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[PMID]:29355528
[Au] Autor:Zhu J; Li S; Ramelot TA; Kennedy MA; Liu M; Yang Y
[Ad] Endereço:State Key Laboratory of Magnetic Resonance and Atomic Molecular Physics, Wuhan Center for Magnetic Resonance, Wuhan Institute of Physics and Mathematics, Chinese Academy of Sciences, Wuhan 430071, China.
[Ti] Título:Structural insights into the impact of two holoprosencephaly-related mutations on human TGIF1 homeodomain.
[So] Source:Biochem Biophys Res Commun;496(2):575-581, 2018 02 05.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Human protein TGIF1 is an essential regulator of cell fate with broad roles in different tissues, and has been implicated in holoprosencephaly (HPE) and many cancers. The function of TGIF1 in transcriptional regulation depends on its three-amino acid loop extension (TALE) type of homeodomain (HD). Two missense mutations that led to P192A and R219C substitutions in TGIF1-HD were previously found in HPE patients and suggested to be the causes for these cases. However, how these mutations affected TGIF1 function has not been investigated from a structural view. Here, we investigated the roles of P192 and R219 in TGIF1-HD structure packing through determining the NMR structure of TGIF1-HD. Surprisingly, P192 and R219 were found to play roles in packing α1 and α2 to α3 together with A190 and F215 through side-chain interactions. Circular dichroism (CD) showed that P192A and R219C mutants displayed structural change and less folding compared with wild-type TGIF1-HD, and H- N HSQC spectrum of P192A mutant exhibited chemical shift perturbations in all three helices of TGIF1-HD. Thus, it is suggested that P192A and R219C mutations led to structure disturbances of TGIF1-HD, which subsequently reduced the DNA-binding affinity of TGIF1-HD by 23-fold and 10-fold respectively, as revealed by the isothermal titration calorimetry (ITC) experiments. Our study provides structural insights of the probable pathogenesis mechanism of two TGIF1-related HPE cases, and evidences for the roles of P192 and R219 in HD folding.
[Mh] Termos MeSH primário: Holoprosencefalia/genética
Proteínas de Homeodomínio/química
Proteínas de Homeodomínio/genética
Mutação Puntual
Proteínas Repressoras/química
Proteínas Repressoras/genética
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
DNA/metabolismo
Holoprosencefalia/metabolismo
Proteínas de Homeodomínio/metabolismo
Seres Humanos
Modelos Moleculares
Mutação de Sentido Incorreto
Ressonância Magnética Nuclear Biomolecular
Conformação Proteica
Dobramento de Proteína
Proteínas Repressoras/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 (Homeodomain Proteins); 0 (Repressor Proteins); 0 (TGIF1 protein, human); 9007-49-2 (DNA)
[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:180123
[St] Status:MEDLINE


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[PMID]:28466892
[Au] Autor:Bondí R; Longo F; Messina M; D'Angelo F; Visca P; Leoni L; Rampioni G
[Ad] Endereço:Department of Science, University Roma Tre, Rome, Italy. giordano.rampioni@uniroma3.it.
[Ti] Título:The multi-output incoherent feedforward loop constituted by the transcriptional regulators LasR and RsaL confers robustness to a subset of quorum sensing genes in Pseudomonas aeruginosa.
[So] Source:Mol Biosyst;13(6):1080-1089, 2017 Jun 01.
