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Pesquisa : D08.811.277.656.350.100.160 [Categoria DeCS]
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  1 / 2142 MEDLINE  
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[PMID]:28387421
[Au] Autor:Gerbaud P; Guibourdenche J; Jarray R; Conti M; Palmic P; Leclerc-Mercier S; Bruneau J; Hermine O; Lepelletier Y; Raynaud F
[Ad] Endereço:INSERM, Université Paris Descartes, Paris, France.
[Ti] Título:APN/CD13 is over-expressed by Psoriatic fibroblasts and is modulated by CGRP and IL-4 but not by retinoic acid treatment.
[So] Source:J Cell Physiol;233(2):958-967, 2018 Feb.
[Is] ISSN:1097-4652
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Psoriasis vulgaris is a common skin inflammatory disease characterized by recurrent flare episodes associated with scaly well-demarcated skin plaques. Skin biopsies from psoriatic patients with high PASI score (22.67 ± 8.67) and from HD were used to study APN/CD13. APN/CD13 is over-expressed in LP and nLP compare to HD skins and fibroblasts. This over-expression is positively correlated with specific enzymatic activity enhancement. However, discrepancies between APN/CD13 expression in LP and nLP prompt us to focus our study on APN/CD13 modulation. Calcitonin Gene Related Peptide (CGRP), a neuropeptide, positively modulated expression and activity of APN/CD13. CGRP consistently induced IL4 secretion, which is also involved in the increase of APN/CD13 expression and activity, which is significantly reversed using IL-4 blocking antibody. Surprisingly, retinoic acid altered the APN/CD13 enzymatic activity only in nLP fibroblasts without modification of APN/CD13 expression. APN/CD13 is over-expressed on psoriatic fibroblasts and exerted high level of activity compare to HD fibroblasts. Taken together, several factors such as CGRP and IL-4 acted on positive regulation of APN/CD13 expression and activity. This study highlighted the interest of APN/CD13 as a new potential target, which should be investigated in psoriasis.
[Mh] Termos MeSH primário: Antígenos CD13/metabolismo
Peptídeo Relacionado com Gene de Calcitonina/farmacologia
Fibroblastos/efeitos dos fármacos
Interleucina-4/farmacologia
Psoríase/enzimologia
Pele/efeitos dos fármacos
Tretinoína/farmacologia
[Mh] Termos MeSH secundário: Adulto
Idoso
Antígenos CD13/genética
Estudos de Casos e Controles
Células Cultivadas
Feminino
Fibroblastos/enzimologia
Fibroblastos/patologia
Seres Humanos
Masculino
Meia-Idade
Psoríase/genética
Psoríase/patologia
Pele/enzimologia
Pele/patologia
Fatores de Tempo
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (IL4 protein, human); 207137-56-2 (Interleukin-4); 5688UTC01R (Tretinoin); 83652-28-2 (Calcitonin Gene-Related Peptide); EC 3.4.11.2 (CD13 Antigens)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171128
[Lr] Data última revisão:
171128
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170408
[St] Status:MEDLINE
[do] DOI:10.1002/jcp.25941


  2 / 2142 MEDLINE  
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[PMID]:28915252
[Au] Autor:Jando J; Camargo SMR; Herzog B; Verrey F
[Ad] Endereço:Institute of Physiology, Zurich Center of Integrative Human Physiology and NCCR Kidney.CH, University of Zurich, Zurich, Switzerland.
[Ti] Título:Expression and regulation of the neutral amino acid transporter B0AT1 in rat small intestine.
