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  1 / 22342 MEDLINE  
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[PMID]:29391274
[Au] Autor:Chen YL; Li TJ; Hao Y; Wu BG; Li H; Geng N; Sun ZQ; Zheng LQ; Sun YX
[Ad] Endereço:Department of Cardiology, The First Hospital of China Medical University, Shenyang, Liaoning, PR China.
[Ti] Título:Association of rs2271037 and rs3749585 polymorphisms in CORIN with susceptibility to hypertension in a Chinese Han population: A case-control study.
[So] Source:Gene;651:79-85, 2018 Apr 20.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Corins are membrane-bound protease that regulates blood pressure by activating the natriuretic peptides. These pro-atrial natriuretic peptide convertases are essential for sodium homeostasis and normal blood pressure. CORIN variants have been identified in humans and other animals, but no studies of CORIN polymorphisms have been conducted in northeastern China. This study aims to investigate the association of 2 single nucleotide polymorphisms (SNPs) in CORIN (rs2271037 and rs3749585) with hypertension, as well as their potential interactions with some risk factors of hypertension in a Han population of northeastern China. A case-control study, including 402 patients with hypertension and 406 participants with normal blood pressure, was conducted in Liaoning province. SNP genotyping was carried out by high resolution melting (HRM) after polymerase chain reaction amplifications. Since rs3749585 is located in 3' untranslated region (UTR) of CORIN, in silico analysis was used to predict target micro RNAs on TargetScan, miRanda, and DIANA-microT. As a result, mutant T allele in rs2271037 (odds ratio [OR], 1.693; 95% confidence [CI], 1.528-1.877; p < 0.001) and C allele in rs3749585 (OR, 1.114; 95% CI 1.011-1.227; p = 0.029) increased the risk of hypertension, comparing with wild G allele and T allele, respectively. Patients with genotype TT (OR, 10.209; 95% CI, 6.414-16.250; p < 0.001) and GT (OR, 1.730; 95% CI, 1.226-2.443; p = 0.002) have higher risk of hypertension than those with genotype GG. SNP rs2271037 was significantly associated with susceptibility to hypertension in all genetic models (dominant model: OR, 2.879; 95% CI, 2.080-3.986; p < 0.001; recessive model: OR, 7.159; 95% CI, 4.779-10.724; p < 0.001; additive model: OR, 1.535; 95% CI, 1.163-2.027; p = 0.002). SNP rs3749585 was significantly correlated with hypertension susceptibility only in dominant model (OR, 1.533; 95% CI, 1.073-2.189; p = 0.019), but not in recessive model (OR, 1.220; 95% CI, 0.906-1.644; p = 0.191) or additive model (OR, 0.915; 95% CI, 0.694-1.205; p = 0.527). After adjusting for age, gender, body mass index (BMI), smoking, low-density lipoprotein cholesterol, and serum sodium level in logistic models, the same statistical results were obtained. Interaction study showed the association between CORIN polymorphisms and hypertension could be changed by overweight (BMI ≥ 25 kg/m ). In silico analyses implicated hsa-miR-495 as a target miRNA that potentially interacts with the 3' UTR of CORIN. In conclusion, polymorphisms of rs2271037 and rs3749585 in CORIN were significantly associated with hypertension in a Han population of northeastern China. The mutant-type T allele of rs2271037 and C allele of rs3749585 might increase the susceptibility to hypertension in this population.
[Mh] Termos MeSH primário: Grupo com Ancestrais do Continente Asiático/genética
Hipertensão/genética
Polimorfismo de Nucleotídeo Único
Serina Endopeptidases/genética
[Mh] Termos MeSH secundário: Alelos
Estudos de Casos e Controles
Feminino
Interação Gene-Ambiente
Estudos de Associação Genética
Predisposição Genética para Doença
Genótipo
Seres Humanos
Masculino
MicroRNAs/metabolismo
Meia-Idade
RNA Mensageiro/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (MicroRNAs); 0 (RNA, Messenger); EC 3.4.21.- (CORIN protein, human); EC 3.4.21.- (Serine Endopeptidases)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180203
[St] Status:MEDLINE


  2 / 22342 MEDLINE  
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[PMID]:29272270
[Au] Autor:Badet T; Voisin D; Mbengue M; Barascud M; Sucher J; Sadon P; Balagué C; Roby D; Raffaele S
[Ad] Endereço:LIPM, Université de Toulouse, INRA, CNRS, Castanet-Tolosan, France.
