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[PMID]:29214786
[Au] Autor:Kim KY; Bae YS; Ji W; Shin D; Kim HS; Kim DS
[Ad] Endereço:Department of Pediatrics, Yonsei University College of Medicine, Severance Children's Hospital, Seoul, Korea.
[Ti] Título:ITPKC and SLC11A1 Gene Polymorphisms and Gene-Gene Interactions in Korean Patients with Kawasaki Disease.
[So] Source:Yonsei Med J;59(1):119-127, 2018 Jan.
[Is] ISSN:1976-2437
[Cp] País de publicação:Korea (South)
[La] Idioma:eng
[Ab] Resumo:PURPOSE: Kawasaki disease (KD) is an acute systemic vasculitis. Both the etiology of KD and the erythema of Bacille Calmette-Guérin (BCG) injection sites observed in the disease are poorly understood. We investigated the association between KD and single nucleotide polymorphisms (SNPs) in two candidate genes: inositol 1,4,5-triphosphate 3-kinase (ITPKC), a well-studied KD-associated gene, and solute carrier 11a1 (SLC11A1), which is associated with the hypersensitive reaction to the BCG strain in Koreans. MATERIALS AND METHODS: Associations between KD and SNPs in two genes were evaluated. Potential associations between BCG injection site erythema and SNPs in two genes were also evaluated. Gene-gene interactions between ITPKC and SLC11A1 in KD and BCG injection site erythema were also analyzed. RESULTS: Three tagging SNPs in ITPKC and five tagging SNPs in SLC11A1 were genotyped in 299 KD patients and 210 control children. SNP rs28493229 in ITPKC was associated with KD and coronary artery complications. SNP rs77624405 in SLC11A1 was associated with KD. Comparisons of KD patients with and without BCG injection site erythema revealed that SNP rs17235409 in SLC11A1 was associated with erythema; no erythema-associated SNPs in ITPKC were identified. Interactions between ITPKC rs28493229_GG and SLC11A1 rs17235409_GA and between ITPKC rs10420685_GG and SLC11A1 rs17235409_AA were strongly associated with BCG injection site erythema. CONCLUSION: This study identified several important polymorphisms in the ITPKC and SLC11A1 genes in Koreans. The genetic variants identified in this study affected KD and erythema of BCG injection sites independently and through gene-gene interactions. Also, the effects of the polymorphisms were age-dependent.
[Mh] Termos MeSH primário: Grupo com Ancestrais do Continente Asiático/genética
Proteínas de Transporte de Cátions/genética
Epistasia Genética
Predisposição Genética para Doença
Síndrome de Linfonodos Mucocutâneos/genética
Fosfotransferases (Aceptor do Grupo Álcool)/genética
Polimorfismo de Nucleotídeo Único/genética
[Mh] Termos MeSH secundário: Vacina BCG/administração & dosagem
Estudos de Casos e Controles
Criança
Pré-Escolar
Eritema/complicações
Feminino
Estudos de Associação Genética
Seres Humanos
Lactente
Masculino
Taxa de Mutação
República da Coreia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (BCG Vaccine); 0 (Cation Transport Proteins); 0 (natural resistance-associated macrophage protein 1); EC 2.7.1.- (Phosphotransferases (Alcohol Group Acceptor)); EC 2.7.1.127 (Inositol 1,4,5-trisphosphate 3-kinase)
[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:171208
[St] Status:MEDLINE
[do] DOI:10.3349/ymj.2018.59.1.119


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[PMID]:29441964
[Au] Autor:Kono Y; Miyoshi S; Fujita T
[Ti] Título:Dextran sodium sulfate alters cytokine production in macrophages .
[So] Source:Pharmazie;71(11):619-624, 2016 Nov 02.
