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[PMID]:29254295
[Au] Autor:Walkiewicz K; Nowakowska-Zajdel E; Strzelczyk J; Dziegielewska-Gesiak S; Muc-Wierzgon M
[Ad] Endereço:Department of Internal Medicine, School of Public Health in Bytom, Medical University of Silesia, Katowice, Poland.
[Ti] Título:Serum levels of ADAM10, ADAM12, ADAM17 AND ADAM28 in colorectal cancer patients.
[So] Source:J Biol Regul Homeost Agents;31(4):929-934, 2017 Oct-Dec.
[Is] ISSN:0393-974X
[Cp] País de publicação:Italy
[La] Idioma:eng
[Ab] Resumo:Colorectal cancer is the third most common cancer in the world. Our study analyzed the potential significance of serum levels of selected adamalysines (ADAM10, ADAM12, ADAM17, ADAM28) in colorectal cancer patients. The study was performed on a group of 85 colorectal cancer patients (48 men, 37 women). Serum protein concentrations were measured by ELISA. The ADAMs serum level changes were analyzed according to selected clinical parameters (BMI, sex, age, clinical stage of disease). The following ranges of concentration of analyzed proteins were obtained: ADAM10 min=1.7, max=321.8 [ng/ml]; ADAM12 min=0.6, max=26.7 [ng/ml]; ADAM17 min=0.4, max=9.8 [ng/ml]; ADAM28 min=17.1, max=1545.8 [ng/ml]. In addition, it was stated that there is a relationship between the serum level of ADAM28 and the degree of the clinical stage (p less than 0.04). The obtained results could be the starting point for further research into the role of adamalysines in the development of colorectal cancer, as well as the potential predictive and prognostic value of these proteins.
[Mh] Termos MeSH primário: Proteínas ADAM/genética
Adenocarcinoma/genética
Biomarcadores Tumorais/genética
Colo/metabolismo
Neoplasias Colorretais/genética
Regulação Neoplásica da Expressão Gênica
[Mh] Termos MeSH secundário: Proteínas ADAM/sangue
Proteína ADAM10/sangue
Proteína ADAM10/genética
Proteína ADAM12/sangue
Proteína ADAM12/genética
Proteína ADAM17/sangue
Proteína ADAM17/genética
Adenocarcinoma/sangue
Adenocarcinoma/diagnóstico
Adenocarcinoma/patologia
Adulto
Fatores Etários
Idoso
Idoso de 80 Anos ou mais
Secretases da Proteína Precursora do Amiloide/sangue
Secretases da Proteína Precursora do Amiloide/genética
Biomarcadores Tumorais/sangue
Índice de Massa Corporal
Colo/patologia
Neoplasias Colorretais/sangue
Neoplasias Colorretais/diagnóstico
Neoplasias Colorretais/patologia
Feminino
Seres Humanos
Masculino
Proteínas de Membrana/sangue
Proteínas de Membrana/genética
Meia-Idade
Estadiamento de Neoplasias
Fatores Sexuais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (Membrane Proteins); EC 3.4.- (Amyloid Precursor Protein Secretases); EC 3.4.24.- (ADAM Proteins); EC 3.4.24.- (ADAM12 Protein); EC 3.4.24.- (ADAM12 protein, human); EC 3.4.24.- (ADAM28 protein, human); EC 3.4.24.81 (ADAM10 Protein); EC 3.4.24.81 (ADAM10 protein, human); EC 3.4.24.86 (ADAM17 Protein); EC 3.4.24.86 (ADAM17 protein, human)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171220
[St] Status:MEDLINE


  2 / 1469 MEDLINE  
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[PMID]:29286859
[Au] Autor:Otulakowski G; Engelberts D; Post M; Masterson C; Kavanagh BP
[Ad] Endereço:1 Hospital for Sick Children Toronto, Ontario, Canada and.
[Ti] Título:Hypercapnic Acidosis Regulates Mer Tyrosine Kinase Receptor Shedding and Activity.
[So] Source:Am J Respir Cell Mol Biol;58(1):132-134, 2018 01.