[So] Source:PLoS One;12(9):e0184845, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Absorption of neutral amino acids across the luminal membrane of intestinal enterocytes is mediated by the broad neutral amino acid transporter B0AT1 (SLC6A19). Its intestinal expression depends on co-expression of the membrane-anchored peptidase angiotensin converting enzyme 2 (ACE2) and is additionally enhanced by aminopeptidase N (CD13). We investigated in this study the expression of B0AT1 and its auxiliary peptidases as well as its transport function along the rat small intestine. Additionally, we tested its possible short- and long-term regulation by dietary proteins and amino acids. We showed by immunofluorescence that B0AT1, ACE2 and CD13 co-localize on the luminal membrane of small intestinal villi and by Western blotting that their protein expression increases in distal direction. Furthermore, we observed an elevated transport activity of the neutral amino acid L-isoleucine during the nocturnal active phase compared to the inactive one. Gastric emptying was delayed by intragastric application of an amino acid cocktail but we observed no acute dietary regulation of B0AT1 protein expression and L-isoleucine transport. Investigation of the chronic dietary regulation of B0AT1, ACE2 and CD13 by different diets revealed an increased B0AT1 protein expression under amino acid-supplemented diet in the proximal section but not in the distal one and for ACE2 protein expression a reverse localization of the effect. Dietary regulation for CD13 protein expression was not as distinct as for the two other proteins. Ring uptake experiments showed a tendency for increased L-isoleucine uptake under amino acid-supplemented diet and in vivo L-isoleucine absorption was more efficient under high protein and amino acid-supplemented diet. Additionally, plasma levels of branched-chain amino acids were elevated under high protein and amino acid diet. Taken together, our experiments did not reveal an acute amino acid-induced regulation of B0AT1 but revealed a chronic dietary adaptation mainly restricted to the proximal segment of the small intestine.
[Mh] Termos MeSH primário: Sistemas de Transporte de Aminoácidos Neutros/biossíntese
Antígenos CD13/metabolismo
Regulação da Expressão Gênica/efeitos dos fármacos
Intestino Delgado/metabolismo
Isoleucina/farmacologia
Peptidil Dipeptidase A/metabolismo
[Mh] Termos MeSH secundário: Animais
Suplementos Nutricionais
Masculino
Ratos
Ratos Wistar
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Amino Acid Transport Systems, Neutral); 0 (SLC6A19 protein, rat); 04Y7590D77 (Isoleucine); EC 3.4.11.2 (CD13 Antigens); EC 3.4.15.1 (Peptidyl-Dipeptidase A); EC 3.4.17.- (angiotensin converting enzyme 2)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170916
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0184845


  3 / 2142 MEDLINE  
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[PMID]:28859152
[Au] Autor:Khatun A; Rahman MS; Ryu DY; Kwon WS; Pang MG
[Ad] Endereço:Department of Animal Science and Technology, Chung-Ang University, Anseong, Republic of Korea.
[Ti] Título:Elevated aminopeptidase N affects sperm motility and early embryo development.
[So] Source:PLoS One;12(8):e0184294, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Aminopeptidase N (APN) is a naturally occurring ectopeptidase present in mammalian semen. Previous studies have demonstrated that APN adversely affects male fertility through the alteration of sperm motility. This enzyme constitutes 0.5 to 1% of the seminal plasma proteins, which can be transferred from the prostasomes to sperms by a fusion process. In the present study, we investigated the molecular mechanism of action of APN and its role in regulating sperm functions and male fertility. In this in vitro study, epididymal mouse spermatozoa were incubated in a capacitating media (pH 7) containing 20 ng/mL of recombinant mouse APN for 90 min. Our results demonstrated that the supplementation of recombinant APN in sperm culture medium significantly increased APN activity, and subsequently altered motility, hyperactivated motility, rapid and medium swimming speeds, viability, and the acrosome reaction of mouse spermatozoa. These effects were potentially caused by increased toxicity in the spermatozoa. Further, altered APN activity in sperm culture medium affected early embryonic development. Interestingly, the effect of elevated APN activity in sperm culture medium was independent of protein tyrosine phosphorylation and protein kinase A activity. On the basis of these results, we concluded that APN plays a significant role in the regulation of several sperm functions and early embryonic development. In addition, increased APN activity could potentially lead to several adverse consequences related to male fertility.