[Is] ISSN:0031-7144
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Macrophages have been assumed to have a crucial role in the development of inflammatory bowel disease (IBD). However, involvement of intestinal macrophages in IBD onset and functional alterations of macrophages during IBD development has not been clarified. We investigated the effect of exposure of compounds used in the induction of colitis in mice on the immune responses of peritoneal macrophages in mice. 2,4,6- trinitrobenzenesulfonic acid and oxazolone did not affect the production of interleukin (IL)-10 and IL-12 from lipopolysaccharide (LPS)-stimulated peritoneal macrophages from BALB/c mice. A significant increase in IL-10 secretion and decrease in IL-12 production from LPS-stimulated macrophages were observed upon exposure to dextran sodium sulfate (DSS). TNF-α production was enhanced significantly by exposure to DSS and LPS. The level of nitric-oxide production from macrophages was increased slightly by exposure to DSS and LPS. Expression of sphingosine kinase-1 and LIGHT (both of which are specific biomarkers of M2b macrophages) was observed in macrophages upon DSS exposure. Alteration of cytokine production in macrophages was observed upon DSS exposure in the absence of LPS stimulation. Peritoneal macrophages from C57BL/6 mice showed similar responses to peritoneal macrophages from BALB/c mice against DSS. These results suggest that DSS directs the immune response of macrophages towards the M2b phenotype.
[Mh] Termos MeSH primário: Citocinas/biossíntese
Sulfato de Dextrana/farmacologia
Macrófagos Peritoneais/metabolismo
[Mh] Termos MeSH secundário: Animais
Colite/induzido quimicamente
Colite/patologia
Feminino
Técnicas In Vitro
Interleucina-10/biossíntese
Interleucina-10/genética
Interleucina-12/biossíntese
Interleucina-12/genética
Lipopolissacarídeos/farmacologia
Macrófagos Peritoneais/efeitos dos fármacos
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Endogâmicos C57BL
Óxido Nítrico/biossíntese
Fosfotransferases (Aceptor do Grupo Álcool)/biossíntese
Fosfotransferases (Aceptor do Grupo Álcool)/genética
Especificidade da Espécie
Membro 14 da Superfamília de Ligantes de Fatores de Necrose Tumoral/biossíntese
Membro 14 da Superfamília de Ligantes de Fatores de Necrose Tumoral/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (IL10 protein, mouse); 0 (Lipopolysaccharides); 0 (Tnfsf14 protein, mouse); 0 (Tumor Necrosis Factor Ligand Superfamily Member 14); 130068-27-8 (Interleukin-10); 187348-17-0 (Interleukin-12); 31C4KY9ESH (Nitric Oxide); 9042-14-2 (Dextran Sulfate); EC 2.7.1.- (Phosphotransferases (Alcohol Group Acceptor)); EC 2.7.1.- (sphingosine kinase)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180215
[St] Status:MEDLINE
[do] DOI:10.1691/ph.2016.6688


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[PMID]:28460443
[Au] Autor:Fan Q; Cheng Y; Chang HM; Deguchi M; Hsueh AJ; Leung PCK
[Ad] Endereço:Department of Obstetrics and Gynaecology, British Columbia Children's Hospital Research Institute, University of British Columbia, Vancouver, British Columbia, V5Z 4H4, Canada.
[Ti] Título:Sphingosine-1-phosphate promotes ovarian cancer cell proliferation by disrupting Hippo signaling.
[So] Source:Oncotarget;8(16):27166-27176, 2017 Apr 18.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Epithelial ovarian carcinomas account for more than 90% of human ovarian cancers and have become the primary cause of death for gynecological malignancies. Unlimited cell proliferation and resistance to cell apoptosis contribute to the development of ovarian cancers. However, the underlying mechanisms involved in these processes in epithelial ovarian carcinomas are yet poorly understood. In the present study, we examined the Hippo signaling gene expression and investigated the effects of Sphingosine 1-phosphate (S1P) on cell proliferation and the underlying mechanisms in human ovarian cancer cell lines, OVCAR3 and SKOV3. Our results demonstrate that S1P disrupts Hippo signaling by reducing YAP phosphorylation and increasing the expression of CCN1 and CCN2 in both ovarian cancer cells. Furthermore, the increase in CCN1/CCN2 expression contributes to the S1P-induced increase in cancer cell proliferation.