[Ti] Título:Parallel evolution of the POQR prolyl oligo peptidase gene conferring plant quantitative disease resistance.
[So] Source:PLoS Genet;13(12):e1007143, 2017 12.
[Is] ISSN:1553-7404
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Plant pathogens with a broad host range are able to infect plant lineages that diverged over 100 million years ago. They exert similar and recurring constraints on the evolution of unrelated plant populations. Plants generally respond with quantitative disease resistance (QDR), a form of immunity relying on complex genetic determinants. In most cases, the molecular determinants of QDR and how they evolve is unknown. Here we identify in Arabidopsis thaliana a gene mediating QDR against Sclerotinia sclerotiorum, agent of the white mold disease, and provide evidence of its convergent evolution in multiple plant species. Using genome wide association mapping in A. thaliana, we associated the gene encoding the POQR prolyl-oligopeptidase with QDR against S. sclerotiorum. Loss of this gene compromised QDR against S. sclerotiorum but not against a bacterial pathogen. Natural diversity analysis associated POQR sequence with QDR. Remarkably, the same amino acid changes occurred after independent duplications of POQR in ancestors of multiple plant species, including A. thaliana and tomato. Genome-scale expression analyses revealed that parallel divergence in gene expression upon S. sclerotiorum infection is a frequent pattern in genes, such as POQR, that duplicated both in A. thaliana and tomato. Our study identifies a previously uncharacterized gene mediating QDR against S. sclerotiorum. It shows that some QDR determinants are conserved in distantly related plants and have emerged through the repeated use of similar genetic polymorphisms at different evolutionary time scales.
[Mh] Termos MeSH primário: Resistência à Doença/genética
Serina Endopeptidases/genética
[Mh] Termos MeSH secundário: Arabidopsis/genética
Ascomicetos/genética
Ascomicetos/patogenicidade
Mapeamento Cromossômico
Regulação da Expressão Gênica de Plantas
Estudo de Associação Genômica Ampla
Doenças das Plantas/genética
Imunidade Vegetal/genética
Proteínas de Plantas/genética
Serina Endopeptidases/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Plant Proteins); EC 3.4.21.- (Serine Endopeptidases); EC 3.4.21.26 (prolyl oligopeptidase)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180227
[Lr] Data última revisão:
180227
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171223
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pgen.1007143


  3 / 22342 MEDLINE  
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[PMID]:28461069
[Au] Autor:Shiryaev SA; Farhy C; Pinto A; Huang CT; Simonetti N; Elong Ngono A; Dewing A; Shresta S; Pinkerton AB; Cieplak P; Strongin AY; Terskikh AV
[Ad] Endereço:Sanford-Burnham-Prebys Medical Discovery Institute, Center for Neuroscience, Aging, and Stem Cell Research, La Jolla, CA 92037, United States.
[Ti] Título:Characterization of the Zika virus two-component NS2B-NS3 protease and structure-assisted identification of allosteric small-molecule antagonists.
[So] Source:Antiviral Res;143:218-229, 2017 07.