[Is] ISSN:1535-4989
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Acidose Respiratória/metabolismo
Hipercapnia/metabolismo
c-Mer Tirosina Quinase/metabolismo
[Mh] Termos MeSH secundário: Proteína ADAM17/metabolismo
Acidose Respiratória/patologia
Animais
Linhagem Celular
Hipercapnia/patologia
Camundongos
[Pt] Tipo de publicação:LETTER; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
EC 2.7.10.1 (Mertk protein, mouse); EC 2.7.10.1 (c-Mer Tyrosine Kinase); EC 3.4.24.86 (ADAM17 Protein); EC 3.4.24.86 (Adam17 protein, mouse)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180221
[Lr] Data última revisão:
180221
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171230
[St] Status:MEDLINE
[do] DOI:10.1165/rcmb.2017-0316LE


  3 / 1469 MEDLINE  
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[PMID]:29180185
[Au] Autor:Fang W; Qian J; Wu Q; Chen Y; Yu G
[Ad] Endereço:Department of Oncology, Longhua Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai, People's Republic of China; Department of Oncology, Fuzhou General Hospital, Fuzhou, Fujian Province, People's Republic of China.
[Ti] Título:ADAM-17 expression is enhanced by FoxM1 and is a poor prognostic sign in gastric carcinoma.
[So] Source:J Surg Res;220:223-233, 2017 Dec.
[Is] ISSN:1095-8673
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The ADAMs proteases are a multifunctional family of proteins, many of which participate in the pathogenesis of cancers. The expression and regulation of ADAMs has not yet been fully examined in gastric cancer. MATERIALS AND METHODS: Using reverse transcription-PCR, messenger RNA expression of ADAM-9, ADAM-10, ADAM-11, ADAM-12, ADAM-15, ADAM-17, ADAM-28, and ADAM-33 was detected in gastric cancer. ADAM-10, ADAM-17, ADAM-28, and FoxM1 expression in gastric cancer was detected by Western blot and immunohistochemistry. The correlation between ADAM-17 and FoxM1 was analyzed in vivo and in vitro. RESULTS: The messenger RNA levels of ADAM-9, ADAM-10, ADAM-15, ADAM-17, ADAM-28, and ADAM-33 were increased in tumor tissues compared with adjacent normal tissue, especially ADAM-10, ADAM-17, and ADAM-28. FoxM1 expression correlated significantly with ADAM-17 expression. FoxM1 regulates ADAM-17 expression in vivo and in vitro, which in turn influences proliferation and tumor growth of gastric cancer cells. Furthermore, Cox regression analysis revealed that FoxM1 and ADAM-17 are independent prognostic factors for patients with gastric cancer. CONCLUSIONS: These results indicate that overexpression of ADAMs may contribute to gastric cancer progression and that ADAM-17 is a downstream target of FoxM1. Overall, the present study highlights the potential for FoxM1 and ADAMs as potential therapeutic targets for patients with gastric carcinoma.
[Mh] Termos MeSH primário: Proteína ADAM17/metabolismo
Adenocarcinoma/enzimologia
Proteína Forkhead Box M1/metabolismo
Neoplasias Gástricas/enzimologia
[Mh] Termos MeSH secundário: Adenocarcinoma/mortalidade
Biomarcadores Tumorais/metabolismo
Linhagem Celular Tumoral
China/epidemiologia
Feminino
Seres Humanos
Masculino
Meia-Idade
Neoplasias Gástricas/mortalidade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (FOXM1 protein, human); 0 (Forkhead Box Protein M1); EC 3.4.24.86 (ADAM17 Protein); EC 3.4.24.86 (ADAM17 protein, human)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171211
[Lr] Data última revisão:
171211
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171129
[St] Status:MEDLINE


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[PMID]:28982863
[Au] Autor:Pham DH; Kim JS; Kim SK; Shin DJ; Uong NT; Hyun H; Yoon MS; Kang SJ; Ryu YJ; Cho JS; Yoon JH; Lee JS; Cho D; Lee SH; Park MH
[Ad] Endereço:Department of Biomedical Sciences, Chonnam National University Medical School, Gwangju, Republic of Korea.
[Ti] Título:Effects of ADAM10 and ADAM17 Inhibitors on Natural Killer Cell Expansion and Antibody-dependent Cellular Cytotoxicity Against Breast Cancer Cells .
