrin and metallopeptidase domain 17 Mus musculus 83-89 23678045-7 2013 These effects of glucose were inhibited when cells were pretreated with TMI-005 and/or transfected with small interfering ADAM17. Glucose 17-24 a disintegrin and metallopeptidase domain 17 Mus musculus 122-128 23801765-5 2013 Activation of heparin-binding EGF or Kit ligand 2 shedding by ADAM17 in iRhom2(-/-) mEFs can be rescued by wild-type iRhom2 but not by iRhom2 lacking its N-terminal cytoplasmic domain. Heparin 14-21 a disintegrin and metallopeptidase domain 17 Mus musculus 62-68 23299479-2 2013 Previous studies showed that inactivation of A disintegrin and metalloproteinase 17 (ADAM17), a membrane-anchored metalloproteinase that regulates epidermal growth factor receptor (EGFR) signaling, reduces pathological retinal neovascularization in a mouse model of oxygen-induced retinopathy (OIR). Oxygen 266-272 a disintegrin and metallopeptidase domain 17 Mus musculus 85-91 23474306-8 2013 CS appeared to affect the APP processing since differences in levels of ADAM17, BACE1 and C99/C83 ratio were found. Cesium 0-2 a disintegrin and metallopeptidase domain 17 Mus musculus 72-78 23646149-6 2013 Rosiglitazone treatment of db/db mice normalized hyperglycemia, attenuated renal injury and decreased urinary ACE2 and renal ADAM17 protein expression. Rosiglitazone 0-13 a disintegrin and metallopeptidase domain 17 Mus musculus 125-131 23646149-10 2013 Therefore, it is tempting to speculate that renoprotection of rosiglitazone could be partially mediated via downregulation of renal ADAM17 and ACE2 shedding. Rosiglitazone 62-75 a disintegrin and metallopeptidase domain 17 Mus musculus 132-138 23299479-2 2013 Previous studies showed that inactivation of A disintegrin and metalloproteinase 17 (ADAM17), a membrane-anchored metalloproteinase that regulates epidermal growth factor receptor (EGFR) signaling, reduces pathological retinal neovascularization in a mouse model of oxygen-induced retinopathy (OIR). Oxygen 266-272 a disintegrin and metallopeptidase domain 17 Mus musculus 45-83 23274494-3 2013 Inhibition of TACE resulted in the improvement in glucose and insulin levels in diabetic animals, suggesting a crucial role of TACE activity in glucose metabolism. Glucose 50-57 a disintegrin and metallopeptidase domain 17 Mus musculus 14-18 23299479-11 2013 CONCLUSIONS: These studies demonstrate that TIMP3 and erlotinib inhibit pathological neovascularization in the mouse retina, most likely due to inactivation of ADAM17 and the EGFR, respectively. Erlotinib Hydrochloride 54-63 a disintegrin and metallopeptidase domain 17 Mus musculus 160-166 23274494-3 2013 Inhibition of TACE resulted in the improvement in glucose and insulin levels in diabetic animals, suggesting a crucial role of TACE activity in glucose metabolism. Glucose 50-57 a disintegrin and metallopeptidase domain 17 Mus musculus 127-131 23274494-3 2013 Inhibition of TACE resulted in the improvement in glucose and insulin levels in diabetic animals, suggesting a crucial role of TACE activity in glucose metabolism. Glucose 144-151 a disintegrin and metallopeptidase domain 17 Mus musculus 14-18 23274494-3 2013 Inhibition of TACE resulted in the improvement in glucose and insulin levels in diabetic animals, suggesting a crucial role of TACE activity in glucose metabolism. Glucose 144-151 a disintegrin and metallopeptidase domain 17 Mus musculus 127-131 23274494-11 2013 Ay-CR showed significantly lower TACE, JNK and p38MAPK activities in VAT and serum TNFalpha level compared with those of Ay-AL. ay-cr 0-5 a disintegrin and metallopeptidase domain 17 Mus musculus 33-37 22626981-6 2013 Moreover, huprine X and huperzine A activate protein kinase C/mitogen-activated protein kinase pathway signalling, alpha-secretases (ADAM 10 and TACE) and increase the fraction of phospho-glycogen synthase kinase 3-beta. huprine X 10-19 a disintegrin and metallopeptidase domain 17 Mus musculus 145-149 23147225-5 2013 However, the transgene-derived TACE could be converted to an active form by furin in vitro and by phorbol myristate acetate (PMA) in vivo. Tetradecanoylphorbol Acetate 98-123 a disintegrin and metallopeptidase domain 17 Mus musculus 31-35 23147225-5 2013 However, the transgene-derived TACE could be converted to an active form by furin in vitro and by phorbol myristate acetate (PMA) in vivo. Tetradecanoylphorbol Acetate 125-128 a disintegrin and metallopeptidase domain 17 Mus musculus 31-35 22626981-6 2013 Moreover, huprine X and huperzine A activate protein kinase C/mitogen-activated protein kinase pathway signalling, alpha-secretases (ADAM 10 and TACE) and increase the fraction of phospho-glycogen synthase kinase 3-beta. huperzine A 24-35 a disintegrin and metallopeptidase domain 17 Mus musculus 145-149 22031879-6 2011 Similar effects were seen with TAPI-1, an inhibitor of another enzyme required for notch activity (TACE). N-((2-(hydroxyaminocarbonyl)methyl)-4-methylpentanoyl)-3-(2'-naphthyl)alanylalanine, 2-aminoethylamide 31-37 a disintegrin and metallopeptidase domain 17 Mus musculus 99-103 22796523-11 2012 mRNA levels of NEP and alpha-secretase (ADAM10 and ADAM17) were significantly lower in cholesterol-treated RPE cells than non-treated cells. Cholesterol 87-98 a disintegrin and metallopeptidase domain 17 Mus musculus 51-57 