[Mh] Termos MeSH primário: Antígenos CD13/genética
Desenvolvimento Embrionário/genética
Espermatozoides/enzimologia
[Mh] Termos MeSH secundário: Acrossomo/enzimologia
Animais
Antígenos CD13/química
Antígenos CD13/metabolismo
Infertilidade Masculina/enzimologia
Infertilidade Masculina/genética
Masculino
Camundongos
Sêmen/enzimologia
Motilidade Espermática/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
EC 3.4.11.2 (CD13 Antigens)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170901
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0184294


  4 / 2142 MEDLINE  
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[PMID]:28739875
[Au] Autor:Resheq YJ; Menzner AK; Bosch J; Tickle J; Li KK; Wilhelm A; Hepburn E; Murihead G; Ward ST; Curbishley SM; Zimmermann HW; Bruns T; Gilbert DF; Tripal P; Mackensen A; Adams DH; Weston CJ
[Ad] Endereço:Institute of Immunology and Immunotherapy, Centre for Liver Research and National Institute for Health Research Birmingham Liver Biomedical Research Centre, College of Medicine and Dentistry, University of Birmingham, Edgbaston, Birmingham B15 2TT, United Kingdom; yazid.resheq@uk-erlangen.de.
[Ti] Título:Impaired Transmigration of Myeloid-Derived Suppressor Cells across Human Sinusoidal Endothelium Is Associated with Decreased Expression of CD13.
[So] Source:J Immunol;199(5):1672-1681, 2017 Sep 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Human monocytic myeloid-derived suppressor cells (MO-MDSCs) within the hepatic compartment suppress inflammation and impair immune surveillance in liver cancer. It is currently not known whether recruitment of MO-MDSCs from blood via hepatic sinusoidal endothelium (HSEC) contributes to their enrichment within the hepatic compartment. We compared the transmigratory potential of MO-MDSCs and monocytes after adhesion to hepatic endothelial monolayers in flow-based assays that mimic in vivo shear stress in the sinusoids. Despite comparable binding to HSEC monolayers, proportionally fewer MO-MDSCs underwent transendothelial migration, indicating that the final steps of extravasation, where actin polymerization plays an important role, are impaired in MO-MDSCs. In this article, we found reduced levels of CD13 on MO-MDSCs, which has recently been reported to control cell motility in monocytes, alongside reduced VLA-4 expression, an integrin predominantly involved in adherence to the apical side of the endothelium. CD13 and VLA-4 blocking and activating Abs were used in flow-based adhesion assays, live-cell imaging of motility, and actin polymerization studies to confirm a role for CD13 in impaired MO-MDSC transmigration. These findings indicate that CD13 significantly contributes to tissue infiltration by MO-MDSCs and monocytes, thereby contributing to the pathogenesis of hepatic inflammation.
[Mh] Termos MeSH primário: Antígenos CD13/metabolismo
Epitélio Posterior/fisiologia
Hemocromatose/imunologia
Hepatite/imunologia
Fígado/imunologia
Células Supressoras Mieloides/imunologia
Migração Transendotelial e Transepitelial
[Mh] Termos MeSH secundário: Actinas/metabolismo
Anticorpos Bloqueadores/farmacologia
Antígenos CD13/genética
Antígenos CD13/imunologia
Adesão Celular
Movimento Celular
Células Cultivadas
Regulação para Baixo
Seres Humanos
Integrina alfa4beta1/genética
Integrina alfa4beta1/imunologia
Integrina alfa4beta1/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Actins); 0 (Antibodies, Blocking); 0 (Integrin alpha4beta1); EC 3.4.11.2 (CD13 Antigens)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170726
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1600466


  5 / 2142 MEDLINE  
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[PMID]:28728898
[Au] Autor:González-Bacerio J; Maluf SEC; Méndez Y; Pascual I; Florent I; Melo PMS; Budu A; Ferreira JC; Moreno E; Carmona AK; Rivera DG; Alonso Del Rivero M; Gazarini ML
[Ad] Endereço:Centro de Estudio de Proteínas, Facultad de Biología, Universidad de La Habana, Calle 25 #455 entre I y J, 10400, Vedado, La Habana, Cuba. Electronic address: jogoba@fbio.uh.cu.
[Ti] Título:KBE009: An antimalarial bestatin-like inhibitor of the Plasmodium falciparum M1 aminopeptidase discovered in an Ugi multicomponent reaction-derived peptidomimetic library.
[So] Source:Bioorg Med Chem;25(17):4628-4636, 2017 Sep 01.