[So] Source:Anticancer Res;37(10):5507-5513, 2017 10.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIM: The inhibition of a disintegrin and metalloproteinase (ADAM) has the potential to become a novel approach for natural killer (NK) cell-based cancer immunotherapy. Thus, the aim of this study was to investigate the influence of ADAM10 and ADAM17 inhibitors on expanded NK cell to enhance antibody-dependent cellular cytotoxicity (ADCC) in breast cancer cell lines. MATERIALS AND METHODS: NK cells were expanded in medium supplemented with an ADAM10 or ADAM17 inhibitor to prevent the shedding of soluble CD16/FcγRIII. The expression level of CD16 and production of interferon-gamma (IFN-γ) was detected by flow cytometry using specific antibodies. ADCC activity of expanded NK cells was estimated in trastuzumab treated breast cancer cell lines such as MCF-7, MDA-MB-231, SKBR3, and BT-474 cells. RESULTS: The ADAM17 inhibitor increased the purity of expanded NK cells to 90% after 14 days at 5 and 10 µM in vitro (p=0.043). However, the expansion rate of NK cells was decreased at 10 µM of the ADAM 17 inhibitor (p=0.043). Inhibition of ADAM10 suppressed the expansion of NK cells, although the NK purity was increased at 1 µM of the inhibitor. The expression of CD16 was significantly increased at 1 and 5 µM of the ADAM17 inhibitor (p=0.046, 0.028, respectively) during the culturing period. Inhibition of ADAM10 reduced the expression of CD16 on NK cells. The cytotoxic activity of the ADAM17 inhibitor treated NK cells against MCF-7 (p=0.039) and BT-474 (p=0.027) cells was significantly elevated. The ADCC activity of NK cells treated with 5 µM of ADAM17 inhibitor was significantly increased against SKBR-3 and BT-474 (p=0.027). Inhibition of ADAM17 increased the production of IFN-γ in expanded NK cells. CONCLUSION: The inhibition of ADAM17 enhanced the purity of expanded NK cells and the ADCC activity of these cells against trastuzumab treated breast cancer cell lines.
[Mh] Termos MeSH primário: Proteína ADAM10/antagonistas & inibidores
Proteína ADAM17/antagonistas & inibidores
Secretases da Proteína Precursora do Amiloide/antagonistas & inibidores
Citotoxicidade Celular Dependente de Anticorpos/efeitos dos fármacos
Antineoplásicos/farmacologia
Neoplasias da Mama/tratamento farmacológico
Proliferação Celular/efeitos dos fármacos
Células Matadoras Naturais/efeitos dos fármacos
Ativação Linfocitária/efeitos dos fármacos
Proteínas de Membrana/antagonistas & inibidores
Inibidores de Proteases/farmacologia
[Mh] Termos MeSH secundário: Proteína ADAM10/metabolismo
Proteína ADAM17/metabolismo
Secretases da Proteína Precursora do Amiloide/metabolismo
Protocolos de Quimioterapia Combinada Antineoplásica/farmacologia
Neoplasias da Mama/enzimologia
Neoplasias da Mama/imunologia
Neoplasias da Mama/patologia
Técnicas de Cocultura
Relação Dose-Resposta a Droga
Feminino
Proteínas Ligadas por GPI/metabolismo
Seres Humanos
Interferon gama/metabolismo
Células Matadoras Naturais/enzimologia
Células Matadoras Naturais/imunologia
Células MCF-7
Proteínas de Membrana/metabolismo
Receptores de IgG/metabolismo
Fatores de Tempo
Trastuzumab/farmacologia
Microambiente Tumoral
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (FCGR3B protein, human); 0 (GPI-Linked Proteins); 0 (IFNG protein, human); 0 (Membrane Proteins); 0 (Protease Inhibitors); 0 (Receptors, IgG); 82115-62-6 (Interferon-gamma); EC 3.4.- (Amyloid Precursor Protein Secretases); EC 3.4.24.81 (ADAM10 Protein); EC 3.4.24.81 (ADAM10 protein, human); EC 3.4.24.86 (ADAM17 Protein); EC 3.4.24.86 (ADAM17 protein, human); P188ANX8CK (Trastuzumab)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171007
[St] Status:MEDLINE


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[PMID]:28947615
[Au] Autor:Kawai T; Takayanagi T; Forrester SJ; Preston KJ; Obama T; Tsuji T; Kobayashi T; Boyer MJ; Cooper HA; Kwok HF; Hashimoto T; Scalia R; Rizzo V; Eguchi S
[Ad] Endereço:From the Cardiovascular Research Center, Department of Physiology, Lewis Katz School of Medicine at Temple University, Philadelphia, PA (T. Kawai, T. Takayanagi, S.J.F., K.J.P., T.O., T. Tsuji, T. Kobayashi, M.J.B., H.A.C., R.S., V.R., S.E.); Faculty of Health Sciences, Macau Special Administrative
[Ti] Título:Vascular ADAM17 (a Disintegrin and Metalloproteinase Domain 17) Is Required for Angiotensin II/ß-Aminopropionitrile-Induced Abdominal Aortic Aneurysm.