21827363-2 2012 TNF-alpha is an important proinflammatory cytokine and is released by the action of a Zn(2+)-containing converting enzyme (TACE/ADAM-17). Zinc 86-92 a disintegrin and metallopeptidase domain 17 Mus musculus 123-127 21827363-2 2012 TNF-alpha is an important proinflammatory cytokine and is released by the action of a Zn(2+)-containing converting enzyme (TACE/ADAM-17). Zinc 86-92 a disintegrin and metallopeptidase domain 17 Mus musculus 128-135 22687607-4 2012 During bleomycin-induced acute lung injury in mice, membrane-bound Mer expression decreased, but production of soluble Mer and activity as well as expression of disintegrin and metalloproteinase 17 (ADAM17) were enhanced . Bleomycin 7-16 a disintegrin and metallopeptidase domain 17 Mus musculus 199-205 22770404-8 2012 When CD16b expressing cell line was overexpressed with ADAM10, shedding of CD16b was increased after stimulation with ionomycin but not PMA; when the cell line overexpressed with ADAM17, shedding of CD16b was increased after stimulation with PMA but not ionomycin. Ionomycin 254-263 a disintegrin and metallopeptidase domain 17 Mus musculus 179-185 22770404-9 2012 Similarly, when ADAM10 was suppressed by short hairpin RNA, CD16b shedding was decreased after stimulation with ionomycin; when ADAM17 was suppressed by short hairpin RNA, CD16b shedding was decreased after stimulation with PMA. Tetradecanoylphorbol Acetate 224-227 a disintegrin and metallopeptidase domain 17 Mus musculus 128-134 21828049-0 2011 Shedding of the Mer tyrosine kinase receptor is mediated by ADAM17 protein through a pathway involving reactive oxygen species, protein kinase Cdelta, and p38 mitogen-activated protein kinase (MAPK). Reactive Oxygen Species 103-126 a disintegrin and metallopeptidase domain 17 Mus musculus 60-66 21041656-5 2010 N-ethyl-N-nitrosourea (ENU)-induced mutations in Adam17 (which is required for AREG and EREG processing) and in Egfr both produce a strong DSS colitis phenotype, and the Adam17 mutation exerts its deleterious effect in the nonhematopoietic compartment. Ethylnitrosourea 0-21 a disintegrin and metallopeptidase domain 17 Mus musculus 170-176 21519143-8 2011 Endothelial deletion of the TNF-alpha converting enzyme (TACE) prevented the TNF-alpha receptor shedding response, which suggests that exposure of microvascular endothelium to sTNF-alpha induced a Ca2+-dependent increase of mitochondrial H2O2 that caused TNFR1 shedding through TACE activation. Hydrogen Peroxide 238-242 a disintegrin and metallopeptidase domain 17 Mus musculus 28-55 21519143-8 2011 Endothelial deletion of the TNF-alpha converting enzyme (TACE) prevented the TNF-alpha receptor shedding response, which suggests that exposure of microvascular endothelium to sTNF-alpha induced a Ca2+-dependent increase of mitochondrial H2O2 that caused TNFR1 shedding through TACE activation. Hydrogen Peroxide 238-242 a disintegrin and metallopeptidase domain 17 Mus musculus 57-61 21041656-5 2010 N-ethyl-N-nitrosourea (ENU)-induced mutations in Adam17 (which is required for AREG and EREG processing) and in Egfr both produce a strong DSS colitis phenotype, and the Adam17 mutation exerts its deleterious effect in the nonhematopoietic compartment. Ethylnitrosourea 0-21 a disintegrin and metallopeptidase domain 17 Mus musculus 49-55 21857648-8 2011 These data demonstrate that a PA-PLA(1)alpha-LPA-P2Y5 axis regulates differentiation and maturation of hair follicles via a TACE-TGFalpha-EGFR pathway, thus underscoring the physiological importance of LPA-induced EGFR transactivation. lysophosphatidic acid 45-48 a disintegrin and metallopeptidase domain 17 Mus musculus 124-128 21785222-4 2011 The increased body, liver and epididymal adipose tissue (EAT) weights, systolic blood pressure, and fasting glucose and lipid levels and decreased serum adiponectin level 12 weeks after starting a HFD were suppressed by Tace inactivation. Glucose 108-115 a disintegrin and metallopeptidase domain 17 Mus musculus 220-224 21980496-3 2011 We hypothesized that treatment with the pharmacologic tumor necrosis factor-alpha converting enzyme (TACE)-inhibitor Marimastat would reverse established steatosis, leading to improved outcome following hepatectomy. marimastat 117-127 a disintegrin and metallopeptidase domain 17 Mus musculus 54-99 21980496-3 2011 We hypothesized that treatment with the pharmacologic tumor necrosis factor-alpha converting enzyme (TACE)-inhibitor Marimastat would reverse established steatosis, leading to improved outcome following hepatectomy. marimastat 117-127 a disintegrin and metallopeptidase domain 17 Mus musculus 101-105 21980496-12 2011 CONCLUSION/SIGNIFICANCE: Treatment with the TACE-inhibitor Marimastat improved surrogate markers for insulin sensitivity and reversed steatosis in mouse models of diet-induced obesity and leptin deficiency, thereby attenuating post-operative injury following hepatectomy. marimastat 59-69 a disintegrin and metallopeptidase domain 17 Mus musculus 44-48 20583103-8 2010 ADAM-17, a proteinase involved in Notch activation, was overexpressed in the skin of mice and patients in response to the local production of reactive oxygen species. Reactive Oxygen Species 142-165 a disintegrin and metallopeptidase domain 17 Mus musculus 0-7 20583103-10 2010 CONCLUSION: Our results show the