[Mh] Termos MeSH primário: Lisofosfolipídeos/farmacologia
Neoplasias Ovarianas/metabolismo
Proteínas Serina-Treonina Quinases/metabolismo
Transdução de Sinais/efeitos dos fármacos
Esfingosina/análogos & derivados
[Mh] Termos MeSH secundário: Transporte Ativo do Núcleo Celular
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Fator de Crescimento do Tecido Conjuntivo/genética
Fator de Crescimento do Tecido Conjuntivo/metabolismo
Proteína Rica em Cisteína 61/genética
Proteína Rica em Cisteína 61/metabolismo
Feminino
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Seres Humanos
Proteínas Nucleares/metabolismo
Neoplasias Ovarianas/genética
Neoplasias Ovarianas/mortalidade
Neoplasias Ovarianas/patologia
Fosforilação
Fosfotransferases (Aceptor do Grupo Álcool)/genética
Fosfotransferases (Aceptor do Grupo Álcool)/metabolismo
Prognóstico
Esfingosina/farmacologia
Fatores de Transcrição/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cysteine-Rich Protein 61); 0 (Lysophospholipids); 0 (Nuclear Proteins); 0 (Transcription Factors); 0 (YY1AP1 protein, human); 139568-91-5 (Connective Tissue Growth Factor); 26993-30-6 (sphingosine 1-phosphate); EC 2.7.1.- (Phosphotransferases (Alcohol Group Acceptor)); EC 2.7.1.- (sphingosine kinase); EC 2.7.1.91 (sphingosine kinase 2, human); EC 2.7.11.1 (Hippo protein, human); EC 2.7.11.1 (Protein-Serine-Threonine Kinases); NGZ37HRE42 (Sphingosine)
[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:170503
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.15677


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[PMID]:28450417
[Au] Autor:Li H; Li Y; Xiang L; Zhang J; Zhu B; Xiang L; Dong J; Liu M; Xiang G
[Ad] Endereço:Department of Endocrinology, Wuhan General Hospital of Guangzhou Command, Wuhan, Hubei Province, China.
[Ti] Título:GDF11 Attenuates Development of Type 2 Diabetes via Improvement of Islet ß-Cell Function and Survival.
[So] Source:Diabetes;66(7):1914-1927, 2017 07.
[Is] ISSN:1939-327X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Growth differentiation factor 11 (GDF11) has been implicated in the regulation of islet development and a variety of aging conditions, but little is known about the physiological functions of GDF11 in adult pancreatic islets. Here, we showed that systematic replenishment of GDF11 not only preserved insulin secretion but also improved the survival and morphology of ß-cells and improved glucose metabolism in both nongenetic and genetic mouse models of type 2 diabetes (T2D). Conversely, anti-GDF11 monoclonal antibody treatment caused ß-cell failure and lethal T2D. In vitro treatment of isolated murine islets and MIN6 cells with recombinant GDF11 attenuated glucotoxicity-induced ß-cell dysfunction and apoptosis. Mechanistically, the GDF11-mediated protective effects could be attributed to the activation of transforming growth factor-ß/Smad2 and phosphatidylinositol-4,5-bisphosphate 3-kinase-AKT-FoxO1 signaling. These findings suggest that GDF11 repletion may improve ß-cell function and mass and thus may lead to a new therapeutic approach for T2D.