[Is] ISSN:1872-9096
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The recent re-emergence of Zika virus (ZIKV) , a member of the Flaviviridae family, has become a global emergency. Currently, there are no effective methods of preventing or treating ZIKV infection, which causes severe neuroimmunopathology and is particularly harmful to the developing fetuses of infected pregnant women. However, the pathology induced by ZIKV is unique among flaviviruses, and knowledge of the biology of other family members cannot easily be extrapolated to ZIKV. Thus, structure-function studies of ZIKV proteins are urgently needed to facilitate the development of effective preventative and therapeutic agents. Like other flaviviruses, ZIKV expresses an NS2B-NS3 protease, which consists of the NS2B cofactor and the NS3 protease domain and is essential for cleavage of the ZIKV polyprotein precursor and generation of fully functional viral proteins. Here, we report the enzymatic characterization of ZIKV protease, and we identify structural scaffolds for allosteric small-molecule inhibitors of this protease. Molecular modeling of the protease-inhibitor complexes suggests that these compounds bind to the druggable cavity in the NS2B-NS3 protease interface and affect productive interactions of the protease domain with its cofactor. The most potent compound demonstrated efficient inhibition of ZIKV propagation in vitro in human fetal neural progenitor cells and in vivo in SJL mice. The inhibitory scaffolds could be further developed into valuable research reagents and, ultimately, provide a roadmap for the selection of efficient inhibitors of ZIKV infection.
[Mh] Termos MeSH primário: Sítio Alostérico
Inibidores de Proteases/química
Inibidores de Proteases/farmacologia
Proteínas não Estruturais Virais/química
Zika virus/enzimologia
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Animais
Antivirais/antagonistas & inibidores
Antivirais/química
Sequência de Bases
Ativação Enzimática
Feminino
Flavivirus/química
Expressão Gênica
Seres Humanos
Concentração Inibidora 50
Camundongos
Modelos Moleculares
Ligação Proteica
Conformação Proteica
Domínios e Motivos de Interação entre Proteínas
RNA Helicases/química
RNA Helicases/efeitos dos fármacos
Fatores de Transcrição SOXB1/genética
Alinhamento de Sequência
Serina Endopeptidases/química
Serina Endopeptidases/efeitos dos fármacos
Células-Tronco
Proteínas não Estruturais Virais/efeitos dos fármacos
Proteínas Virais/química
Proteínas Virais/genética
Zika virus/química
Zika virus/genética
Zika virus/crescimento & desenvolvimento
Infecção pelo Zika virus/virologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Antiviral Agents); 0 (NS2B protein, flavivirus); 0 (NS3 protein, flavivirus); 0 (Protease Inhibitors); 0 (SOX2 protein, human); 0 (SOXB1 Transcription Factors); 0 (Viral Nonstructural Proteins); 0 (Viral Proteins); EC 3.4.21.- (Serine Endopeptidases); EC 3.6.4.13 (RNA Helicases)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180228
[Lr] Data última revisão:
180228
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE


  4 / 22342 MEDLINE  
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[PMID]:28951254
[Au] Autor:Palanisamy N; Akaberi D; Lennerstrand J
[Ad] Endereço:Molecular and Cellular Engineering Group, BioQuant, University of Heidelberg, Heidelberg, Germany; The Hartmut Hoffmann-Berling International Graduate School of Molecular and Cellular Biology (HBIGS), University of Heidelberg, Heidelberg, Germany. Electronic address: navaneethan.palanisamy@bioquant.uni-heidelberg.de.
[Ti] Título:Protein backbone flexibility pattern is evolutionarily conserved in the Flaviviridae family: A case of NS3 protease in Flavivirus and Hepacivirus.
[So] Source:Mol Phylogenet Evol;118:58-63, 2018 Jan.
[Is] ISSN:1095-9513
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Viruses belonging to the Flaviviridae family have been an important health concern for humans, animals and birds alike. No specific treatment is available yet for many of the viral infections caused by the members of this family. Lack of specific drugs against these viruses is mainly due to lack of protein structure information. It has been known that protein backbone fluctuation pattern is highly conserved in protein pairs with similar folds, in spite of the lack of sequence similarity. We hypothesized that this concept should also hold true for proteins (especially enzymes) of viruses included in different genera of the Flaviviridae family, as we know that the sequence similarity between them is low. Using available NS3 protease crystal structures of the Flaviviridae family, our preliminary results have shown that the Cα (i.e. backbone) fluctuation patterns are highly similar between Flaviviruses and a Hepacivirus (i.e. hepatitis C virus, HCV). This has to be validated further experimentally.