pivotal role of the ADAM-17/Notch pathway in SSc following activation by reactive oxygen species. Reactive Oxygen Species 106-129 a disintegrin and metallopeptidase domain 17 Mus musculus 53-60 20603312-7 2010 Unexpectedly, although the intestine of unchallenged homozygous ADAM17(ex/ex) mice was normal, ADAM17(ex/ex) mice showed substantially increased susceptibility to inflammation in dextran sulfate sodium colitis. Dextran Sulfate 179-201 a disintegrin and metallopeptidase domain 17 Mus musculus 95-101 20236926-8 2010 TACE activity was 2-3-fold higher in asm(-/-) macrophages as compared with asm(+/+) macrophages and was suppressed when cells were treated with exogenous ceramide and sphingomyelinase. Ceramides 154-162 a disintegrin and metallopeptidase domain 17 Mus musculus 0-4 20628198-8 2010 Finally, adenoviral delivery of Adam17 prevented acetaminophen-induced liver failure in a clinically relevant model of Fas-dependent fulminant hepatitis. Acetaminophen 49-62 a disintegrin and metallopeptidase domain 17 Mus musculus 32-38 20628198-8 2010 Finally, adenoviral delivery of Adam17 prevented acetaminophen-induced liver failure in a clinically relevant model of Fas-dependent fulminant hepatitis. ammonium ferrous sulfate 119-122 a disintegrin and metallopeptidase domain 17 Mus musculus 32-38 19959661-0 2009 Vitamin B12 deficiency reduces proliferation and promotes differentiation of neuroblastoma cells and up-regulates PP2A, proNGF, and TACE. Vitamin B 12 0-11 a disintegrin and metallopeptidase domain 17 Mus musculus 132-136 20593020-4 2010 We hypothesized that treatment with a broad-spectrum MMP and TACE-inhibitor (Marimastat) would ameliorate injury and inflammation, leading to decreased fibrogenesis during repeated hepatotoxin-induced liver injury. marimastat 77-87 a disintegrin and metallopeptidase domain 17 Mus musculus 61-65 19877183-3 2010 In mouse hepatocytes, C(2)C(12) myocytes, and 3T3F442A adipocytes, TACE activity was triggered by palmitic acid, lipolysaccharide, high glucose, and high insulin. Palmitic Acid 98-111 a disintegrin and metallopeptidase domain 17 Mus musculus 67-71 19877183-3 2010 In mouse hepatocytes, C(2)C(12) myocytes, and 3T3F442A adipocytes, TACE activity was triggered by palmitic acid, lipolysaccharide, high glucose, and high insulin. lipolysaccharide 113-129 a disintegrin and metallopeptidase domain 17 Mus musculus 67-71 19877183-3 2010 In mouse hepatocytes, C(2)C(12) myocytes, and 3T3F442A adipocytes, TACE activity was triggered by palmitic acid, lipolysaccharide, high glucose, and high insulin. Glucose 136-143 a disintegrin and metallopeptidase domain 17 Mus musculus 67-71 19846666-0 2009 Mitochondrial reactive oxygen species mediate GPCR-induced TACE/ADAM17-dependent transforming growth factor-alpha shedding. Reactive Oxygen Species 14-37 a disintegrin and metallopeptidase domain 17 Mus musculus 59-63 19846666-4 2009 We report that ATP stimulates TGF-alpha proteolysis with concomitant EGFR activation and that this process requires TACE/ADAM17 activity in both murine fibroblasts and CHO cells. Adenosine Triphosphate 15-18 a disintegrin and metallopeptidase domain 17 Mus musculus 121-127 19846666-0 2009 Mitochondrial reactive oxygen species mediate GPCR-induced TACE/ADAM17-dependent transforming growth factor-alpha shedding. Reactive Oxygen Species 14-37 a disintegrin and metallopeptidase domain 17 Mus musculus 64-70 19846666-9 2009 Instead, mitochondrial ROS production increased in response to ATP and mitochondrial oxidative complex activity was required to activate TACE-dependent shedding. Reactive Oxygen Species 23-26 a disintegrin and metallopeptidase domain 17 Mus musculus 137-141 19543557-0 2009 Exogenous nitric oxide inhibits shedding of ADAM17 substrates. Nitric Oxide 10-22 a disintegrin and metallopeptidase domain 17 Mus musculus 44-50 19426283-0 2009 Serotonin stimulates platelet receptor shedding by tumor necrosis factor-alpha-converting enzyme (ADAM17). Serotonin 0-9 a disintegrin and metallopeptidase domain 17 Mus musculus 98-104 19534723-1 2009 To evaluate the anti-angiogenic efficacy of CB-12181 [an azasugar derivative that has inhibitory actions against matrix metalloproteinases (MMPs) and tumor necrosis factor-alpha (TNF-alpha) converting enzyme (TACE)], we investigated the suppressing ability on in vitro (tube formation by endothelial cells) and in vivo (retinal neovascularization on murine ischemia-induced proliferative retinopathy) models of angiogenesis. 3,4,5-trihydroxy-1-(4'-phenoxybenzenesulfonyl)piperidine-2-hydroxy amide 44-52 a disintegrin and metallopeptidase domain 17 Mus musculus 179-207 19534723-1 2009 To evaluate the anti-angiogenic efficacy of CB-12181 [an azasugar derivative that has inhibitory actions against matrix metalloproteinases (MMPs) and tumor necrosis factor-alpha (TNF-alpha) converting enzyme (TACE)], we investigated the suppressing ability on in vitro (tube formation by endothelial cells) and in vivo (retinal neovascularization on murine ischemia-induced proliferative retinopathy) models of angiogenesis. 