[Mh] Termos MeSH primário: Glicemia/efeitos dos fármacos
Proteínas Morfogenéticas Ósseas/farmacologia
Diabetes Mellitus Experimental/metabolismo
Diabetes Mellitus Tipo 2/metabolismo
Fatores de Diferenciação de Crescimento/farmacologia
Células Secretoras de Insulina/efeitos dos fármacos
Insulina/secreção
[Mh] Termos MeSH secundário: Animais
Anticorpos Monoclonais/farmacologia
Apoptose
Glicemia/metabolismo
Western Blotting
Proteínas Morfogenéticas Ósseas/antagonistas & inibidores
Linhagem Celular
Sobrevivência Celular/efeitos dos fármacos
Dieta Hiperlipídica
Modelos Animais de Doenças
Proteína Forkhead Box O1/efeitos dos fármacos
Proteína Forkhead Box O1/metabolismo
Teste de Tolerância a Glucose
Fatores de Diferenciação de Crescimento/antagonistas & inibidores
Células Secretoras de Insulina/secreção
Ilhotas Pancreáticas/efeitos dos fármacos
Ilhotas Pancreáticas/secreção
Camundongos
Fosfotransferases (Aceptor do Grupo Álcool)/efeitos dos fármacos
Fosfotransferases (Aceptor do Grupo Álcool)/metabolismo
Proteínas Proto-Oncogênicas c-akt/efeitos dos fármacos
Proteínas Proto-Oncogênicas c-akt/metabolismo
Reação em Cadeia da Polimerase em Tempo Real
Receptores para Leptina/genética
Transdução de Sinais/efeitos dos fármacos
Proteína Smad2/efeitos dos fármacos
Proteína Smad2/metabolismo
Fator de Crescimento Transformador beta/efeitos dos fármacos
Fator de Crescimento Transformador beta/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Blood Glucose); 0 (Bone Morphogenetic Proteins); 0 (Forkhead Box Protein O1); 0 (Foxo1 protein, mouse); 0 (Gdf11 protein, mouse); 0 (Growth Differentiation Factors); 0 (Insulin); 0 (Receptors, Leptin); 0 (Smad2 Protein); 0 (Smad2 protein, mouse); 0 (Transforming Growth Factor beta); 0 (leptin receptor, mouse); EC 2.7.1.- (Phosphotransferases (Alcohol Group Acceptor)); EC 2.7.1.- (phosphatidylinositol 4,5-biphosphate kinase); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:180108
[Lr] Data última revisão:
180108
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.2337/db17-0086


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[PMID]:29175388
[Au] Autor:Chen Q; Zheng Y; Luo L; Yang Y; Hu X; Kong X
[Ad] Endereço:Key Laboratory for Plant Diversity and Biogeography of East Asia, Kunming Institute of Botany, Chinese Academy of Sciences, Kunming 650201, China.
[Ti] Título:Functional FRIGIDA allele enhances drought tolerance by regulating the P5CS1 pathway in Arabidopsis thaliana.
[So] Source:Biochem Biophys Res Commun;495(1):1102-1107, 2018 01 01.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Flowering at the right time is important for the reproductive success of plants and their response to environmental stress. In Arabidopsis, a major determinant of natural variation in flowering time is FRIGIDA (FRI). In the present study, we show that overexpression of the functional FRIGIDA gene in wild-type Col background (ColFRI) positively enhances the drought tolerance by activating P5CS1 expression and promoting proline accumulation during water stress. Furthermore, no significant changes in FRI gene and protein expression levels were observed with drought treatment, whereas P5CS1 protein expression significantly increased. In contrast, vernalization treatment efficiently reduced P5CS1 expression levels and resulted in a decrease in drought tolerance in the ColFRI plants. The flc mutants with a functional FRI background also relieved FRI-mediated activation of P5CS1 during drought tolerance. Taken together, our findings reveal the novel function of FRI in enhancing drought resistance through its downstream P5CS1 pathway during water-deficit stress, which is dependent on its target, the FLC gene.