[Mh] Termos MeSH primário: Evolução Molecular
Flavivirus/enzimologia
Hepacivirus/enzimologia
Proteínas não Estruturais Virais/classificação
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Animais
Seres Humanos
Funções Verossimilhança
Filogenia
Estrutura Terciária de Proteína
RNA Helicases/química
RNA Helicases/classificação
RNA Helicases/genética
Alinhamento de Sequência
Serina Endopeptidases/química
Serina Endopeptidases/classificação
Serina Endopeptidases/genética
Proteínas não Estruturais Virais/química
Proteínas não Estruturais Virais/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (NS3 protein, flavivirus); 0 (NS3 protein, hepatitis C virus); 0 (Viral Nonstructural Proteins); EC 3.4.21.- (Serine Endopeptidases); EC 3.6.4.13 (RNA Helicases)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170928
[St] Status:MEDLINE


  5 / 22342 MEDLINE  
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[PMID]:29254316
[Au] Autor:Liu GT; Shen C; Ren XH; Yang L; Yu YM; Xiu YX; Li RH; Jiang L; Zhang CL; Li YW
[Ad] Endereço:Department of Thoracic Surgery, Affiliated Hongqi Hospital of Mudanjiang Medical University, Mu Danjiang, China.
[Ti] Título:Relationship between transmembrane serine protease expression and prognosis of esophageal squamous cell carcinoma.
[So] Source:J Biol Regul Homeost Agents;31(4):1067-1072, 2017 Oct-Dec.
[Is] ISSN:0393-974X
[Cp] País de publicação:Italy
[La] Idioma:eng
[Ab] Resumo:Esophageal squamous cell carcinoma is the most common type of esophageal cancer in Eastern Europe and Asia, being the 6th most common cause of cancer deaths worldwide. The aim of this study was to analyze the expression of transmembrane serine protein in esophageal squamous cell carcinoma, and to correlate it with the clinical biological features of esophageal cancer. The expression of transmembrane protease serine 4 (TMPRSS4) mRNA and protein in carcinoma tissues and corresponding adjacent tissues and non-tumorous esophageal tissues was determined using PCR (qRT-PCR). The results show that both TMPRSS4 mRNA and protein expression were remarkably lower in adjacent normal tissues than in tumorous tissues. TMPRSS4 protein expression in esophageal carcinoma was correlated with patient demographic characteristics, tumor type, high TNM stages and overall survival (OS). Based on the experimental results, we conclude that TMPRSS4 is closely related to the occurrence, development and metastasis of esophageal squamous cell carcinoma.
[Mh] Termos MeSH primário: Biomarcadores Tumorais/genética
Carcinoma de Células Escamosas/diagnóstico
Carcinoma de Células Escamosas/genética
Neoplasias Esofágicas/diagnóstico
Neoplasias Esofágicas/genética
Regulação Neoplásica da Expressão Gênica
Proteínas de Membrana/genética
RNA Mensageiro/genética
Serina Endopeptidases/genética
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Biomarcadores Tumorais/metabolismo
Carcinoma de Células Escamosas/mortalidade
Carcinoma de Células Escamosas/patologia
Neoplasias Esofágicas/mortalidade
Neoplasias Esofágicas/patologia
Feminino
Seres Humanos
Metástase Linfática
Masculino
Proteínas de Membrana/metabolismo
Meia-Idade
Estadiamento de Neoplasias
Prognóstico
RNA Mensageiro/metabolismo
Serina Endopeptidases/metabolismo
Análise de Sobrevida
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (Membrane Proteins); 0 (RNA, Messenger); EC 3.4.21.- (Serine Endopeptidases); EC 3.4.21.- (TMPRSS4 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


  6 / 22342 MEDLINE  
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[PMID]:29265467
[Au] Autor:Guan J; Zhang J; Yuan S; Yang B; Clark KD; Ling E; Huang W
[Ad] Endereço:Key Laboratory of Insect Developmental and Evolutionary Biology, Institute of Plant Physiology and Ecology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China.