[Is] ISSN:1742-2051
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Quorum sensing (QS) is an intercellular communication system which controls virulence-related phenotypes in the human pathogen Pseudomonas aeruginosa. LasR is the QS receptor protein which responds to the signal molecule N-(3-oxododecanoyl)homoserine lactone (3OC -HSL) and promotes signal production by increasing the transcription of the 3OC -HSL synthase gene, lasI. LasR also activates the expression of other genes, including rsaL, coding for the RsaL protein which acts as a transcriptional repressor of lasI. Direct gene activation and RsaL-mediated gene repression, both exerted by LasR on the expression of the output gene lasI, generate a regulatory network motif known as the type 1 incoherent feedforward loop (IFFL-1) that governs 3OC -HSL production. In addition to lasI, RsaL directly represses a set of LasR-activated genes; hence, the IFFL-1 generated by LasR and RsaL is a multi-output IFFL-1. Here we demonstrate that the multi-output IFFL-1 constituted by LasR and RsaL confers robustness with respect to fluctuations in the levels of LasR to the phenotypes controlled by both these transcriptional regulators (e.g. 3OC -HSL synthesis and pyocyanin production). In contrast, other virulence-related phenotypes controlled by LasR but not by RsaL (e.g. elastase and protease production) are sensitive to changes in LasR levels. Overall, the multi-output IFFL-1 generated by LasR and RsaL splits the QS regulon into two distinct sub-regulons with different robustness with respect to LasR fluctuations. This emerging regulatory property enhances the phenotypic plasticity of P. aeruginosa, thus contributing to its adaptation to changing environments.
[Mh] Termos MeSH primário: Proteínas de Bactérias/metabolismo
Pseudomonas aeruginosa/metabolismo
Pseudomonas aeruginosa/fisiologia
Percepção de Quorum
Proteínas Repressoras/metabolismo
Transativadores/metabolismo
[Mh] Termos MeSH secundário: 4-Butirolactona/análogos & derivados
4-Butirolactona/metabolismo
Proteínas de Bactérias/genética
Regulação da Expressão Gênica
Homosserina/análogos & derivados
Homosserina/metabolismo
Proteínas Repressoras/genética
Transativadores/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bacterial Proteins); 0 (LasR protein, Pseudomonas aeruginosa); 0 (N-(3-oxododecanoyl)homoserine lactone); 0 (Repressor Proteins); 0 (Trans-Activators); 0 (rsaL protein, Pseudomonas aeruginosa); 1192-20-7 (homoserine lactone); 6KA95X0IVO (Homoserine); OL659KIY4X (4-Butyrolactone)
[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:170504
[St] Status:MEDLINE
[do] DOI:10.1039/c7mb00040e


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[PMID]:29182018
[Au] Autor:Amin SA; Adhikari N; Jha T
[Ad] Endereço:Natural Science Laboratory, Department of Pharmaceutical Technology, Division of Medicinal & Pharmaceutical Chemistry, PO Box 17020, Jadavpur University, Kolkata 700032, West Bengal, India.
[Ti] Título:Structure-activity relationships of hydroxamate-based histone deacetylase-8 inhibitors: reality behind anticancer drug discovery.
[So] Source:Future Med Chem;9(18):2211-2237, 2017 12.
[Is] ISSN:1756-8927
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The pan-histone deacetylase (HDAC) inhibitors comprise a fish-like structural orientation where hydrophobic aryl- and zinc-binding groups act as head and tail, respectively of a fish. The linker moiety correlates the body of the fish linking head and tail groups. Despite these pan-HDAC inhibitors, selective HDAC-8 inhibitors are still in demand as a safe remedy. HDAC-8 is involved in invasion and metastasis in cancer. This review deals with the rationale behind HDAC-8 inhibitory activity and selectivity along with detailed structure-activity relationships of diverse hydroxamate-based HDAC-8 inhibitors. HDAC-8 inhibitory potency may be increased by modifying the fish-like pharmacophoric features of such type of pan-HDAC inhibitors. This review may provide a preliminary basis to design and optimize new lead molecules with higher HDAC-8 inhibitory activity. This work may surely enlighten in providing useful information in the field of target-specific anticancer therapy.