[Is] ISSN:1464-3391
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Malaria is a global human parasitic disease mainly caused by the protozoon Plasmodium falciparum. Increased parasite resistance to current drugs determines the relevance of finding new treatments against new targets. A novel target is the M1 alanyl-aminopeptidase from P. falciparum (PfA-M1), which is essential for parasite development in human erythrocytes and is inhibited by the pseudo-peptide bestatin. In this work, we used a combinatorial multicomponent approach to produce a library of peptidomimetics and screened it for the inhibition of recombinant PfA-M1 (rPfA-M1) and the in vitro growth of P. falciparum erythrocytic stages (3D7 and FcB1 strains). Dose-response studies with selected compounds allowed identifying the bestatin-based peptidomimetic KBE009 as a submicromolar rPfA-M1 inhibitor (K =0.4µM) and an in vitro antimalarial compound as potent as bestatin (IC =18µM; without promoting erythrocyte lysis). At therapeutic-relevant concentrations, KBE009 is selective for rPfA-M1 over porcine APN (a model of these enzymes from mammals), and is not cytotoxic against HUVEC cells. Docking simulations indicate that this compound binds PfA-M1 without Zn coordination, establishing mainly hydrophobic interactions and showing a remarkable shape complementarity with the active site of the enzyme. Moreover, KBE009 inhibits the M1-type aminopeptidase activity (Ala-7-amido-4-methylcoumarin substrate) in isolated live parasites with a potency similar to that of the antimalarial activity (IC =82µM), strongly suggesting that the antimalarial effect is directly related to the inhibition of the endogenous PfA-M1. These results support the value of this multicomponent strategy to identify PfA-M1 inhibitors, and make KBE009 a promising hit for drug development against malaria.
[Mh] Termos MeSH primário: Antimaláricos/química
Antígenos CD13/antagonistas & inibidores
Dipeptídeos/química
Plasmodium falciparum/enzimologia
Proteínas de Protozoários/antagonistas & inibidores
[Mh] Termos MeSH secundário: Antimaláricos/síntese química
Antimaláricos/farmacologia
Sítios de Ligação
Antígenos CD13/genética
Antígenos CD13/metabolismo
Domínio Catalítico
Sobrevivência Celular/efeitos dos fármacos
Dipeptídeos/síntese química
Dipeptídeos/farmacologia
Eritrócitos/citologia
Eritrócitos/efeitos dos fármacos
Eritrócitos/parasitologia
Células Endoteliais da Veia Umbilical Humana
Seres Humanos
Leucina/análogos & derivados
Leucina/química
Leucina/farmacologia
Simulação de Acoplamento Molecular
Peptidomiméticos
Plasmodium falciparum/efeitos dos fármacos
Proteínas de Protozoários/metabolismo
Proteínas Recombinantes/biossíntese
Proteínas Recombinantes/química
Proteínas Recombinantes/isolamento & purificação
Relação Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antimalarials); 0 (Dipeptides); 0 (KBE009); 0 (Peptidomimetics); 0 (Protozoan Proteins); 0 (Recombinant Proteins); EC 3.4.11.2 (CD13 Antigens); GMW67QNF9C (Leucine); I0J33N5627 (ubenimex)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170722
[St] Status:MEDLINE


  6 / 2142 MEDLINE  
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[PMID]:28669053
[Au] Autor:Grieger E; Gresch G; Niesen J; Woitok M; Barth S; Fischer R; Fendel R; Stein C
[Ad] Endereço:Department of Immunotherapy, Fraunhofer Institute for Molecular Biology and Applied Ecology IME, Forckenbeckstr. 6, 52074, Aachen, Germany. elena.grieger@ime.fraunhofer.de.
[Ti] Título:Efficient targeting of CD13 on cancer cells by the immunotoxin scFv13-ETA' and the bispecific scFv [13xds16].
[So] Source:J Cancer Res Clin Oncol;143(11):2159-2170, 2017 Nov.