3,4,5-trihydroxy-1-(4'-phenoxybenzenesulfonyl)piperidine-2-hydroxy amide 44-52 a disintegrin and metallopeptidase domain 17 Mus musculus 209-213 19543557-2 2009 We analyzed the effect of endogenous and exogenous nitric oxide on the expression and activity of ADAM17 in murine endothelial cells and a monocyte/macrophage cell line. Nitric Oxide 51-63 a disintegrin and metallopeptidase domain 17 Mus musculus 98-104 19543557-5 2009 Our data seem contrary to a previous report that showed the activation of ADAM17 by nitric oxide (Zhang et al., 2000, J Biol Chem 275: 15839-15844). Nitric Oxide 84-96 a disintegrin and metallopeptidase domain 17 Mus musculus 74-80 19005070-5 2008 We have examined the effects of the highly selective TACE inhibitor, BMS-561392, on APP processing in vitro and in vivo. BMS561392 69-79 a disintegrin and metallopeptidase domain 17 Mus musculus 53-57 18953638-4 2009 Here we generated floxed ERalpha mice using a self-excising ACN (tACE-Cre/Neo) cassette. 3-hydroxy-5-estrane-17-carbonitrile 60-63 a disintegrin and metallopeptidase domain 17 Mus musculus 65-69 19005070-9 2008 Despite this, we observed competition for APP when TACE activity was enhanced via phorbol ester treatment or if APP was modified such that it was retained within the trans-Golgi network (TGN). Phorbol Esters 82-95 a disintegrin and metallopeptidase domain 17 Mus musculus 51-55 17606376-1 2007 A series of beta-sulfonyl hydroxamate TACE inhibitors, bearing a butynylamino or a butynyloxy P1" group, was designed and synthesized. beta-sulfonyl hydroxamate 12-37 a disintegrin and metallopeptidase domain 17 Mus musculus 38-42 17606376-1 2007 A series of beta-sulfonyl hydroxamate TACE inhibitors, bearing a butynylamino or a butynyloxy P1" group, was designed and synthesized. butynylamino 65-77 a disintegrin and metallopeptidase domain 17 Mus musculus 38-42 17606376-1 2007 A series of beta-sulfonyl hydroxamate TACE inhibitors, bearing a butynylamino or a butynyloxy P1" group, was designed and synthesized. butynyloxy p1 83-96 a disintegrin and metallopeptidase domain 17 Mus musculus 38-42 17341609-5 2006 ROS, in turn, act as second message signals and control the activation of TACE (TNF-alpha converting enzyme), a member of a disintegrin and metalloproteinase family. Reactive Oxygen Species 0-3 a disintegrin and metallopeptidase domain 17 Mus musculus 74-78 17344430-0 2007 Different ADAMs have distinct influences on Kit ligand processing: phorbol-ester-stimulated ectodomain shedding of Kitl1 by ADAM17 is reduced by ADAM19. Phorbol Esters 67-80 a disintegrin and metallopeptidase domain 17 Mus musculus 124-130 17344430-6 2007 ADAM17 was identified as the major phorbol-ester-stimulated sheddase of Kitl1, whereas ADAMs 8, 9, 10, 12 and 15 were not required for this process. Phorbol Esters 35-48 a disintegrin and metallopeptidase domain 17 Mus musculus 0-6 17344430-7 2007 ADAM17 also emerged as the major constitutive and phorbol-ester-stimulated sheddase of Kitl2 in mouse embryonic fibroblasts. Phorbol Esters 50-63 a disintegrin and metallopeptidase domain 17 Mus musculus 0-6 17344430-9 2007 Taken together, this study identifies a novel sheddase, ADAM17, for Kitl1 and Kitl2, and demonstrates that ADAM19 can reduce ADAM17-dependent phorbol-ester-stimulated Kitl1 ectodomain shedding. Phorbol Esters 142-155 a disintegrin and metallopeptidase domain 17 Mus musculus 56-62 17344430-9 2007 Taken together, this study identifies a novel sheddase, ADAM17, for Kitl1 and Kitl2, and demonstrates that ADAM19 can reduce ADAM17-dependent phorbol-ester-stimulated Kitl1 ectodomain shedding. Phorbol Esters 142-155 a disintegrin and metallopeptidase domain 17 Mus musculus 125-131 16844679-4 2006 We hypothesized that Marimastat, a broad-spectrum MMP and TNF-alpha converting enzyme (TACE) inhibitor, might modulate this injury through interruption of inflammatory pathways. marimastat 21-31 a disintegrin and metallopeptidase domain 17 Mus musculus 58-85 16844679-4 2006 We hypothesized that Marimastat, a broad-spectrum MMP and TNF-alpha converting enzyme (TACE) inhibitor, might modulate this injury through interruption of inflammatory pathways. marimastat 21-31 a disintegrin and metallopeptidase domain 17 Mus musculus 87-91 17341609-5 2006 ROS, in turn, act as second message signals and control the activation of TACE (TNF-alpha converting enzyme), a member of a disintegrin and metalloproteinase family. Reactive Oxygen Species 0-3 a disintegrin and metallopeptidase domain 17 Mus musculus 80-107 16298020-4 2006 15,16-Dihydotanshinoe I suppressed the expression of not only inducible nitric oxide synthase but also of interleukin-1beta, tumor necrosis factor-alpha, and of TNF-alpha converting enzyme. 15,16-dihydotanshinoe i 0-23 a disintegrin and metallopeptidase domain 17 Mus musculus 161-188 16723229-0 2006 Design and synthesis of butynyloxyphenyl beta-sulfone piperidine hydroxamates as TACE inhibitors. butynyloxyphenyl beta-sulfone piperidine hydroxamates 24-77 a disintegrin and metallopeptidase domain 17 Mus musculus 81-85 16723229-1 2006 A series of butynyloxyphenyl beta-sulfone piperidine hydroxamate TACE inhibitors was designed and synthesized. butynyloxyphenyl beta-sulfone piperidine hydroxamate 12-64 a disintegrin and metallopeptidase domain 17 Mus musculus 65-69 16723229-3 2006 Of the compounds investigated, 17s has excellent in vitro potency against isolated TACE enzyme, shows good selectivity over MMP-1, -2, -7, -8, -9, -13, and -14, and oral activity in an in vivo mouse model of TNF-alpha production. 