[Mh] Termos MeSH primário: Antineoplásicos/química
Inibidores de Histona Desacetilases/química
Ácidos Hidroxâmicos/química
Proteínas Repressoras/antagonistas & inibidores
[Mh] Termos MeSH secundário: Animais
Antineoplásicos/uso terapêutico
Sítios de Ligação
Desenho de Drogas
Inibidores de Histona Desacetilases/uso terapêutico
Histona Desacetilases/metabolismo
Seres Humanos
Ácidos Hidroxâmicos/uso terapêutico
Simulação de Acoplamento Molecular
Neoplasias/tratamento farmacológico
Neoplasias/patologia
Proteínas Repressoras/metabolismo
Relação Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Histone Deacetylase Inhibitors); 0 (Hydroxamic Acids); 0 (Repressor Proteins); EC 3.5.1.98 (HDAC8 protein, human); EC 3.5.1.98 (Histone Deacetylases)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171129
[St] Status:MEDLINE
[do] DOI:10.4155/fmc-2017-0130


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[PMID]:29206995
[Au] Autor:Wyatt AW; Annala M; Aggarwal R; Beja K; Feng F; Youngren J; Foye A; Lloyd P; Nykter M; Beer TM; Alumkal JJ; Thomas GV; Reiter RE; Rettig MB; Evans CP; Gao AC; Chi KN; Small EJ; Gleave ME
[Ad] Endereço:Department of Urologic Sciences, Vancouver Prostate Centre, University of British Columbia, Vancouver, Canada; Institute of Biosciences and Medical Technology, University of Tampere, Tampere, Finland; Department of Medicine and Department of Radiation Oncology, UCSF Helen Diller Family Comprehensive
[Ti] Título:Concordance of Circulating Tumor DNA and Matched Metastatic Tissue Biopsy in Prostate Cancer.
[So] Source:J Natl Cancer Inst;109(12), 2017 Dec 01.
[Is] ISSN:1460-2105
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Background: Real-time knowledge of the somatic genome can influence management of patients with metastatic castration-resistant prostate cancer (mCRPC). While routine metastatic tissue biopsy is challenging in mCRPC, plasma circulating tumor DNA (ctDNA) has emerged as a minimally invasive tool to sample the tumor genome. However, no systematic comparisons of matched "liquid" and "solid" biopsies have been performed that would enable ctDNA profiling to replace the need for direct tissue sampling. Methods: We performed targeted sequencing across 72 clinically relevant genes in 45 plasma cell-free DNA (cfDNA) samples collected at time of metastatic tissue biopsy. We compared ctDNA alterations with exome sequencing data generated from matched tissue and quantified the concordance of mutations and copy number alterations using the Fisher exact test and Pearson correlations. Results: Seventy-five point six percent of cfDNA samples had a ctDNA proportion greater than 2% of total cfDNA. In these patients, all somatic mutations identified in matched metastatic tissue biopsies were concurrently present in ctDNA. Furthermore, the hierarchy of variant allele fractions for shared mutations was remarkably similar between ctDNA and tissue. Copy number profiles between matched liquid and solid biopsy were highly correlated, and individual copy number calls in clinically actionable genes were 88.9% concordant. Detected alterations included AR amplifications in 22 (64.7%) samples, SPOP mutations in three (8.8%) samples, and inactivating alterations in tumor suppressors TP53 , PTEN , RB1 , APC , CDKN1B , BRCA2 , and PIK3R1 . In several patients, ctDNA sequencing revealed robust changes not present in paired solid biopsy, including clinically relevant alterations in the AR, WNT, and PI3K pathways. Conclusions: Our study shows that, in the majority of patients, a ctDNA assay is sufficient to identify all driver DNA alterations present in matched metastatic tissue and supports development of DNA biomarkers to guide mCRPC patient management based on ctDNA alone.