[Is] ISSN:1432-1335
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:PURPOSE: Treatment of cancer using standard chemotherapy still offers a poor prognosis combined with severe side effects. Novel antibody-based therapies have been shown to overcome low efficiency and lack of selectivity by targeting cancer-associated antigens, such as aminopeptidase CD13. METHODS: We isolated a high-affinity CD13-specific single-chain fragment variable (scFv13) from a phage display library of V-genes from mice immunized with soluble antigen. An immunotoxin comprising the scFv13 and a truncated version of the exotoxin A of Pseudomonas aeruginosa (ETA', scFv13-ETA') and a bispecific scFv targeting CD13 and CD16 simultaneously (bsscFv[13xds16]) was generated and investigated for their therapeutic potential. RESULTS: Both fusion proteins bound specifically to target cells with high affinity. Furthermore, scFv13-ETA' inhibited the proliferation of human cancer cell lines efficiently at low concentrations (IC values of 408 pM-7 nM) and induced apoptosis (40-85% of target cells). The bsscFv triggered dose-dependent antibody-dependent cell-mediated cytotoxicity, resulting in the lysis of up to 23.9% A2058 cells, 18.0% MDA-MB-468 cells and 19.1% HL-60 cells. CONCLUSION: The provided data demonstrate potent therapeutic activity of the scFv13-ETA' and the bsscFv[13xds16]. The CD13-specific scFv is therefore suitable for the direct and specific delivery of both cytotoxic agents and effector cells to cancer-derived cells, making it ideal for further therapeutic evaluation.
[Mh] Termos MeSH primário: ADP Ribose Transferases/imunologia
Anticorpos Biespecíficos/farmacologia
Apoptose/efeitos dos fármacos
Toxinas Bacterianas/imunologia
Antígenos CD13/antagonistas & inibidores
Proliferação Celular/efeitos dos fármacos
Exotoxinas/imunologia
Imunotoxinas/farmacologia
Neoplasias/tratamento farmacológico
Anticorpos de Cadeia Única/imunologia
Fatores de Virulência/imunologia
[Mh] Termos MeSH secundário: Antígenos CD13/imunologia
Seres Humanos
Neoplasias/imunologia
Neoplasias/patologia
Proteínas Recombinantes/farmacologia
Células Tumorais Cultivadas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Bispecific); 0 (Bacterial Toxins); 0 (Exotoxins); 0 (Immunotoxins); 0 (Recombinant Proteins); 0 (Single-Chain Antibodies); 0 (Virulence Factors); EC 2.4.2.- (ADP Ribose Transferases); EC 2.4.2.31 (toxA protein, Pseudomonas aeruginosa); EC 3.4.11.2 (CD13 Antigens)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170703
[St] Status:MEDLINE
[do] DOI:10.1007/s00432-017-2468-5


  7 / 2142 MEDLINE  
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[PMID]:28475015
[Au] Autor:Wang G; Yuan N; Huang S; Feng L; Han R; Zhang Y; Ren J; Meng M; Zhao X
[Ad] Endereço:1 Department of Medical Oncology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, People's Republic of China.
[Ti] Título:The CNGRCLLII(KLAKLAK)2 peptide shows cytotoxicity against HUVECs by inducing apoptosis: An in vitro and in vivo study.
[So] Source:Tumour Biol;39(5):1010428317701649, 2017 May.
[Is] ISSN:1423-0380
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Fibrinogen Asn-Gly-Arg motif can specifically recognize and bind to Aminopeptidase N (CD13) on vascular endothelial cells in newly formed tumor vessels. Adipose-derived stem cells can serve as ideal vectors for gene therapy because of their ability of migrating to tumor tissues. First, this study was aimed to design a new peptide (CNGRCLLII(KLAKLAK)2) named CNAK which contains cyclic Asn-Gly-Arg motif and test its biological activity against human umbilical vein endothelial cells. Second, we aimed to construct stably transfected adipose-derived stem cells which express the CNAK peptide and investigate their anti-angiogenic activity in vivo. Adipose-derived stem cells were employed to localize CNAK on vascular endothelial cells in tumors based on their homing property. First of all, the new peptide was synthesized, which effectively entered into CD13+ human umbilical vein endothelial cells and showed cytotoxicity against human umbilical vein endothelial cells. The peptide induced apoptosis of human umbilical vein endothelial cells in a time- and dose-dependent manner, inhibited the expression of Bcl-2, and promoted the expression of Caspase-3 in human umbilical vein endothelial cells. Furthermore, the migration and tube formation of human umbilical vein endothelial cells were inhibited by CNAK. Primary adipose-derived stem cells were then isolated and identified. Stably transfected adipose-derived stem cells which express CNAK peptide (CNAK-ASCs) were successfully established, and the migration of CNAK-ASCs was assessed. In vivo, CNAK-ASCs were found to inhibit the growth and angiogenesis of breast cancer xenografts. This effect may be through inhibiting the secretion of matrix metalloproteinase-2 and membrane type 1-matrix metalloproteinase in vivo. It was also found that CNAK-ASCs reduced the quantity of breast cancer stem cells in tumor tissues. Our data suggested that the new peptide CNAK containing Asn-Gly-Arg motif had anti-angiogenic activity in vitro and in vivo.