[Mh] Termos MeSH primário: Proteínas de Arabidopsis/genética
Proteínas de Arabidopsis/metabolismo
Arabidopsis/fisiologia
Secas
Regulação da Expressão Gênica de Plantas/fisiologia
Glutamato-5-Semialdeído Desidrogenase/metabolismo
Redes e Vias Metabólicas/fisiologia
Complexos Multienzimáticos/metabolismo
Fosfotransferases (Aceptor do Grupo Álcool)/metabolismo
Estresse Fisiológico/fisiologia
[Mh] Termos MeSH secundário: Alelos
Flores/genética
Flores/crescimento & desenvolvimento
Glutamato-5-Semialdeído Desidrogenase/genética
Complexos Multienzimáticos/genética
Fosfotransferases (Aceptor do Grupo Álcool)/genética
Plantas Geneticamente Modificadas/fisiologia
Prolina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Arabidopsis Proteins); 0 (FRI protein, Arabidopsis); 0 (Multienzyme Complexes); 0 (delta(1)-pyrroline-5-carboxylate synthetase, Arabidopsis); 9DLQ4CIU6V (Proline); EC 1.2.1.41 (Glutamate-5-Semialdehyde Dehydrogenase); EC 2.7.1.- (Phosphotransferases (Alcohol Group Acceptor))
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180105
[Lr] Data última revisão:
180105
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171128
[St] Status:MEDLINE


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[PMID]:29277765
[Au] Autor:Yang G; Qiu J; Wang D; Tao Y; Song Y; Wang H; Tang J; Wang X; Sun YU; Yang Z; Hoffman RM
[Ad] Endereço:Hangzhou Third Hospital, Hangzhou, P.R. China.
[Ti] Título:Traditional Chinese Medicine Curcumin Sensitizes Human Colon Cancer to Radiation by Altering the Expression of DNA Repair-related Genes.
[So] Source:Anticancer Res;38(1):131-136, 2018 01.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIM: The aim of the present study was to investigate the radio-sensitizing efficacy of curcumin, a traditional Chinese medicine (TCM) on colon cancer cells in vitro and in vivo. MATERIALS AND METHODS: Human colon cancer HT-29 cells were treated with curcumin (2.5 µM), irradiation (10 Gy) and the combination of irradiation and curcumin. Cell proliferation was assessed using the MTT assay. Apoptotic cells were detected by Annexin V-PE/7-AAD analysis. PCR was performed to determine differential-expression profiling of 95 DNA-repair genes in irradiated cells and cells treated with both irradiation and curcumin. Differentially-expressed genes were confirmed by Western blotting. In vivo radio-sensitizing efficacy of curcumin was assessed in a xenograft mouse model of HT-29 colon cancer. Curcumin was administrated daily by intraperitoneal injection at 20 mg/kg/dose. Mice received irradiation (10 Gy) twice weekly. Apoptosis of the cancer cells following treatment was determined by TUNEL staining. RESULTS: Irradiation induced proliferation inhibition and apoptosis of HT-29 cells in vitro. Concurrent curcumin treatment sensitized the HT-29 tumor to irradiation (p<0.01). DNA repair-related genes CCNH and XRCC5 were upregulated and LIG4 and PNKP downregulated by the combination of curcumin and irradiation compared with irradiation alone (p<0.05). Combined treatment of curcumin and irradiation resulted in a significantly greater tumor-growth inhibition and apoptosis compared to irradiation treatment alone (p<0.01). CONCLUSION: Curcumin sensitizes human colon cancer in vitro and in vivo to radiation. Downregulation of LIG4 and PNKP and upregulation of XRCC5 and CCNH DNA-repair-related genes were involved in the radio-sensitizing efficacy of curcumin in colon cancer.