[Mh] Termos MeSH primário: DNA Tumoral Circulante/sangue
Neoplasias de Próstata Resistentes à Castração/genética
Neoplasias de Próstata Resistentes à Castração/patologia
[Mh] Termos MeSH secundário: Proteína da Polipose Adenomatosa do Colo/genética
Proteína BRCA2/genética
Biomarcadores Tumorais/sangue
Biomarcadores Tumorais/genética
Inibidor de Quinase Dependente de Ciclina p27/genética
Variações do Número de Cópias de DNA
Seres Humanos
Biópsia Líquida
Masculino
Mutação
Metástase Neoplásica
Proteínas Nucleares/genética
PTEN Fosfo-Hidrolase/genética
Fosfatidilinositol 3-Quinases/genética
Receptores Androgênicos/genética
Proteínas Repressoras/genética
Proteínas de Ligação a Retinoblastoma/genética
Proteína Supressora de Tumor p53/genética
Ubiquitina-Proteína Ligases/genética
Via de Sinalização Wnt/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (APC protein, human); 0 (Adenomatous Polyposis Coli Protein); 0 (BRCA2 Protein); 0 (BRCA2 protein, human); 0 (Biomarkers, Tumor); 0 (CDKN1B protein, human); 0 (Circulating Tumor DNA); 0 (Nuclear Proteins); 0 (RB1 protein, human); 0 (Receptors, Androgen); 0 (Repressor Proteins); 0 (Retinoblastoma Binding Proteins); 0 (SPOP protein, human); 0 (TP53 protein, human); 0 (Tumor Suppressor Protein p53); 147604-94-2 (Cyclin-Dependent Kinase Inhibitor p27); EC 2.3.2.27 (Ubiquitin-Protein Ligases); EC 2.7.1.- (PIK3R1 protein, human); EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 3.1.3.67 (PTEN Phosphohydrolase); EC 3.1.3.67 (PTEN protein, human)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171206
[St] Status:MEDLINE
[do] DOI:10.1093/jnci/djx118


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[PMID]:28453729
[Au] Autor:Chen Z; Xie J; Hao H; Lin H; Wang L; Zhang Y; Chen L; Cao S; Huang X; Liao W; Bin J; Liao Y
[Ad] Endereço:State Key Laboratory of Organ Failure Research, Department of Cardiology, Nanfang Hospital, Southern Medical University, 1838, Guangzhou Avenue North, Guangzhou 510515, China.
[Ti] Título:Ablation of periostin inhibits post-infarction myocardial regeneration in neonatal mice mediated by the phosphatidylinositol 3 kinase/glycogen synthase kinase 3ß/cyclin D1 signalling pathway.
[So] Source:Cardiovasc Res;113(6):620-632, 2017 May 01.
[Is] ISSN:1755-3245
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Aims: To resolve the controversy as to whether periostin plays a role in myocardial regeneration after myocardial infarction (MI), we created a neonatal mouse model of MI to investigate the influence of periostin ablation on myocardial regeneration and clarify the underlying mechanisms. Methods and results: Neonatal periostin-knockout mice and their wildtype littermates were subjected to MI or sham surgery. In the wildtype mice after MI, fibrosis was detectable at 3 days and fibrotic tissue was completely replaced by regenerated myocardium at 21 days. In contrast, in the knockout mice, significant fibrosis in the infarcted area was present at even 3 weeks after MI. Levels of phosphorylated-histone 3 and aurora B in the myocardium, detected by immunofluorescence and western blotting, were significantly lower in knockout than in wildtype mice at 7 days after MI. Similarly, angiogenesis was decreased in the knockout mice after MI. Expression of both the endothelial marker CD-31 and α-smooth muscle actin was markedly lower in the knockout than in wildtype mice at 7 days after MI. The knockout MI group had elevated levels of glycogen synthase kinase (GSK) 3ß and decreased phosphatidylinositol 3-kinase (PI3K), phosphorylated serine/threonine protein kinase B (p-Akt), and cyclin D1, compared with the wildtype MI group. Similar effects were observed in experiments using cultured cardiomyocytes from neonatal wildtype or periostin knockout mice. Administration of SB216763, a GSK3ß inhibitor, to knockout neonatal mice decreased myocardial fibrosis and increased angiogenesis in the infarcted area after MI. Conclusion: Ablation of periostin suppresses post-infarction myocardial regeneration by inhibiting the PI3K/GSK3ß/cyclin D1 signalling pathway, indicating that periostin is essential for myocardial regeneration.