[Ti] Título:Analysis of the functions of the signal peptidase complex in the midgut of Tribolium castaneum.
[So] Source:Arch Insect Biochem Physiol;97(3), 2018 Mar.
[Is] ISSN:1520-6327
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Signal peptidase complexes (SPCs) are conserved from bacteria to human beings, and are typically composed of four to five subunits. There are four genes encoding SPC proteins in the red flour beetle, Tribolium castaneum. To understand their importance to insect development, double-stranded RNA for each SPC gene was injected into red flour beetles at the early larval and adult stages. Knockdown of all four signal peptidase genes was lethal to larvae. Moreover, larvae had difficulty with old cuticle ecdysis. Knockdown of TcSPC12 alone did not affect pupal or adult development. When TcSPC12, TcSPC18, and TcSPC25 were knocked down in larvae, the melanization of hemocytes and midguts was observed. When knocked down in larvae and adults, TcSPC18 induced severe cell apoptosis in midguts, and the adult midgut lost the ability to maintain crypts after knockdown of TcSPC18, indicating its importance to midgut cell proliferation and differentiation. Knockdown of TcSPC22 or TcSPC25 also resulted in many apoptotic cells in the midguts. However, TcSPC12 appeared to be unimportant for midgut development. We conclude that TcSPC18 is essential for maintaining the adult midgut crypts.
[Mh] Termos MeSH primário: Proteínas de Membrana/metabolismo
Serina Endopeptidases/metabolismo
Tribolium/enzimologia
[Mh] Termos MeSH secundário: Animais
Feminino
Trato Gastrointestinal/enzimologia
Hemócitos/metabolismo
Proteínas de Insetos/metabolismo
Melaninas/metabolismo
Interferência de RNA
Tribolium/crescimento & desenvolvimento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Insect Proteins); 0 (Melanins); 0 (Membrane Proteins); EC 3.4.21.- (Serine Endopeptidases); EC 3.4.21.89 (type I signal peptidase)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180216
[Lr] Data última revisão:
180216
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171222
[St] Status:MEDLINE
[do] DOI:10.1002/arch.21441


  7 / 22342 MEDLINE  
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[PMID]:28457855
[Au] Autor:Tan CW; Sam IC; Chong WL; Lee VS; Chan YF
[Ad] Endereço:Department of Medical Microbiology, Faculty of Medicine, University of Malaya, 50603 Kuala Lumpur, Malaysia. Electronic address: tancw86@gmail.com.
[Ti] Título:Polysulfonate suramin inhibits Zika virus infection.
[So] Source:Antiviral Res;143:186-194, 2017 07.
[Is] ISSN:1872-9096
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Zika virus (ZIKV) is an arthropod-borne flavivirus that causes newborn microcephaly and Guillian-Barré syndrome in adults. No therapeutics are available to treat ZIKV infection or other flaviviruses. In this study, we explored the inhibitory effect of glycosaminoglycans and analogues against ZIKV infection. Highly sulfated heparin, dextran sulfate and suramin significantly inhibited ZIKV infection in Vero cells. De-sulfated heparin analogues lose inhibitory effect, implying that sulfonate groups are critical for viral inhibition. Suramin, an FDA-approved anti-parasitic drug, inhibits ZIKV infection with 3-5 log PFU viral reduction with IC value of ∼2.5-5 µg/ml (1.93 µM-3.85 µM). A time-of-drug-addition study revealed that suramin remains potent even when administrated at 1-24 hpi. Suramin inhibits ZIKV infection by preventing viral adsorption, entry and replication. Molecular dynamics simulation revealed stronger interaction of suramin with ZIKV NS3 helicase than with the envelope protein. Suramin warrants further investigation as a potential antiviral candidate for ZIKV infection. Heparan sulfate (HS) is a cellular attachment receptor for multiple flaviviruses. However, no direct ZIKV-heparin interaction was observed in heparin-binding analysis, and downregulate or removal of cellular HS with sodium chlorate or heparinase I/III did not inhibit ZIKV infection. This indicates that cell surface HS is not utilized by ZIKV as an attachment receptor.