3mrx 31-34 a disintegrin and metallopeptidase domain 17 Mus musculus 83-87 15691827-4 2005 This shedding was inhibited by the broad range metalloproteinase inhibitor GM6001, the two potent ADAM17 inhibitors GW280264X and TAPI-2, and was absent in mice lacking functional ADAM17 (ADAM17 lacking Zn-binding domain; ADAM17(DeltaZn/DeltaZn)). N-(2(R)-2-(hydroxamidocarbonylmethyl)-4-methylpentanoyl)-L-tryptophan methylamide 75-81 a disintegrin and metallopeptidase domain 17 Mus musculus 98-104 16179345-0 2005 Aspirin induces platelet receptor shedding via ADAM17 (TACE). Aspirin 0-7 a disintegrin and metallopeptidase domain 17 Mus musculus 47-53 16179345-0 2005 Aspirin induces platelet receptor shedding via ADAM17 (TACE). Aspirin 0-7 a disintegrin and metallopeptidase domain 17 Mus musculus 55-59 16179345-9 2005 These data demonstrate that aspirin at high concentrations induces shedding of GPIbalpha and GPV by an ADAM17-dependent mechanism and that this process can occur in vivo. Aspirin 28-35 a disintegrin and metallopeptidase domain 17 Mus musculus 103-109 15985531-0 2005 Reactive oxygen species-dependent TNF-alpha converting enzyme activation through stimulation of 5-HT2B and alpha1D autoreceptors in neuronal cells. Oxygen 9-15 a disintegrin and metallopeptidase domain 17 Mus musculus 34-61 16227584-3 2005 Spontaneous and inducible Axl cleavage was inhibited by the broad-spectrum metalloproteinase inhibitor GM6001 and by hydroxamate GW280264X, which is capable of blocking ADAM10 and ADAM17. N-(2(R)-2-(hydroxamidocarbonylmethyl)-4-methylpentanoyl)-L-tryptophan methylamide 103-109 a disintegrin and metallopeptidase domain 17 Mus musculus 180-186 16227584-3 2005 Spontaneous and inducible Axl cleavage was inhibited by the broad-spectrum metalloproteinase inhibitor GM6001 and by hydroxamate GW280264X, which is capable of blocking ADAM10 and ADAM17. GW280264X 129-138 a disintegrin and metallopeptidase domain 17 Mus musculus 180-186 15691827-4 2005 This shedding was inhibited by the broad range metalloproteinase inhibitor GM6001, the two potent ADAM17 inhibitors GW280264X and TAPI-2, and was absent in mice lacking functional ADAM17 (ADAM17 lacking Zn-binding domain; ADAM17(DeltaZn/DeltaZn)). N-(2(R)-2-(hydroxamidocarbonylmethyl)-4-methylpentanoyl)-L-tryptophan methylamide 75-81 a disintegrin and metallopeptidase domain 17 Mus musculus 180-186 15691827-4 2005 This shedding was inhibited by the broad range metalloproteinase inhibitor GM6001, the two potent ADAM17 inhibitors GW280264X and TAPI-2, and was absent in mice lacking functional ADAM17 (ADAM17 lacking Zn-binding domain; ADAM17(DeltaZn/DeltaZn)). N-(2(R)-2-(hydroxamidocarbonylmethyl)-4-methylpentanoyl)-L-tryptophan methylamide 75-81 a disintegrin and metallopeptidase domain 17 Mus musculus 180-186 15691827-4 2005 This shedding was inhibited by the broad range metalloproteinase inhibitor GM6001, the two potent ADAM17 inhibitors GW280264X and TAPI-2, and was absent in mice lacking functional ADAM17 (ADAM17 lacking Zn-binding domain; ADAM17(DeltaZn/DeltaZn)). N-(2(R)-2-(hydroxamidocarbonylmethyl)-4-methylpentanoyl)-L-tryptophan methylamide 75-81 a disintegrin and metallopeptidase domain 17 Mus musculus 180-186 15691827-4 2005 This shedding was inhibited by the broad range metalloproteinase inhibitor GM6001, the two potent ADAM17 inhibitors GW280264X and TAPI-2, and was absent in mice lacking functional ADAM17 (ADAM17 lacking Zn-binding domain; ADAM17(DeltaZn/DeltaZn)). Zinc 203-205 a disintegrin and metallopeptidase domain 17 Mus musculus 180-186 15691827-4 2005 This shedding was inhibited by the broad range metalloproteinase inhibitor GM6001, the two potent ADAM17 inhibitors GW280264X and TAPI-2, and was absent in mice lacking functional ADAM17 (ADAM17 lacking Zn-binding domain; ADAM17(DeltaZn/DeltaZn)). Zinc 203-205 a disintegrin and metallopeptidase domain 17 Mus musculus 180-186 15691827-4 2005 This shedding was inhibited by the broad range metalloproteinase inhibitor GM6001, the two potent ADAM17 inhibitors GW280264X and TAPI-2, and was absent in mice lacking functional ADAM17 (ADAM17 lacking Zn-binding domain; ADAM17(DeltaZn/DeltaZn)). Zinc 203-205 a disintegrin and metallopeptidase domain 17 Mus musculus 180-186 12207026-8 2002 Furthermore, phorbol ester-stimulated shedding of the TACE substrate tumor necrosis factor-alpha was decreased in cells expressing catalytically active PTPH1 compared with inactive PTPH1. Phorbol Esters 13-26 a disintegrin and metallopeptidase domain 17 Mus musculus 54-58 15292243-5 2004 Our results corroborate that ADAM17, but not ADAM9, -10, or -19, is critical for phorbol ester- and pervanadate-stimulated release of TNFalpha in mouse embryonic fibroblasts. Phorbol Esters 81-94 a disintegrin and metallopeptidase domain 17 Mus musculus 29-35 15292243-5 2004 Our results corroborate that ADAM17, but not ADAM9, -10, or -19, is critical for phorbol ester- and pervanadate-stimulated release of TNFalpha in mouse embryonic fibroblasts. pervanadate 100-111 a disintegrin and metallopeptidase domain 17 Mus musculus 29-35 15215246-4 2004 Transmembrane IL-15Ralpha is constitutively converted into its soluble form by proteolytic cleavage that involves tumor necrosis factor-alpha-converting enzyme (TACE), and this process is further enhanced by phorbol 12-myristate 13-acetate (PMA) stimulation. Tetradecanoylphorbol Acetate 241-244 a disintegrin and metallopeptidase domain 17 Mus musculus 161-165 15215246-5 2004 The hydroxamate GW280264X, which is capable of blocking TACE and the closely related disintegrin-like metalloproteinase 10 (ADAM10), effectively inhibited both spontaneous and PMA-inducible cleavage of IL-15Ralpha, whereas GI254023X, which preferentially blocks ADAM10, was ineffective. hydroxamate 4-15 a disintegrin and metallopeptidase domain 17 Mus musculus 56-60 15215246-5 2004 The hydroxamate GW280264X, which is capable of blocking TACE and the closely related disintegrin-like metalloproteinase 10 (ADAM10), effectively inhibited both spontaneous and PMA-inducible cleavage of IL-15Ralpha, whereas GI254023X, which preferentially blocks ADAM10, was ineffective. GW280264X 16-25 a disintegrin and metallopeptidase domain 17 Mus musculus 56-60 15215246-7 2004 Moreover, murine fibroblasts deficient in TACE but not ADAM10 expression exhibited a significant reduction in the spontaneous and inducible IL-15Ralpha shedding, whereas a reconstitution of TACE in these cells restored the release of sIL-15Ralpha, thereby suggesting that TACE-mediated proteolysis may represent a major mechanism for sIL-15Ralpha generation in mice. sil-15ralpha 234-246 a disintegrin and metallopeptidase domain 17 Mus musculus 42-46 15215246-7 2004 Moreover, murine fibroblasts deficient in TACE but not ADAM10 expression exhibited a significant reduction in the spontaneous and inducible IL-15Ralpha shedding, whereas a reconstitution of TACE in these cells restored the release of sIL-15Ralpha, thereby suggesting that TACE-mediated proteolysis may represent a major mechanism for sIL-15Ralpha generation in mice. sil-15ralpha 234-246 a disintegrin and metallopeptidase domain 17 Mus musculus 190-194 15215246-7 2004 Moreover, murine fibroblasts deficient in TACE but not ADAM10 expression exhibited a significant reduction in the spontaneous and inducible IL-15Ralpha shedding, whereas a reconstitution of TACE in these cells restored the release of sIL-15Ralpha, thereby suggesting that TACE-mediated proteolysis may represent a major mechanism for sIL-15Ralpha generation in mice. sil-15ralpha 234-246 a disintegrin and metallopeptidase domain 17 Mus musculus 190-194 15215246-7 2004 Moreover, murine fibroblasts deficient in TACE but not ADAM10 expression exhibited a significant reduction in the spontaneous and inducible IL-15Ralpha shedding, whereas a reconstitution of TACE in these cells restored the release of sIL-15Ralpha, thereby suggesting that TACE-mediated proteolysis may represent a major mechanism for sIL-15Ralpha generation in mice. sil-15ralpha 334-346 a disintegrin and metallopeptidase domain 17 Mus musculus 42-46 15357971-0 2004 Synthesis and structure-activity relationship of a novel sulfone series of TNF-alpha converting enzyme inhibitors. Sulfones 57-64 a disintegrin and metallopeptidase domain 17 Mus musculus 75-102 15357971-1 2004 Replacement of the amide functionality in IM491 (N-hydroxy-(5S,6S)-1-methyl-6-[[4-(2-methyl-4-quinolinylmethoxy)anilinyl]carbonyl]5-piperidinecarboxamide) with a sulfonyl group led to a new series of alpha,beta-cyclic and beta,beta-cyclic gamma-sulfonyl hydroxamic acids, which were potent TNF-alpha converting enzyme (TACE) inhibitors. Amides 19-24 a disintegrin and metallopeptidase domain 17 Mus musculus 290-317 15357971-1 2004 Replacement of the amide functionality in IM491 (N-hydroxy-(5S,6S)-1-methyl-6-[[4-(2-methyl-4-quinolinylmethoxy)anilinyl]carbonyl]5-piperidinecarboxamide) with a sulfonyl group led to a new series of alpha,beta-cyclic and beta,beta-cyclic gamma-sulfonyl hydroxamic acids, which were potent TNF-alpha converting enzyme (TACE) inhibitors. Amides 19-24 a disintegrin and metallopeptidase domain 17 Mus musculus 319-323 15075334-7 2004 Further mutagenesis and functional analyses demonstrated that Cys(600) was absolutely essential for ectodomain shedding, suggesting that Cys(600), similar to Cys(225), participates in disulfide bonding, which is critical for both the processing and catalysis of TACE. Cysteine 62-65 a disintegrin and metallopeptidase domain 17 Mus musculus 262-266 15075334-7 2004 Further mutagenesis and functional analyses demonstrated that Cys(600) was absolutely essential for ectodomain shedding, suggesting that Cys(600), similar to Cys(225), participates in disulfide bonding, which is critical for both the processing and catalysis of TACE. Cysteine 137-140 a disintegrin and metallopeptidase domain 17 Mus musculus 262-266 15075334-7 2004 Further mutagenesis and functional analyses demonstrated that Cys(600) was absolutely essential for ectodomain shedding, suggesting that Cys(600), similar to Cys(225), participates in disulfide bonding, which is critical for both the processing and catalysis of TACE. Cysteine 137-140 a disintegrin and metallopeptidase domain 17 Mus musculus 262-266 15075334-7 2004 Further mutagenesis and functional analyses demonstrated that Cys(600) was absolutely essential for ectodomain shedding, suggesting that Cys(600), similar to Cys(225), participates in disulfide bonding, which is critical for both the processing and catalysis of TACE. Disulfides 184-193 a disintegrin and metallopeptidase domain 17 Mus musculus 262-266 14559850-6 2003 Using the TNF-alpha