[Mh] Termos MeSH primário: Moléculas de Adesão Celular/deficiência
Ciclina D1/metabolismo
Infarto do Miocárdio/enzimologia
Miocárdio/enzimologia
Fosfatidilinositol 3-Quinase/metabolismo
Regeneração
Proteínas Repressoras/metabolismo
Transdução de Sinais
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Moléculas de Adesão Celular/genética
Células Cultivadas
Modelos Animais de Doenças
Fibrose
Camundongos Knockout
Infarto do Miocárdio/genética
Infarto do Miocárdio/patologia
Infarto do Miocárdio/fisiopatologia
Miocárdio/patologia
Neovascularização Fisiológica
Fosforilação
Inibidores de Proteínas Quinases/farmacologia
Proteínas Proto-Oncogênicas c-akt/metabolismo
Regeneração/efeitos dos fármacos
Proteínas Repressoras/antagonistas & inibidores
Transdução de Sinais/efeitos dos fármacos
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Ccnd1 protein, mouse); 0 (Cell Adhesion Molecules); 0 (GSKIP protein, mouse); 0 (Postn protein, mouse); 0 (Protein Kinase Inhibitors); 0 (Repressor Proteins); 136601-57-5 (Cyclin D1); EC 2.7.1.137 (Phosphatidylinositol 3-Kinase); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1093/cvr/cvx001


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[PMID]:28449057
[Au] Autor:Schumacher MA; Zeng W; Findlay KC; Buttner MJ; Brennan RG; Tschowri N
[Ad] Endereço:Department of Biochemistry, Duke University School of Medicine, Durham, NC 27701, USA.
[Ti] Título:The Streptomyces master regulator BldD binds c-di-GMP sequentially to create a functional BldD2-(c-di-GMP)4 complex.
[So] Source:Nucleic Acids Res;45(11):6923-6933, 2017 Jun 20.
[Is] ISSN:1362-4962
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Streptomyces are ubiquitous soil bacteria that undergo a complex developmental transition coinciding with their production of antibiotics. This transition is controlled by binding of a novel tetrameric form of the second messenger, 3΄-5΄ cyclic diguanylic acid (c-di-GMP) to the master repressor, BldD. In all domains of life, nucleotide-based second messengers allow a rapid integration of external and internal signals into regulatory pathways that control cellular responses to changing conditions. c-di-GMP can assume alternative oligomeric states to effect different functions, binding to effector proteins as monomers, intercalated dimers or, uniquely in the case of BldD, as a tetramer. However, at physiological concentrations c-di-GMP is a monomer and little is known about how higher oligomeric complexes assemble on effector proteins and if intermediates in assembly pathways have regulatory significance. Here, we show that c-di-GMP binds BldD using an ordered, sequential mechanism and that BldD function necessitates the assembly of the BldD2-(c-di-GMP)4 complex.
[Mh] Termos MeSH primário: Proteínas de Bactérias/química
GMP Cíclico/análogos & derivados
Proteínas Repressoras/química
Streptomyces
[Mh] Termos MeSH secundário: Sítios de Ligação
Cristalografia por Raios X
GMP Cíclico/química
Ligações de Hidrogênio
Modelos Moleculares
Ligação Proteica
Domínios Proteicos
Estabilidade Proteica
Estrutura Quaternária de Proteína
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bacterial Proteins); 0 (Repressor Proteins); 61093-23-0 (bis(3',5')-cyclic diguanylic acid); H2D2X058MU (Cyclic GMP)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:180307
[Lr] Data última revisão:
180307
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170428
[St] Status:MEDLINE
[do] DOI:10.1093/nar/gkx287


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[PMID]:29388837
[Au] Autor:Martinez-Jaramillo E; Garza-Morales R; Wechman SL; Montes de Oca-Luna R; Saucedo-Cardenas O; Shirwan H; Yolcu E; McMasters KM; Gomez-Gutierrez JG
[Ad] Endereço:a The Hiram C. Polk Jr., MD, Department of Surgery , University of Louisville School of Medicine , Louisville , USA.