[Mh] Termos MeSH primário: Suramina/antagonistas & inibidores
Infecção pelo Zika virus/prevenção & controle
Zika virus/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Anticorpos Antivirais
Cercopithecus aethiops
Cloratos/farmacologia
DNA Helicases/metabolismo
Sulfato de Dextrana/antagonistas & inibidores
Flavivirus/efeitos dos fármacos
Glicosaminoglicanos/farmacologia
Heparina/análogos & derivados
Heparina/química
Heparina/farmacologia
Heparitina Sulfato/farmacologia
Concentração Inibidora 50
Camundongos
Simulação de Acoplamento Molecular
Simulação de Dinâmica Molecular
RNA Helicases/química
RNA Helicases/efeitos dos fármacos
Serina Endopeptidases/química
Serina Endopeptidases/efeitos dos fármacos
Suramina/administração & dosagem
Células Vero
Proteínas do Envelope Viral/metabolismo
Proteínas não Estruturais Virais/química
Proteínas não Estruturais Virais/efeitos dos fármacos
Internalização do Vírus/efeitos dos fármacos
Replicação Viral/efeitos dos fármacos
Zika virus/fisiologia
Infecção pelo Zika virus/virologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antibodies, Viral); 0 (Chlorates); 0 (Glycosaminoglycans); 0 (NS3 protein, flavivirus); 0 (Viral Envelope Proteins); 0 (Viral Nonstructural Proteins); 6032D45BEM (Suramin); 9005-49-6 (Heparin); 9042-14-2 (Dextran Sulfate); 9050-30-0 (Heparitin Sulfate); EC 3.4.21.- (Serine Endopeptidases); EC 3.6.4.- (DNA Helicases); EC 3.6.4.13 (RNA Helicases); T95DR77GMR (sodium chlorate)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180213
[Lr] Data última revisão:
180213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE


  8 / 22342 MEDLINE  
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[PMID]:27776350
[Au] Autor:Kong J; Du J; Wang Y; Yang M; Gao J; Wei X; Fang W; Zhan J; Zhang H
[Ad] Endereço:Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), State Key Laboratory of Natural and Biomimetic Drugs, Department of Anatomy, Histology and Embryology, Peking University Health Science Center, Beijing 100191, China.
[Ti] Título:Focal adhesion molecule Kindlin-1 mediates activation of TGF-ß signaling by interacting with TGF-ßRI, SARA and Smad3 in colorectal cancer cells.
[So] Source:Oncotarget;7(46):76224-76237, 2016 11 15.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Kindlin-1, an integrin-interacting protein, has been implicated in TGF-ß/Smad3 signaling. However, the molecular mechanism underlying Kindlin-1 regulation of TGF-ß/Smad3 signaling remains elusive. Here, we reported that Kindlin-1 is an important mediator of TGF-ß/Smad3 signaling by showing that Kindlin-1 physically interacts with TGF-ß receptor I (TßRI), Smad anchor for receptor activation (SARA) and Smad3. Kindlin-1 is required for the interaction of Smad3 with TßRI, Smad3 phosphorylation, nuclear translocation, and finally the activation of TGF-ß/Smad3 signaling pathway. Functionally, Kindlin-1 promoted colorectal cancer (CRC) cell proliferation in vitro and tumor growth in vivo, and was also required for CRC cell migration and invasion via an epithelial to mesenchymal transition. Kindlin-1 was found to be increased with the CRC progression from stages I to IV. Importantly, raised expression level of Kindlin-1 correlates with poor outcome in CRC patients. Taken together, we demonstrated that Kindlin-1 promotes CRC progression by recruiting SARA and Smad3 to TßRI and thereby activates TGF-ß/Smad3 signaling. Thus, Kindlin-1 is a novel regulator of TGF-ß/Smad3 signaling and may also be a potential target for CRC therapeutics.