[Mh] Termos MeSH primário: Neoplasias do Colo/tratamento farmacológico
Neoplasias do Colo/radioterapia
Curcumina/farmacologia
Curcumina/uso terapêutico
Radiossensibilizantes/farmacologia
Radiossensibilizantes/uso terapêutico
[Mh] Termos MeSH secundário: Animais
Apoptose/efeitos dos fármacos
Apoptose/efeitos da radiação
Proliferação Celular/efeitos dos fármacos
Proliferação Celular/efeitos da radiação
Neoplasias do Colo/metabolismo
Neoplasias do Colo/patologia
Ciclina H/genética
Ciclina H/metabolismo
DNA Ligase Dependente de ATP/genética
DNA Ligase Dependente de ATP/metabolismo
Reparo do DNA/genética
Enzimas Reparadoras do DNA/genética
Enzimas Reparadoras do DNA/metabolismo
Feminino
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Regulação Neoplásica da Expressão Gênica/efeitos da radiação
Células HT29
Seres Humanos
Autoantígeno Ku/genética
Autoantígeno Ku/metabolismo
Medicina Tradicional Chinesa
Camundongos Endogâmicos BALB C
Camundongos Nus
Fosfotransferases (Aceptor do Grupo Álcool)/genética
Fosfotransferases (Aceptor do Grupo Álcool)/metabolismo
Carga Tumoral/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CCNH protein, human); 0 (Cyclin H); 0 (LIG4 protein, human); 0 (Radiation-Sensitizing Agents); EC 2.7.1.- (PNKP protein, human); EC 2.7.1.- (Phosphotransferases (Alcohol Group Acceptor)); EC 3.6.4.12 (XRCC5 protein, human); EC 4.2.99.- (Ku Autoantigen); EC 6.5.1.- (DNA Repair Enzymes); EC 6.5.1.1 (DNA Ligase ATP); IT942ZTH98 (Curcumin)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180104
[Lr] Data última revisão:
180104
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171227
[St] Status:MEDLINE


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[PMID]:29233590
[Au] Autor:Spry C; Sewell AL; Hering Y; Villa MVJ; Weber J; Hobson SJ; Harnor SJ; Gul S; Marquez R; Saliba KJ
[Ad] Endereço:Research School of Biology, The Australian National University, Canberra, ACT 2601, Australia.
[Ti] Título:Structure-activity analysis of CJ-15,801 analogues that interact with Plasmodium falciparum pantothenate kinase and inhibit parasite proliferation.
[So] Source:Eur J Med Chem;143:1139-1147, 2018 Jan 01.
[Is] ISSN:1768-3254
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:Survival of the human malaria parasite Plasmodium falciparum is dependent on pantothenate (vitamin B ), a precursor of the fundamental enzyme cofactor coenzyme A. CJ-15,801, an enamide analogue of pantothenate isolated from the fungus Seimatosporium sp. CL28611, was previously shown to inhibit P. falciparum proliferation in vitro by targeting pantothenate utilization. To inform the design of next generation analogues, we set out to synthesize and test a series of synthetic enamide-bearing pantothenate analogues. We demonstrate that conservation of the R-pantoyl moiety and the trans-substituted double bond of CJ-15,801 is important for the selective, on-target antiplasmodial effect, while replacement of the carboxyl group is permitted, and, in one case, favored. Additionally, we show that the antiplasmodial potency of CJ-15,801 analogues that retain the R-pantoyl and trans-substituted enamide moieties correlates with inhibition of P. falciparum pantothenate kinase (PfPanK)-catalyzed pantothenate phosphorylation, implicating the interaction with PfPanK as a key determinant of antiplasmodial activity.
[Mh] Termos MeSH primário: Antimaláricos/farmacologia
Ácido Pantotênico/análogos & derivados
Fosfotransferases (Aceptor do Grupo Álcool)/antagonistas & inibidores
Plasmodium falciparum/efeitos dos fármacos
[Mh] Termos MeSH secundário: Antimaláricos/síntese química
Antimaláricos/química
Proliferação Celular/efeitos dos fármacos
Relação Dose-Resposta a Droga
Seres Humanos
Estrutura Molecular
Ácido Pantotênico/síntese química
Ácido Pantotênico/química
Ácido Pantotênico/farmacologia
Testes de Sensibilidade Parasitária
Fosfotransferases (Aceptor do Grupo Álcool)/metabolismo
Plasmodium falciparum/enzimologia
Relação Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antimalarials); 0 (CJ-15,801); 19F5HK2737 (Pantothenic Acid); EC 2.7.1.- (Phosphotransferases (Alcohol Group Acceptor)); EC 2.7.1.33 (pantothenate kinase)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180101
[Lr] Data última revisão:
180101
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171214
[St] Status:MEDLINE


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[PMID]:28471356
[Au] Autor:Ha JH; Eo Y; Ahn HC; Ryu KS
[Ad] Endereço:Protein Structure Group, Korea Basic Science Institute, 162 Yeongudanji-ro, Ochang-eup, Cheongju-si, Chungcheongbuk-do 28119, Republic of Korea.