[So] Source:Hypertension;70(5):959-963, 2017 Nov.
[Is] ISSN:1524-4563
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Angiotensin II (AngII)-activated epidermal growth factor receptor has been implicated in abdominal aortic aneurysm (AAA) development. In vascular smooth muscle cells (VSMCs), AngII activates epidermal growth factor receptor via a metalloproteinase, ADAM17 (a disintegrin and metalloproteinase domain 17). We hypothesized that AngII-dependent AAA development would be prevented in mice lacking ADAM17 in VSMCs. To test this concept, control and VSMC ADAM17-deficient mice were cotreated with AngII and a lysyl oxidase inhibitor, ß-aminopropionitrile, to induce AAA. We found that 52.4% of control mice did not survive because of aortic rupture. All other surviving control mice developed AAA and demonstrated enhanced expression of ADAM17 in the AAA lesions. In contrast, all AngII and ß-aminopropionitrile-treated VSMC ADAM17-deficient mice survived and showed reduction in external/internal diameters (51%/28%, respectively). VSMC ADAM17 deficiency was associated with lack of epidermal growth factor receptor activation, interleukin-6 induction, endoplasmic reticulum/oxidative stress, and matrix deposition in the abdominal aorta of treated mice. However, both VSMC ADAM17-deficient and control mice treated with AngII and ß-aminopropionitrile developed comparable levels of hypertension. Treatment of C57Bl/6 mice with an ADAM17 inhibitory antibody but not with control IgG also prevented AAA development. In conclusion, VSMC ADAM17 silencing or systemic ADAM17 inhibition seems to protect mice from AAA formation. The mechanism seems to involve suppression of epidermal growth factor receptor activation.
[Mh] Termos MeSH primário: Proteína ADAM17
Aminopropionitrilo/metabolismo
Angiotensina II/metabolismo
Aneurisma da Aorta Abdominal
Hipertensão
Músculo Liso Vascular
[Mh] Termos MeSH secundário: Proteína ADAM17/antagonistas & inibidores
Proteína ADAM17/metabolismo
Animais
Aorta Abdominal/metabolismo
Aorta Abdominal/patologia
Aneurisma da Aorta Abdominal/etiologia
Aneurisma da Aorta Abdominal/metabolismo
Aneurisma da Aorta Abdominal/patologia
Aneurisma da Aorta Abdominal/prevenção & controle
Hipertensão/etiologia
Hipertensão/metabolismo
Hipertensão/prevenção & controle
Camundongos
Camundongos Endogâmicos C57BL
Músculo Liso Vascular/metabolismo
Músculo Liso Vascular/patologia
Proteína-Lisina 6-Oxidase/metabolismo
Proteínas Modificadoras da Atividade de Receptores/metabolismo
Receptor do Fator de Crescimento Epidérmico/metabolismo
Transdução de Sinais/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptor Activity-Modifying Proteins); 11128-99-7 (Angiotensin II); 151-18-8 (Aminopropionitrile); EC 1.4.3.13 (Protein-Lysine 6-Oxidase); EC 2.7.10.1 (Receptor, Epidermal Growth Factor); EC 3.4.24.86 (ADAM17 Protein); EC 3.4.24.86 (Adam17 protein, mouse)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171111
[Lr] Data última revisão:
171111
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170927
[St] Status:MEDLINE
[do] DOI:10.1161/HYPERTENSIONAHA.117.09822


  6 / 1469 MEDLINE  
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[PMID]:28893955
[Au] Autor:Sharma N; Trinidad CV; Trembath AP; Markiewicz MA
[Ad] Endereço:Department of Microbiology, Molecular Genetics and Immunology, University of Kansas Medical Center, Kansas City, KS 66160.