[Mh] Termos MeSH primário: Apoptose/efeitos dos fármacos
Neoplasias da Mama/terapia
Terapia Genética
Oligopeptídeos/administração & dosagem
Peptídeos/administração & dosagem
[Mh] Termos MeSH secundário: Tecido Adiposo/citologia
Animais
Apoptose/genética
Neoplasias da Mama/genética
Neoplasias da Mama/patologia
Antígenos CD13/genética
Linhagem Celular Tumoral
Feminino
Fibrinogênio/química
Fibrinogênio/genética
Fibrinogênio/uso terapêutico
Células Endoteliais da Veia Umbilical Humana/efeitos dos fármacos
Células Endoteliais da Veia Umbilical Humana/metabolismo
Seres Humanos
Camundongos
Oligopeptídeos/química
Oligopeptídeos/genética
Peptídeos/química
Peptídeos/genética
Células-Tronco/química
Células-Tronco/citologia
Transfecção
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (NGR peptide); 0 (Oligopeptides); 0 (Peptides); 9001-32-5 (Fibrinogen); EC 3.4.11.2 (CD13 Antigens)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170506
[St] Status:MEDLINE
[do] DOI:10.1177/1010428317701649


  8 / 2142 MEDLINE  
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[PMID]:28389152
[Au] Autor:Cellier M; James AL; Orenga S; Perry JD; Rasul AK; Stanforth SP
[Ad] Endereço:Research & Development Microbiology, bioMérieux SA, 3 route de Port Michaud, 38 390 La-Balme-les-Grottes, France.
[Ti] Título:Detection of l-alanylaminopeptidase activity in microorganisms using chromogenic self-immolative enzyme substrates.
[So] Source:Bioorg Med Chem Lett;27(10):2102-2106, 2017 05 15.
[Is] ISSN:1464-3405
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Three potential chromogenic enzymatic probes, each possessing a self-immolative spacer unit, were synthesised for the purpose of detecting l-alanylaminopeptidase activity in microorganisms. An Alizarin-based probe was the most effective, allowing several species to generate strongly coloured colonies in the presence of metal ions.
[Mh] Termos MeSH primário: Antraquinonas/química
Antígenos CD13/metabolismo
Compostos Cromogênicos/química
[Mh] Termos MeSH secundário: Antraquinonas/metabolismo
Compostos Cromogênicos/metabolismo
Bactérias Gram-Negativas/enzimologia
Bactérias Gram-Negativas/crescimento & desenvolvimento
Bactérias Gram-Positivas/enzimologia
Bactérias Gram-Positivas/crescimento & desenvolvimento
Metais/química
Especificidade por Substrato
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Anthraquinones); 0 (Chromogenic Compounds); 0 (Metals); 60MEW57T9G (alizarin); EC 3.4.11.2 (CD13 Antigens)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171124
[Lr] Data última revisão:
171124
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170409
[St] Status:MEDLINE


  9 / 2142 MEDLINE  
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[PMID]:28383782
[Au] Autor:Tsai SC; Lin CC; Shih TC; Tseng RJ; Yu MC; Lin YJ; Hsieh SY
[Ad] Endereço:Department of Gastroenterology and Hepatology, Chang Gung Memorial Hospital, Linkou, Taoyuan, Taiwan.
[Ti] Título:The miR-200b-ZEB1 circuit regulates diverse stemness of human hepatocellular carcinoma.
[So] Source:Mol Carcinog;56(9):2035-2047, 2017 Sep.