[Ti] Título:Increasing the soluble expression and crystallization of the Escherichia coli quorum-sensing protein LsrK.
[So] Source:Acta Crystallogr F Struct Biol Commun;73(Pt 5):253-258, 2017 May 01.
[Is] ISSN:2053-230X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:LsrK is one of the key components of the luxS-regulated (lsr) operon in Escherichia coli and plays an important role during the quorum-sensing (QS) process mediated by autoinducer-2 (AI-2). The AI-2 molecule is imported into the cell by the LsrACB transporter and is subsequently phosphorylated (to AI-2-P) by LsrK. AI-2-P binds to the repressor protein of the lsr operon (LsrR) and triggers various cellular responses related to QS by dissociating LsrR from the DNA. Although a large amount of purified LsrK is required for structural studies, recombinant GST-LsrK was mostly expressed in an insoluble form. To enhance the soluble expression of LsrK, an attempt was made to increase the expression of the cellular chaperone proteins that are well known to support proper protein folding. Transformed E. coli was cultured in high-salt LB medium and heat shock was applied prior to subsequent IPTG induction at 20°C. These procedures increased the yield of purified LsrK by about tenfold compared with standard IPTG induction at 20°C. The expressed LsrK was readily purified by GST-affinity chromatography. Crystals of LsrK were grown by the hanging-drop vapour-diffusion method. The X-ray diffraction data of the crystal were processed in a primitive hexagonal space group to 2.9 Šresolution.
[Mh] Termos MeSH primário: Cristalização/métodos
Proteínas de Escherichia coli/química
Escherichia coli/genética
Fosfotransferases (Aceptor do Grupo Álcool)/química
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Clonagem Molecular
Cristalografia por Raios X
Meios de Cultura/farmacologia
Escherichia coli/efeitos dos fármacos
Escherichia coli/metabolismo
Proteínas de Escherichia coli/genética
Proteínas de Escherichia coli/metabolismo
Expressão Gênica
Vetores Genéticos/química
Vetores Genéticos/metabolismo
Temperatura Alta
Isopropiltiogalactosídeo/farmacologia
Óperon
Fosfotransferases (Aceptor do Grupo Álcool)/genética
Fosfotransferases (Aceptor do Grupo Álcool)/metabolismo
Percepção de Quorum/genética
Proteínas Recombinantes/química
Proteínas Recombinantes/genética
Proteínas Recombinantes/metabolismo
Solubilidade
Difração de Raios X
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Culture Media); 0 (Escherichia coli Proteins); 0 (Recombinant Proteins); 367-93-1 (Isopropyl Thiogalactoside); EC 2.7.1.- (LsrK protein, E coli); EC 2.7.1.- (Phosphotransferases (Alcohol Group Acceptor))
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171204
[Lr] Data última revisão:
171204
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1107/S2053230X1700468X


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[PMID]:27776973
[Au] Autor:Ramazzotti G; Faenza I; Fiume R; Billi AM; Manzoli L; Mongiorgi S; Ratti S; McCubrey JA; Suh PG; Cocco L; Follo MY
[Ad] Endereço:Cellular Signalling Laboratory, Department of Biomedical and Neuromotor Sciences, University of Bologna, Bologna, Italy. Electronic address: giulia.ramazzotti@unibo.it.
[Ti] Título:PLC-ß1 and cell differentiation: An insight into myogenesis and osteogenesis.
[So] Source:Adv Biol Regul;63:1-5, 2017 Jan.