converting enzyme (TACE) inhibitor, TAPI-1, TPA-stimulated TNFalpha shedding could be completely prevented in PKCepsilon transgenic mice and isolated keratinocytes. N-((2-(hydroxyaminocarbonyl)methyl)-4-methylpentanoyl)-3-(2'-naphthyl)alanylalanine, 2-aminoethylamide 56-62 a disintegrin and metallopeptidase domain 17 Mus musculus 10-37 14559850-6 2003 Using the TNF-alpha converting enzyme (TACE) inhibitor, TAPI-1, TPA-stimulated TNFalpha shedding could be completely prevented in PKCepsilon transgenic mice and isolated keratinocytes. N-((2-(hydroxyaminocarbonyl)methyl)-4-methylpentanoyl)-3-(2'-naphthyl)alanylalanine, 2-aminoethylamide 56-62 a disintegrin and metallopeptidase domain 17 Mus musculus 39-43 14559850-6 2003 Using the TNF-alpha converting enzyme (TACE) inhibitor, TAPI-1, TPA-stimulated TNFalpha shedding could be completely prevented in PKCepsilon transgenic mice and isolated keratinocytes. Tetradecanoylphorbol Acetate 64-67 a disintegrin and metallopeptidase domain 17 Mus musculus 10-37 14559850-6 2003 Using the TNF-alpha converting enzyme (TACE) inhibitor, TAPI-1, TPA-stimulated TNFalpha shedding could be completely prevented in PKCepsilon transgenic mice and isolated keratinocytes. Tetradecanoylphorbol Acetate 64-67 a disintegrin and metallopeptidase domain 17 Mus musculus 39-43 14559850-7 2003 These results indicate that PKCepsilon signal transduction pathways to TPA-stimulated TNFalpha ectodomain shedding are mediated by TACE, a transmembrane metalloprotease. Tetradecanoylphorbol Acetate 71-74 a disintegrin and metallopeptidase domain 17 Mus musculus 131-135 14559850-11 2003 Taken together, these results indicate that: (a) PKCepsilon activation is an initial signal in TPA-induced shedding of TNFalpha from epidermal keratinocytes; (b) PKCepsilon-mediated signals to TACE are possibly mediated through reactive oxygen species; and (c) TPA-induced TNFalpha shedding may play a role in the development of mSCC in PKCepsilon transgenic mice. Tetradecanoylphorbol Acetate 95-98 a disintegrin and metallopeptidase domain 17 Mus musculus 193-197 15745814-0 2005 Synthesis and SAR of diazepine and thiazepine TACE and MMP inhibitors. Thiazepines 35-45 a disintegrin and metallopeptidase domain 17 Mus musculus 46-50 15745814-1 2005 Potent and selective TACE and MMP inhibitors utilizing the diazepine and thiazepine ring systems were synthesized and evaluated for biological activity in in vitro and in vivo models of TNF-alpha release. Diazepine 59-68 a disintegrin and metallopeptidase domain 17 Mus musculus 21-25 15745814-1 2005 Potent and selective TACE and MMP inhibitors utilizing the diazepine and thiazepine ring systems were synthesized and evaluated for biological activity in in vitro and in vivo models of TNF-alpha release. Thiazepines 73-83 a disintegrin and metallopeptidase domain 17 Mus musculus 21-25 11472217-1 2001 To search for TNF-alpha (tumor necrosis factor alpha) converting enzyme (TACE) inhibitors, we designed a new class of macrocyclic hydroxamic acids by linking the P1 and P2" residues of acyclic anti-succinate-based hydroxamic acids. Hydroxamic Acids 130-146 a disintegrin and metallopeptidase domain 17 Mus musculus 73-77 12147693-11 2002 Diphenylamine and its related compounds exert this action on L-selectin through a prostaglandin-independent, TACE-dependent mechanism that seems to be linked to the capability of these agents to uncouple the mitochondrial oxidative phosphorylation. Diphenylamine 0-13 a disintegrin and metallopeptidase domain 17 Mus musculus 109-113 11472217-1 2001 To search for TNF-alpha (tumor necrosis factor alpha) converting enzyme (TACE) inhibitors, we designed a new class of macrocyclic hydroxamic acids by linking the P1 and P2" residues of acyclic anti-succinate-based hydroxamic acids. Succinic Acid 198-207 a disintegrin and metallopeptidase domain 17 Mus musculus 73-77 11418640-10 2001 We conclude that the CD44 sheddase and TACE are distinct enzymes, and that Ab- and phorbol ester-enhanced cleavage of CD44 is controlled in a cell type-dependent fashion by Rho GTPases through the cytoskeleton. Phorbol Esters 83-96 a disintegrin and metallopeptidase domain 17 Mus musculus 39-43 11472217-1 2001 To search for TNF-alpha (tumor necrosis factor alpha) converting enzyme (TACE) inhibitors, we designed a new class of macrocyclic hydroxamic acids by linking the P1 and P2" residues of acyclic anti-succinate-based hydroxamic acids. Hydroxamic Acids 214-230 a disintegrin and metallopeptidase domain 17 Mus musculus 73-77 11460998-2 2001 Herein, we have found that TAPI, a synthetic inhibitor of TACE, inhibits embryonic mouse lung branching morphogenesis in culture. tapi 27-31 a disintegrin and metallopeptidase domain 17 Mus musculus 58-62 11460998-5 2001 Furthermore, both aquaporin-5 (Aqp5) and surfactant protein-C (SP-C) mRNA expression and protein immunoreactivity were significantly inhibited in cultured mouse lungs treated with TACE antisense oligonucleotide, indicating defective epithelial cell differentiation in embryonic lungs with decreased TACE expression. Oligonucleotides 195-210 a disintegrin and metallopeptidase domain 17 Mus musculus 180-184 11460998-3 2001 To further investigate the biological significance of TACE as a shedding enzyme during early lung organogenesis, we have devised an antisense