[Ti] Título:NKG2D Signaling between Human NK Cells Enhances TACE-Mediated TNF-α Release.
[So] Source:J Immunol;199(8):2865-2872, 2017 Oct 15.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:NK group 2 member D (NKG2D) is a strong NK cell-activating receptor, with engagement by ligands triggering granule release and cytokine production. The function of NKG2D signaling in NK cells has largely been studied in the context of engagement of the receptor by ligands expressed on the surface of target cells. We report that upon activation with IL-12, IL-15, and IL-18 human NK cells express NKG2D ligands of the UL16 binding protein family on the cell surface. NKG2D-ligand interaction between cytokine-stimulated NK cells increases the activity of the metalloprotease TNF-α-converting enzyme. This enhanced TNF-α-converting enzyme activity significantly increases the release of TNF-α and UL16 binding protein from the surface of the NK cells. These results demonstrate that NKG2D signaling is critical for maximal TNF-α release by NK cells. Further, they demonstrate a role for NKG2D-ligand interaction via homotypic NK cell contact in NK cell effector function.
[Mh] Termos MeSH primário: Proteína ADAM17/metabolismo
Células Matadoras Naturais/imunologia
Subfamília K de Receptores Semelhantes a Lectina de Células NK/metabolismo
[Mh] Termos MeSH secundário: Proteína ADAM17/genética
Comunicação Celular
Células Cultivadas
Citotoxicidade Imunológica
Proteínas Ligadas por GPI/genética
Proteínas Ligadas por GPI/metabolismo
Seres Humanos
Imunidade Inata
Peptídeos e Proteínas de Sinalização Intercelular/genética
Peptídeos e Proteínas de Sinalização Intercelular/metabolismo
Interleucina-12/imunologia
Interleucina-15/imunologia
Interleucina-18/imunologia
Ativação Linfocitária
Transdução de Sinais
Fator de Necrose Tumoral alfa/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (GPI-Linked Proteins); 0 (Intercellular Signaling Peptides and Proteins); 0 (Interleukin-15); 0 (Interleukin-18); 0 (NK Cell Lectin-Like Receptor Subfamily K); 0 (Tumor Necrosis Factor-alpha); 0 (ULBP2 protein, human); 187348-17-0 (Interleukin-12); EC 3.4.24.86 (ADAM17 Protein); EC 3.4.24.86 (ADAM17 protein, human)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171111
[Lr] Data última revisão:
171111
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170913
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1700647


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[PMID]:28877252
[Au] Autor:Link MA; Lücke K; Schmid J; Schumacher V; Eden T; Rose-John S; Mittrücker HW
[Ad] Endereço:Institute of Immunology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
[Ti] Título:The role of ADAM17 in the T-cell response against bacterial pathogens.
[So] Source:PLoS One;12(9):e0184320, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:ADAM17 is a member of the A Disintegrin And Metalloproteinase family of proteases. It is ubiquitously expressed and causes the shedding of a broad spectrum of surface proteins such as adhesion molecules, cytokines and cytokine receptors. By controlled shedding of these proteins from leukocytes, ADAM17 is able to regulate immune responses. Several ADAM17 targets on T cells have been implicated in T-cell migration, differentiation and effector functions. However, the role of ADAM17 in T-cell responses is still unclear. To characterize the function of ADAM17 in T cells, we used Adam17fl/fl×CD4cre+ mice with a T-cell restricted inactivation of the Adam17 gene. Upon stimulation, ADAM17-deficient CD4+ and CD8+ T cells were impaired in shedding of CD62L, IL-6Rα, TNF-α, TNFRI and TNFRII. Surprisingly, we could not detect profound changes in the composition of major T-cell subsets in Adam17fl/fl×CD4cre+ mice. Following infection with Listeria monocytogenes, Adam17fl/fl×CD4cre+ mice mounted regular listeria-specific CD4+ TH1 and CD8+ T-cell responses and were able to control primary and secondary infections. In conclusion, our study indicates that ADAM17 is either not required in T cells under homoeostatic conditions and for control of listeria infection or can be effectively compensated by other mechanisms.