[Ti] Título:Adenovirus Lacking E1b Efficiently Induces Cytopathic Effect in HPV-16-Positive Murine Cancer Cells via Virus Replication and Apoptosis.
[So] Source:Cancer Invest;36(1):19-27, 2018 Jan 02.
[Is] ISSN:1532-4192
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Conditionally replicative adenoviruses (CRAds) replicate poorly in murine cancer cells; however, E1b-deleted CRAds may replicate effectively in HPV16-E6/E7-positive murine cancer cells (TC-1). The HPV16 E7 open reading frame encodes functions analogous to these deleted adenovirus E1 proteins. In this study, an E1b-deleted CRAd (Adhz60) was evaluated for its ability to replicate and induce oncolysis in TC-1 cells. Adhz60-mediated oncolysis was similar in TC-1 and HeLa cells. Productive viral replication was evident based on expression of E1A and hexon, production of infectious virus progeny, and Adhz60-induced apoptosis. The results suggest that TC-1 murine cancer cells allow Adhz60 replication and oncolysis.
[Mh] Termos MeSH primário: Adenoviridae/genética
Proteínas E1B de Adenovirus/genética
Apoptose/genética
Papillomavirus Humano 16/genética
Replicação Viral/genética
[Mh] Termos MeSH secundário: Animais
Apoptose/fisiologia
Linhagem Celular Tumoral
Células HEK293
Células HeLa
Seres Humanos
Camundongos
Camundongos Endogâmicos C57BL
Proteínas Oncogênicas Virais/genética
Proteínas E7 de Papillomavirus/genética
Proteínas Repressoras/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adenovirus E1B Proteins); 0 (E6 protein, Human papillomavirus type 16); 0 (Oncogene Proteins, Viral); 0 (Papillomavirus E7 Proteins); 0 (Repressor Proteins); 0 (oncogene protein E7, Human papillomavirus type 16)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180202
[St] Status:MEDLINE
[do] DOI:10.1080/07357907.2018.1430812


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[PMID]:28454697
[Au] Autor:Tian FY; Hivert MF; Wen X; Xie C; Niu Z; Fan L; Gillman MW; Chen WQ
[Ad] Endereço:Department of Medical Statistics and Epidemiology, Guangzhou Key Laboratory of Environmental Pollution and Health Assessment, Guangdong Provincial Key Laboratory of Food, Nutrition and Health, School of Public Health, Sun Yat-sen University, Guangzhou, Guangdong, China. Electronic address: tianfy@ma
[Ti] Título:Tissue differences in DNA methylation changes at AHRR in full term low birth weight in maternal blood, placenta and cord blood in Chinese.
[So] Source:Placenta;52:49-57, 2017 Apr.