[Mh] Termos MeSH primário: Neoplasias Colorretais/metabolismo
Peptídeos e Proteínas de Sinalização Intracelular/metabolismo
Proteínas de Membrana/metabolismo
Proteínas de Neoplasias/metabolismo
Proteínas Serina-Treonina Quinases/metabolismo
Receptores de Fatores de Crescimento Transformadores beta/metabolismo
Serina Endopeptidases/metabolismo
Transdução de Sinais
Proteína Smad3/metabolismo
Fator de Crescimento Transformador beta/metabolismo
[Mh] Termos MeSH secundário: Proliferação Celular
Neoplasias Colorretais/genética
Neoplasias Colorretais/mortalidade
Neoplasias Colorretais/patologia
Progressão da Doença
Transição Epitelial-Mesenquimal
Expressão Gênica
Seres Humanos
Proteínas de Membrana/genética
Proteínas de Neoplasias/genética
Ligação Proteica
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (FERMT1 protein, human); 0 (Intracellular Signaling Peptides and Proteins); 0 (Membrane Proteins); 0 (Neoplasm Proteins); 0 (Receptors, Transforming Growth Factor beta); 0 (SMAD3 protein, human); 0 (Smad3 Protein); 0 (Transforming Growth Factor beta); EC 2.7.1.11 (TGF-beta type I receptor); EC 2.7.11.1 (Protein-Serine-Threonine Kinases); EC 3.4.21- (ZFYVE16 protein, human); EC 3.4.21.- (Serine Endopeptidases)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180208
[Lr] Data última revisão:
180208
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.12779


  9 / 22342 MEDLINE  
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[PMID]:28741531
[Au] Autor:Ateeq B; Bhatia V; Goel S
[Ad] Endereço:Molecular Oncology Laboratory, Department of Biological Sciences and Bioengineering, Indian Institute of Technology, Kanpur, Uttar Pradesh 208016, India. Electronic address: bushra@iitk.ac.in.
[Ti] Título:Molecular Discriminators of Racial Disparities in Prostate Cancer.
[So] Source:Trends Cancer;2(3):116-120, 2016 Mar.
[Is] ISSN:2405-8025
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Recent molecular characterization of prostate cancer (PCa) identified novel genetic aberrations and disease subtypes. The frequencies of molecular aberrations show racial disparity. Clinical strategies and targeted therapies embracing these racial differences are required. Here we discuss ethnic differences in genetic alterations and their impact on the susceptibility, progression, and treatment of prostate cancer.
[Mh] Termos MeSH primário: Neoplasias da Próstata/etnologia
Neoplasias da Próstata/genética
[Mh] Termos MeSH secundário: Grupos de Populações Continentais
Grupos Étnicos
Predisposição Genética para Doença
Seres Humanos
Masculino
Serina Endopeptidases/genética
Regulador Transcricional ERG/genética
Inibidor da Tripsina Pancreática de Kazal/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ERG protein, human); 0 (SPINK1 protein, human); 0 (Transcriptional Regulator ERG); 50936-63-5 (Trypsin Inhibitor, Kazal Pancreatic); EC 3.4.21.- (Serine Endopeptidases); EC 3.4.21.- (TMPRSS2 protein, human)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180118
[Lr] Data última revisão:
180118
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170726
[St] Status:MEDLINE


  10 / 22342 MEDLINE  
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[PMID]:28464560
[Au] Autor:Wilkinson DJ; Habgood A; Lamb HK; Thompson P; Hawkins AR; Désilets A; Leduc R; Steinmetzer T; Hammami M; Lee MS; Craik CS; Watson S; Lin H; Milner JM; Rowan AD
[Ad] Endereço:Newcastle University, Newcastle upon Tyne, UK.
[Ti] Título:Matriptase Induction of Metalloproteinase-Dependent Aggrecanolysis In Vitro and In Vivo: Promotion of Osteoarthritic Cartilage Damage by Multiple Mechanisms.
[So] Source:Arthritis Rheumatol;69(8):1601-1611, 2017 08.