[Mh] Termos MeSH primário: Proteína ADAM17/metabolismo
Linfócitos T CD4-Positivos/imunologia
Linfócitos T CD8-Positivos/imunologia
Listeriose/imunologia
[Mh] Termos MeSH secundário: Animais
Adesão Celular
Diferenciação Celular
Membrana Celular/metabolismo
Feminino
Selectina L/metabolismo
Listeria monocytogenes
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Receptores de Interleucina-6/metabolismo
Receptores Tipo I de Fatores de Necrose Tumoral/metabolismo
Receptores Tipo II do Fator de Necrose Tumoral/metabolismo
Células Th1/imunologia
Fator de Necrose Tumoral alfa/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, Interleukin-6); 0 (Receptors, Tumor Necrosis Factor, Type I); 0 (Receptors, Tumor Necrosis Factor, Type II); 0 (Tumor Necrosis Factor-alpha); 126880-86-2 (L-Selectin); EC 3.4.24.86 (ADAM17 Protein); EC 3.4.24.86 (Adam17 protein, mouse)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171023
[Lr] Data última revisão:
171023
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170907
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0184320


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[PMID]:28815577
[Au] Autor:Luo WW; Shu HB
[Ad] Endereço:Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan, China.
[Ti] Título:Emerging roles of rhomboid-like pseudoproteases in inflammatory and innate immune responses.
[So] Source:FEBS Lett;591(20):3182-3189, 2017 Oct.
[Is] ISSN:1873-3468
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Rhomboid-like pseudoproteases are a conserved superfamily of proteins related to the rhomboid intramembrane serine proteases that lack key catalytic residues. iRhom2, a member of the rhomboid-like pseudoprotease superfamily, regulates the maturation and trafficking of ADAM17 and is associated with inflammatory arthritis. Recent studies demonstrate that iRhom2 is also involved in innate immunity by regulating the trafficking and stability of MITA (also called STING), which is a central adaptor in innate antiviral signalling pathways. Here, we summarize recent progress on the roles and mechanisms of iRhom2 and its homologues in innate immunity and also discuss the links between the physiological functions of iRhoms and immunological diseases.
[Mh] Termos MeSH primário: Proteína ADAM17/imunologia
Artrite Reumatoide/imunologia
Proteínas de Transporte/imunologia
Imunidade Inata
Proteínas de Membrana/imunologia
[Mh] Termos MeSH secundário: Proteína ADAM17/genética
Animais
Artrite Reumatoide/enzimologia
Artrite Reumatoide/genética
Artrite Reumatoide/patologia
Proteínas de Transporte/genética
Fator de Crescimento Epidérmico/genética
Fator de Crescimento Epidérmico/imunologia
Regulação da Expressão Gênica
Seres Humanos
Proteínas de Membrana/genética
Isoformas de Proteínas/genética
Isoformas de Proteínas/imunologia
Estabilidade Proteica
Transporte Proteico
Receptor do Fator de Crescimento Epidérmico/genética
Receptor do Fator de Crescimento Epidérmico/imunologia
Transdução de Sinais
Fator de Necrose Tumoral alfa/genética
Fator de Necrose Tumoral alfa/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Carrier Proteins); 0 (MPYS protein, human); 0 (Membrane Proteins); 0 (Protein Isoforms); 0 (RHBDF2 protein, human); 0 (Tumor Necrosis Factor-alpha); 62229-50-9 (Epidermal Growth Factor); EC 2.7.10.1 (EGFR protein, human); EC 2.7.10.1 (Receptor, Epidermal Growth Factor); EC 3.4.24.86 (ADAM17 Protein); EC 3.4.24.86 (ADAM17 protein, human)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170818
[St] Status:MEDLINE
[do] DOI:10.1002/1873-3468.12796


  9 / 1469 MEDLINE  
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[PMID]:28778937
[Au] Autor:Bredemeier M; Edimiris P; Mach P; Kubista M; Sjöback R; Rohlova E; Kolostova K; Hauch S; Aktas B; Tewes M; Kimmig R; Kasimir-Bauer S
[Ad] Endereço:Department of Gynecology and Obstetrics, University Hospital Essen, Essen, Germany.
[Ti] Título:Gene Expression Signatures in Circulating Tumor Cells Correlate with Response to Therapy in Metastatic Breast Cancer.
[So] Source:Clin Chem;63(10):1585-1593, 2017 Oct.