[Is] ISSN:1532-3102
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Very few study addressed the relationship between Aryl-hydrocarbon receptor repressor (AHRR) DNA methylation and low birth weight, especially in multiple tissues of mother-infant pairs. In this study, we aimed to investigate AHRR DNA methylation modification in cord blood, placenta and maternal blood between full term low birth weight (FT-LBW) and full term normal birth weight (FT-NBW) newborns. METHODS: We enrolled 90 FT-LBW and 90 FT-NBW mother-infant pairs, of which all placenta and cord blood samples were collected while 45 maternal blood samples of each group were collected. We measured AHRR DNA methylation (Chr5: 373013-373606) using Sequenom MassARRAY, and assessed associations between AHRR DNA methylation and FT-LBW using logistic regression adjusting for maternal age, education, family income, delivery mode, and passive smoking. RESULTS: FT-LBW babies had 3% lower methylation at Chr5: 373378 (CpG 13) in cord blood, and 4-9% higher methylation levels at Chr5: 373315, 373378, 373423, 373476 and 373490/373494 (CpG 10; 13; 15; 16; 17/18 respectively) in maternal blood, comparing with FT-NBW. The methylation of Chr5: 373378 (CpG 13) remained significant association with FT-LBW both in cord blood (OR = 0.90; 95% CI: 0.82, 0.98) and maternal blood (OR = 1.14; 95% CI: 1.04, 1.25) further adjusting for each other in the same model. We observed no significant difference at any CpG sites in placenta. DISCUSSION: AHRR DNA methylation of cord and maternal blood might be independently associated with FT-LBW in different ways.
[Mh] Termos MeSH primário: Fatores de Transcrição Hélice-Alça-Hélice Básicos/metabolismo
Metilação de DNA
Sangue Fetal/metabolismo
Recém-Nascido de Baixo Peso/metabolismo
Placenta/metabolismo
Proteínas Repressoras/metabolismo
[Mh] Termos MeSH secundário: Fatores de Transcrição Hélice-Alça-Hélice Básicos/genética
Estudos de Casos e Controles
China
Feminino
Seres Humanos
Recém-Nascido
Idade Materna
Gravidez
Proteínas Repressoras/genética
Poluição por Fumaça de Tabaco
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (AHRR protein, human); 0 (Basic Helix-Loop-Helix Transcription Factors); 0 (Repressor Proteins); 0 (Tobacco Smoke Pollution)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170430
[St] Status:MEDLINE


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[PMID]:29200284
[Au] Autor:He X; Liao X; Li H; Xia W; Sun H
[Ad] Endereço:MOE Key Laboratory of Bioinorganic and Synthetic Chemistry, School of Chemistry, Sun Yat-sen University , Guangzhou 510275, China.
[Ti] Título:Bismuth-Induced Inactivation of Ferric Uptake Regulator from Helicobacter pylori.
[So] Source:Inorg Chem;56(24):15041-15048, 2017 Dec 18.
[Is] ISSN:1520-510X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Ferric uptake regulator (Fur) of Helicobacter pylori is a global regulator that is important for bacterial colonization and survival within the gastric mucosa. H. pylori Fur (HpFur) is unique in its ability to regulate gene expression in both metal-bound (holo-Fur) and metal-free (apo-Fur) forms. Bismuth-based drugs are widely used for the treatment of H. pylori infection. However, the mechanism of action of bismuth drug was not fully understood. Recently, it has been reported that bismuth drugs could interfere with the bacterial ferric uptake pathway and inhibit bacterial growth, implying intrinsic correlation between bismuth drug and bacterial iron metabolism. Herein, we demonstrate that Bi(III) binds to HpFur protein specifically at the physiologically important S1 site, which further leads to protein oligomerization and loss of DNA binding capability. The targeting of HpFur by bismuth drugs significantly reduced transcription levels of its regulated genes, which are crucial for bacterial physiology and metabolism. Our studies present direct evidence that perturbation of iron metabolism in H. pylori by bismuth might serve as one of the mechanisms for the antimicrobial activity of bismuth drugs.