[Is] ISSN:1098-2744
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Accumulating evidence suggests that human hepatocellular carcinoma (HCC) can be derived from cancer stem cells (CSCs), which contribute to tumor initiation, metastasis, chemoresistance, and recurrence. A great variety of HCC CSCs resulting in diverse clinical manifestations have been reported. However, how CSC diversity is regulated and generated remains unclear. Here we report that the miR-200b-ZEB1 circuit is closely involved with the induction and maintenance of a diverse group of CSCs. We found that miR-200b downregulation occurred in early HCC and associated with poor prognosis. The downregulation was attributable to genome deletion and promoter methylation of the miR-200a/b/429 gene. Ectopic expression of miR-200b or silencing of ZEB1 led to a decrease in CD13 and CD24 HCC CSCs and an increase in EpCAM HCC CSCs. Mechanistically, miR-200b directly suppressed BMI1 and ZEB1 expressions. ZEB1 recognized promoters of CD13, CD24, and EpCAM genes resulting in CD13 and CD24 upregulation and EpCAM downregulation. Neither miR-200b nor ZEB1 had obvious effects on CD133 or CD90 expression. Silencing CD13 or CD24 expression suppressed tumorigenicity of HCC cells. Ectopic expression of CD24 reversed the suppression of tumorigenicity by ectopic expression of miR-200b. Clinically, miR-200b downregulation was coupled with ZEB1 upregulation in approximately two-thirds of HCC patients. ZEB1 expression was positively correlated with CD13 and CD24 expressions in HCCs, while miR-200b expression was positively correlated with EpCAM. Our findings suggest that the miR-200b-ZEB1 circuit is a master regulator of diverse stemness of HCC, which differentiates HCCs into those containing CD13 /CD24 CSCs from those containing EpCAM CSCs.
[Mh] Termos MeSH primário: Carcinoma Hepatocelular/metabolismo
MicroRNAs/metabolismo
Células-Tronco Neoplásicas/metabolismo
Homeobox 1 de Ligação a E-box em Dedo de Zinco/metabolismo
[Mh] Termos MeSH secundário: Antígenos de Diferenciação/metabolismo
Antígenos CD13/metabolismo
Antígeno CD24/metabolismo
Carcinoma Hepatocelular/genética
Diferenciação Celular
Linhagem Celular Tumoral
Transformação Celular Neoplásica
Metilação de DNA
DNA de Neoplasias/metabolismo
Regulação para Baixo
Deleção de Genes
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Células-Tronco Neoplásicas/microbiologia
Regiões Promotoras Genéticas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, Differentiation); 0 (CD24 Antigen); 0 (DNA, Neoplasm); 0 (MIRN200 microRNA, human); 0 (MicroRNAs); 0 (ZEB1 protein, human); 0 (Zinc Finger E-box-Binding Homeobox 1); EC 3.4.11.2 (CD13 Antigens)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170407
[St] Status:MEDLINE
[do] DOI:10.1002/mc.22657


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[PMID]:28038565
[Au] Autor:Wolke C; Teumer A; Endlich K; Endlich N; Rettig R; Stracke S; Fiene B; Aymanns S; Felix SB; Hannemann A; Lendeckel U
[Ad] Endereço:1 Institute of Medical Biochemistry and Molecular Biology, University Medicine Greifswald, Greifswald D-17475, Germany.
[Ti] Título:Serum protease activity in chronic kidney disease patients: The GANI_MED renal cohort.
[So] Source:Exp Biol Med (Maywood);242(5):554-563, 2017 Mar.