[Is] ISSN:2326-5205
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: To assess the ability of matriptase, a type II transmembrane serine proteinase, to promote aggrecan loss from the cartilage of patients with osteoarthritis (OA) and to determine whether its inhibition can prevent aggrecan loss and cartilage damage in experimental OA. METHODS: Aggrecan release from human OA cartilage explants and human stem cell-derived cartilage discs was evaluated, and cartilage-conditioned media were used for Western blotting. Gene expression was analyzed by real-time polymerase chain reaction. Murine OA was induced by surgical destabilization of the medial meniscus, and matriptase inhibitors were administered via osmotic minipump or intraarticular injection. Cartilage damage was scored histologically and aggrecan cleavage was visualized immunohistochemically using specific neoepitope antibodies. RESULTS: The addition of soluble recombinant matriptase promoted a time-dependent release of aggrecan (and collagen) from OA cartilage, which was sensitive to metalloproteinase inhibition and protease-activated receptor 2 antagonism. Although engineered human (normal) cartilage discs failed to release aggrecan following matriptase addition, both matrix metalloproteinase- and aggrecanase-mediated cleavages of aggrecan were detected in human OA cartilage. Additionally, while matriptase did not directly degrade aggrecan, it promoted the accumulation of low-density lipoprotein receptor-related protein 1 (LRP-1) in conditioned media of the OA cartilage explants. Matriptase inhibition via neutralizing antibody or small molecule inhibitor significantly reduced cartilage damage scores in murine OA, which was associated with reduced generation of metalloproteinase-mediated aggrecan cleavage. CONCLUSION: Matriptase potently induces the release of metalloproteinase-generated aggrecan fragments as well as soluble LRP-1 from OA cartilage. Therapeutic targeting of matriptase proteolytic activity reduces metalloproteinase activity, further suggesting that this serine proteinase may have potential as a disease-modifying therapy in OA.
[Mh] Termos MeSH primário: Agrecanas/efeitos dos fármacos
Cartilagem Articular/efeitos dos fármacos
Osteoartrite do Joelho/metabolismo
Serina Endopeptidases/farmacologia
[Mh] Termos MeSH secundário: Proteína ADAMTS4/efeitos dos fármacos
Proteína ADAMTS4/metabolismo
Proteína ADAMTS5/efeitos dos fármacos
Proteína ADAMTS5/metabolismo
Idoso
Idoso de 80 Anos ou mais
Agrecanas/metabolismo
Animais
Anticorpos Neutralizantes/farmacologia
Western Blotting
Cartilagem Articular/metabolismo
Cartilagem Articular/patologia
Endopeptidases/efeitos dos fármacos
Endopeptidases/metabolismo
Feminino
Perfilação da Expressão Gênica
Seres Humanos
Imuno-Histoquímica
Técnicas In Vitro
Proteína-1 Relacionada a Receptor de Lipoproteína de Baixa Densidade/efeitos dos fármacos
Proteína-1 Relacionada a Receptor de Lipoproteína de Baixa Densidade/metabolismo
Masculino
Metaloproteinases da Matriz/efeitos dos fármacos
Metaloproteinases da Matriz/metabolismo
Proteínas de Membrana/antagonistas & inibidores
Proteínas de Membrana/metabolismo
Meniscos Tibiais/cirurgia
Camundongos
Meia-Idade
Osteoartrite do Joelho/patologia
Reação em Cadeia da Polimerase em Tempo Real
Proteínas Recombinantes/farmacologia
Serina Endopeptidases/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Aggrecans); 0 (Antibodies, Neutralizing); 0 (Low Density Lipoprotein Receptor-Related Protein-1); 0 (Membrane Proteins); 0 (Recombinant Proteins); EC 3.4.- (Endopeptidases); EC 3.4.21.- (Serine Endopeptidases); EC 3.4.21.109 (ST14 protein, human); EC 3.4.21.109 (St14 protein, mouse); EC 3.4.24.- (ADAMTS5 Protein); EC 3.4.24.- (Matrix Metalloproteinases); EC 3.4.24.82 (ADAMTS4 Protein); EC 3.4.99.- (aggrecanase)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:180119
[Lr] Data última revisão:
180119
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.1002/art.40133



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