[Mh] Termos MeSH primário: Antibacterianos/farmacologia
Proteínas de Bactérias/antagonistas & inibidores
Bismuto/farmacologia
Inibidores Enzimáticos/farmacologia
Helicobacter pylori/efeitos dos fármacos
Proteínas Repressoras/antagonistas & inibidores
[Mh] Termos MeSH secundário: Proteínas de Bactérias/química
Proteínas de Bactérias/metabolismo
DNA Bacteriano/metabolismo
Estabilidade Enzimática/efeitos dos fármacos
Infecções por Helicobacter/tratamento farmacológico
Infecções por Helicobacter/microbiologia
Helicobacter pylori/metabolismo
Seres Humanos
Modelos Moleculares
Conformação Proteica/efeitos dos fármacos
Multimerização Proteica/efeitos dos fármacos
Proteínas Repressoras/química
Proteínas Repressoras/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Bacterial Agents); 0 (Bacterial Proteins); 0 (DNA, Bacterial); 0 (Enzyme Inhibitors); 0 (Repressor Proteins); 0 (ferric uptake regulating proteins, bacterial); U015TT5I8H (Bismuth)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180228
[Lr] Data última revisão:
180228
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171205
[St] Status:MEDLINE
[do] DOI:10.1021/acs.inorgchem.7b02380


  10 / 43329 MEDLINE  
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[PMID]:29360877
[Au] Autor:Verma V; Kaur C; Grover P; Gupta A; Chaudhary VK
[Ad] Endereço:Centre for Innovation in Infectious Disease Research, Education and Training (CIIDRET), University of Delhi South Campus, New Delhi, India.
[Ti] Título:Biotin-tagged proteins: Reagents for efficient ELISA-based serodiagnosis and phage display-based affinity selection.
[So] Source:PLoS One;13(1):e0191315, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The high-affinity interaction between biotin and streptavidin has opened avenues for using recombinant proteins with site-specific biotinylation to achieve efficient and directional immobilization. The site-specific biotinylation of proteins carrying a 15 amino acid long Biotin Acceptor Peptide tag (BAP; also known as AviTag) is effected on a specific lysine either by co-expressing the E. coli BirA enzyme in vivo or by using purified recombinant E. coli BirA enzyme in the presence of ATP and biotin in vitro. In this paper, we have designed a T7 promoter-lac operator-based expression vector for rapid and efficient cloning, and high-level cytosolic expression of proteins carrying a C-terminal BAP tag in E. coli with TEV protease cleavable N-terminal deca-histidine tag, useful for initial purification. Furthermore, a robust three-step purification pipeline integrated with well-optimized protocols for TEV protease-based H10 tag removal, and recombinant BirA enzyme-based site-specific in vitro biotinylation is described to obtain highly pure biotinylated proteins. Most importantly, the paper demonstrates superior sensitivities in indirect ELISA with directional and efficient immobilization of biotin-tagged proteins on streptavidin-coated surfaces in comparison to passive immobilization. The use of biotin-tagged proteins through specific immobilization also allows more efficient selection of binders from a phage-displayed naïve antibody library. In addition, for both these applications, specific immobilization requires much less amount of protein as compared to passive immobilization and can be easily multiplexed. The simplified strategy described here for the production of highly pure biotin-tagged proteins will find use in numerous applications, including those, which may require immobilization of multiple proteins simultaneously on a solid surface.
[Mh] Termos MeSH primário: Proteínas de Bactérias/isolamento & purificação
Proteínas de Bactérias/metabolismo
Biotina/metabolismo
Ensaio de Imunoadsorção Enzimática/métodos
Biblioteca de Peptídeos
Testes Sorológicos/métodos
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Proteínas de Bactérias/química
Proteínas de Bactérias/genética
Biotinilação
Carbono-Nitrogênio Ligases/metabolismo
Clonagem Molecular
Citosol/metabolismo
Escherichia coli/citologia
Escherichia coli/genética
Proteínas de Escherichia coli/metabolismo
Vetores Genéticos/genética
Indicadores e Reagentes/metabolismo
Mycobacterium tuberculosis/genética
Proteínas Repressoras/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Bacterial Proteins); 0 (Escherichia coli Proteins); 0 (Indicators and Reagents); 0 (Peptide Library); 0 (Repressor Proteins); 6SO6U10H04 (Biotin); EC 6.3.- (Carbon-Nitrogen Ligases); EC 6.3.4.15 (birA protein, E coli)
[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:180124
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191315



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