[Is] ISSN:1535-3699
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Serum or plasma proteases have been associated with various diseases including cancer, inflammation, or reno-cardiovascular diseases. We aimed to investigate whether the enzymatic activities of serum proteases are associated with the estimated glomerular filtration rate (eGFR) in patients with different stages of chronic kidney disease (CKD). Our study population comprised 268 participants of the "Greifswald Approach to Individualized Medicine" (GANI_MED) cohort. Enzymatic activity of aminopeptidase A, aminopeptidase B, alanyl (membrane) aminopeptidase, insulin-regulated aminopeptidase, puromycin-sensitive aminopeptidase, leucine aminopeptidase 3, prolyl-endopeptidase (PEP), dipeptidyl peptidase 4 (DPP4), angiotensin I-converting enzyme, and angiotensin I-converting enzyme 2 (ACE2) proteases was measured in serum. Linear regression of the respective protease was performed on kidney function adjusted for age and sex. Kidney function was modeled either by the continuous Modification of Diet in Renal Disease (MDRD)-based eGFR or dichotomized by eGFR < 15 mL/min/1.73 m or <45 mL/min/1.73 m , respectively. Results with a false discovery rate below 0.05 were deemed statistically significant. Among the 10 proteases investigated, only the activities of ACE2 and DPP4 were correlated with eGFR. Patients with lowest eGFR exhibited highest DPP4 and ACE2 activities. DPP4 and PEP were correlated with age, but all other serum protease activities showed no associations with age or sex. Our data indicate that ACE2 and DPP4 enzymatic activity are associated with the eGFR in patients with CKD. This finding distinguishes ACE2 and DPP4 from other serum peptidases analyzed and clearly indicates that further analyses are warranted to identify the precise role of these serum ectopeptidases in the pathogenesis of CKD and to fully elucidate underlying molecular mechanisms. Impact statement • Renal and cardiac diseases are very common and often occur concomitantly, resulting in increased morbidity and mortality. Understanding of molecular mechanisms linking both diseases is limited, available fragmentary data point to a role of the renin-angiotensin system (RAS) and, in particular, Ras-related peptidases. • Here, a comprehensive analysis of serum peptidase activities in patients with different stages of chronic kidney disease (CKD) is presented, with special emphasis given to RAS peptidases • The serum activities of the peptidases angiotensin I-converting enzyme 2 and dipeptidyl peptidase 4 were identified as closely associated with kidney function, specifically with the estimated glomerular filtration rate. The findings are discussed in the context of available data suggesting protective roles for both enzymes in reno-cardiac diseases. • The data add to our understanding of pathomechanisms underlying development and progression of CKD and indicate that both enzymes might represent potential pharmacological targets for the preservation of renal function.
[Mh] Termos MeSH primário: Peptídeo Hidrolases/sangue
Insuficiência Renal Crônica/enzimologia
[Mh] Termos MeSH secundário: Idoso
Aminopeptidases/sangue
Aminopeptidases/metabolismo
Antígenos CD13/sangue
Antígenos CD13/metabolismo
Creatinina/sangue
Cistinil Aminopeptidase/sangue
Cistinil Aminopeptidase/metabolismo
Dipeptidil Peptidase 4/sangue
Dipeptidil Peptidase 4/metabolismo
Feminino
Taxa de Filtração Glomerular
Glutamil Aminopeptidase/sangue
Glutamil Aminopeptidase/metabolismo
Seres Humanos
Leucil Aminopeptidase/sangue
Leucil Aminopeptidase/metabolismo
Masculino
Meia-Idade
Peptídeo Hidrolases/metabolismo
Peptidil Dipeptidase A/sangue
Peptidil Dipeptidase A/metabolismo
Insuficiência Renal Crônica/sangue
Serina Endopeptidases/sangue
Serina Endopeptidases/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
AYI8EX34EU (Creatinine); EC 3.4.- (Peptide Hydrolases); EC 3.4.11.- (Aminopeptidases); EC 3.4.11.1 (LAP3 protein, human); EC 3.4.11.1 (Leucyl Aminopeptidase); EC 3.4.11.14 (enkephalin degrading enzyme); EC 3.4.11.2 (CD13 Antigens); EC 3.4.11.3 (Cystinyl Aminopeptidase); EC 3.4.11.3 (leucyl-cystinyl aminopeptidase); EC 3.4.11.6 (aminopeptidase B); EC 3.4.11.7 (Glutamyl Aminopeptidase); EC 3.4.14.5 (DPP4 protein, human); EC 3.4.14.5 (Dipeptidyl Peptidase 4); EC 3.4.15.1 (Peptidyl-Dipeptidase A); EC 3.4.17.- (angiotensin converting enzyme 2); EC 3.4.21.- (Serine Endopeptidases); EC 3.4.21.26 (prolyl oligopeptidase)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170101
[St] Status:MEDLINE
[do] DOI:10.1177/1535370216684040



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