oligonucleotide to specifically block endogenous TACE gene expression at both transcriptional and translational levels in embryonic mouse lung explant culture. Oligonucleotides 142-157 a disintegrin and metallopeptidase domain 17 Mus musculus 54-58 11460998-5 2001 Furthermore, both aquaporin-5 (Aqp5) and surfactant protein-C (SP-C) mRNA expression and protein immunoreactivity were significantly inhibited in cultured mouse lungs treated with TACE antisense oligonucleotide, indicating defective epithelial cell differentiation in embryonic lungs with decreased TACE expression. Oligonucleotides 195-210 a disintegrin and metallopeptidase domain 17 Mus musculus 299-303 11460998-8 2001 Soluble TGF-alpha, when included in the lung culture, rescued the TACE antisense oligonucleotide-treated lungs from inhibition of both lung branching morphogenesis and lung epithelial cell differentiation, suggesting an impaired release of circulating regulators necessary for lung development in the absence of TACE gene expression. Oligonucleotides 81-96 a disintegrin and metallopeptidase domain 17 Mus musculus 66-70 11460998-3 2001 To further investigate the biological significance of TACE as a shedding enzyme during early lung organogenesis, we have devised an antisense oligonucleotide to specifically block endogenous TACE gene expression at both transcriptional and translational levels in embryonic mouse lung explant culture. Oligonucleotides 142-157 a disintegrin and metallopeptidase domain 17 Mus musculus 191-195 11460998-8 2001 Soluble TGF-alpha, when included in the lung culture, rescued the TACE antisense oligonucleotide-treated lungs from inhibition of both lung branching morphogenesis and lung epithelial cell differentiation, suggesting an impaired release of circulating regulators necessary for lung development in the absence of TACE gene expression. Oligonucleotides 81-96 a disintegrin and metallopeptidase domain 17 Mus musculus 312-316 11460998-4 2001 Addition of TACE antisense oligonucleotide resulted in a concentration-dependent reduction in lung branching morphogenesis in culture, whereas both scrambled and sense control oligonucleotides showed no adverse effects on lung growth. Oligonucleotides 27-42 a disintegrin and metallopeptidase domain 17 Mus musculus 12-16 10747938-4 2000 Here, we show that nitric oxide (NO) activates TACE-mediated ectodomain shedding. Nitric Oxide 19-31 a disintegrin and metallopeptidase domain 17 Mus musculus 47-51 11160199-7 2001 These data indicated that TACE is required for the TPA-induced M-CSFR cleavage. Tetradecanoylphorbol Acetate 51-54 a disintegrin and metallopeptidase domain 17 Mus musculus 26-30 10785383-4 2000 In experiments with TACE deficient (TACE-/-) fibroblasts we found that 4beta-phorbol 12-myristate 13-acetate (PMA)-induced shedding of the interleukin-6 receptor (IL-6R) is strongly reduced. Tetradecanoylphorbol Acetate 71-108 a disintegrin and metallopeptidase domain 17 Mus musculus 20-24 10785383-4 2000 In experiments with TACE deficient (TACE-/-) fibroblasts we found that 4beta-phorbol 12-myristate 13-acetate (PMA)-induced shedding of the interleukin-6 receptor (IL-6R) is strongly reduced. Tetradecanoylphorbol Acetate 71-108 a disintegrin and metallopeptidase domain 17 Mus musculus 36-40 10785383-4 2000 In experiments with TACE deficient (TACE-/-) fibroblasts we found that 4beta-phorbol 12-myristate 13-acetate (PMA)-induced shedding of the interleukin-6 receptor (IL-6R) is strongly reduced. Tetradecanoylphorbol Acetate 110-113 a disintegrin and metallopeptidase domain 17 Mus musculus 20-24 10785383-4 2000 In experiments with TACE deficient (TACE-/-) fibroblasts we found that 4beta-phorbol 12-myristate 13-acetate (PMA)-induced shedding of the interleukin-6 receptor (IL-6R) is strongly reduced. Tetradecanoylphorbol Acetate 110-113 a disintegrin and metallopeptidase domain 17 Mus musculus 36-40 10785383-7 2000 PMA-induced shedding of IL-6R in TACE deficient mouse fibroblasts could be restored by stable transfection of a TACE cDNA. Tetradecanoylphorbol Acetate 0-3 a disintegrin and metallopeptidase domain 17 Mus musculus 33-37 10785383-7 2000 PMA-induced shedding of IL-6R in TACE deficient mouse fibroblasts could be restored by stable transfection of a TACE cDNA. Tetradecanoylphorbol Acetate 0-3 a disintegrin and metallopeptidase domain 17 Mus musculus 112-116 10727411-5 2000 An additional form of TACE, lacking the pro and cytoplasmic domains, is detected when cell lysates are prepared in the presence of EDTA instead of a hydroxamate-based metalloprotease inhibitor or 1,10-phenanthroline. Edetic Acid 131-135 a disintegrin and metallopeptidase domain 17 Mus musculus 22-26 10727411-5 2000 An additional form of TACE, lacking the pro and cytoplasmic domains, is detected when cell lysates are prepared in the presence of EDTA instead of a hydroxamate-based metalloprotease inhibitor or 1,10-phenanthroline. hydroxamate 149-160 a disintegrin and metallopeptidase domain 17 Mus musculus 22-26 10727411-5 2000 An additional form of TACE, lacking the pro and cytoplasmic domains, is detected when cell lysates are prepared in the presence of EDTA instead of a hydroxamate-based metalloprotease inhibitor or 1,10-phenanthroline. 1,10-phenanthroline 196-215 a disintegrin and metallopeptidase domain 17 Mus musculus 22-26