[Is] ISSN:1530-8561
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Circulating tumor cells (CTCs) are thought to be an ideal surrogate marker to monitor disease progression in metastatic breast cancer (MBC). We investigated the prediction of treatment response in CTCs of MBC patients on the basis of the expression of 46 genes. METHODS: From 45 MBC patients and 20 healthy donors (HD), 2 × 5 mL of blood was collected at the time of disease progression (TP0) and at 2 consecutive clinical staging time points (TP1 and TP2) to proceed with the AdnaTest (QIAGEN). Patients were grouped into (a) responder (R) and non-responder (NR) at TP1 and (b) overall responder (OR) and overall non-responder (ONR) at TP2. A 46-gene PCR assay was used for preamplification and high-throughput gene expression profiling. Data were analyzed by use of GenEx (MultiD) and SAS. RESULTS: The CTC positivity was defined by the four-gene signature ( , , , positivity). Fourteen genes were identified as significantly differentially expressed between CTC+ and CTC- patients ( , , , , , , , , , , , , , and ). was highly expressed in CTC+ patients and in the NR at TP1. A significant differential expression of 4 genes ( , , , and ) was observed between OR and ONR when stratifying the samples into CTC+ or CTC-. CONCLUSIONS: could be a key marker in distinguishing R from NR, and was powerful in identifying CTCs.
[Mh] Termos MeSH primário: Neoplasias da Mama/diagnóstico
Neoplasias da Mama/terapia
Mama/patologia
Células Neoplásicas Circulantes/patologia
Transcriptoma
[Mh] Termos MeSH secundário: Proteína ADAM17/genética
Biomarcadores Tumorais/genética
Neoplasias da Mama/sangue
Neoplasias da Mama/genética
Feminino
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Células Neoplásicas Circulantes/metabolismo
Prognóstico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); EC 3.4.24.86 (ADAM17 Protein); EC 3.4.24.86 (ADAM17 protein, human)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171013
[Lr] Data última revisão:
171013
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170806
[St] Status:MEDLINE
[do] DOI:10.1373/clinchem.2016.269605


  10 / 1469 MEDLINE  
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[PMID]:28711352
[Au] Autor:Tong L; Kim SH; Chen L; Kosinski A; Shankar BB; Girijavallabhan V; Yang DY; Yu W; Zhou G; Shih NY; Chen S; Hu M; Lundell D; Niu X; Umland S; Kozlowski JA
[Ad] Endereço:Department of Medicinal Chemistry, Merck & Co., Inc., 2000 Galloping Hill Road, Kenilworth, NJ 07033, USA. Electronic address: ling.tong@merck.com.
[Ti] Título:Development of a prodrug of hydantoin based TACE inhibitor.
[So] Source:Bioorg Med Chem Lett;27(16):3704-3708, 2017 08 15.
[Is] ISSN:1464-3405
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Our research on hydantoin based TNF-α converting enzyme (TACE) inhibitors led to fused bi-heteroaryl hydantoin series that demonstrate sub-nanomolar potency (Ki) as well as excellent activity in human whole blood (hWBA). However, lead compound 2 posed some formulation challenges which prevented it for further development. A prodrug approach was investigated to address this issue. The pivalate prodrug 3 can be formulated as stable neutral form and demonstrated improved DMPK properties when compared with parent compound.
[Mh] Termos MeSH primário: Proteína ADAM17/antagonistas & inibidores
Hidantoínas/química
Hidantoínas/síntese química
Hidantoínas/farmacologia
Ácidos Pentanoicos/química
Pró-Fármacos/síntese química
Pró-Fármacos/farmacologia
[Mh] Termos MeSH secundário: Proteína ADAM17/metabolismo
Administração Oral
Animais
Área Sob a Curva
Cães
Ativação Enzimática/efeitos dos fármacos
Meia-Vida
Haplorrinos
Seres Humanos
Hidantoínas/administração & dosagem
Hidantoínas/farmacocinética
Ácidos Pentanoicos/administração & dosagem
Ácidos Pentanoicos/farmacocinética
Pró-Fármacos/administração & dosagem
Pró-Fármacos/farmacocinética
Curva ROC
Ratos
Relação Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Hydantoins); 0 (Pentanoic Acids); 0 (Prodrugs); 813RE8BX41 (pivalic acid); EC 3.4.24.86 (ADAM17 Protein)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171125
[Lr] Data última revisão:
171125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170717
[St] Status:MEDLINE



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