[Is] ISSN:2212-4934
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Phosphoinositide-phospholipase C-ß1 (PLC-ß1) plays a crucial role in the initiation of the genetic program responsible for muscle differentiation and osteogenesis. During myogenic differentiation of murine C2C12 myoblasts, PLC-ß1 signaling pathway involves the Inositol Polyphosphate Multikinase (IPMK) and ß-catenin as downstream effectors. By means of c-jun binding to cyclin D3 promoter, the activation of PLC-ß1 pathway determines cyclin D3 accumulation. However, osteogenesis requires PLC-ß1 expression and up-regulation but it does not affect cyclin D3 levels, suggesting that the two processes require the activation of different mediators.
[Mh] Termos MeSH primário: Desenvolvimento Muscular/genética
Mioblastos/metabolismo
Osteoblastos/metabolismo
Osteogênese/genética
Fosfolipase C beta/genética
[Mh] Termos MeSH secundário: Animais
Diferenciação Celular
Linhagem Celular
Ciclina D3/genética
Ciclina D3/metabolismo
Regulação da Expressão Gênica no Desenvolvimento
Proteínas Quinases JNK Ativadas por Mitógeno/genética
Proteínas Quinases JNK Ativadas por Mitógeno/metabolismo
Camundongos
Mioblastos/citologia
Osteoblastos/citologia
Fosfolipase C beta/metabolismo
Fosfotransferases (Aceptor do Grupo Álcool)/genética
Fosfotransferases (Aceptor do Grupo Álcool)/metabolismo
Regiões Promotoras Genéticas
Ligação Proteica
Transdução de Sinais
beta Catenina/genética
beta Catenina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (CTNNB1 protein, mouse); 0 (Ccnd3 protein, mouse); 0 (Cyclin D3); 0 (beta Catenin); EC 2.7.1.- (Phosphotransferases (Alcohol Group Acceptor)); EC 2.7.1.- (inositol polyphosphate multikinase); EC 2.7.11.24 (JNK Mitogen-Activated Protein Kinases); EC 3.1.4.11 (Phospholipase C beta); EC 3.1.4.11 (Plcb1 protein, mouse)
[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:161026
[St] Status:MEDLINE


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[PMID]:29056104
[Au] Autor:Cuthbert CE; Foster JE; Ramdath DD
[Ad] Endereço:1Department of Pre-Clinical Sciences, Faculty of Medical Sciences,The University of the West Indies,St. Augustine,Trinidad and Tobago, West Indies.
[Ti] Título:A maternal high-fat, high-sucrose diet alters insulin sensitivity and expression of insulin signalling and lipid metabolism genes and proteins in male rat offspring: effect of folic acid supplementation.
[So] Source:Br J Nutr;118(8):580-588, 2017 Oct.
[Is] ISSN:1475-2662
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:A maternal high-fat, high-sucrose (HFS) diet alters offspring glucose and lipid homoeostasis through unknown mechanisms and may be modulated by folic acid. We investigated the effect of a maternal HFS diet on glucose homoeostasis, expression of genes and proteins associated with insulin signalling and lipid metabolism and the effect of prenatal folic acid supplementation (HFS/F) in male rat offspring. Pregnant Sprague-Dawley rats were randomly fed control (CON), HFS or HFS/F diets. Offspring were weaned on CON; at postnatal day 70, fasting plasma insulin and glucose and liver and skeletal muscle gene and protein expression were measured. Treatment effects were assessed by one-way ANOVA. Maternal HFS diet induced higher fasting glucose in offspring v. HFS/F (P=0·027) and down-regulation (P<0·05) of genes coding for v-Akt murine thymoma viral oncogene homolog 2, resistin and v-Raf-1 murine leukaemia viral oncogene homolog 1 (Raf1) in offspring skeletal muscle and acetyl-CoA carboxylase (Acaca), fatty acid synthase and phosphatidylinositol-4,5-biphosphate 3-kinase, catalytic subunit ß in offspring liver. Skeletal muscle neuropeptide Y and hepatic Kruppel-like factor 10 were up-regulated in HFS v. CON offspring (P<0·05). Compared with CON, Acaca and Raf1 protein expression levels were significantly lower in HFS offspring. Maternal HFS induced higher homoeostasis model of assessment index of insulin resistance v. CON (P=0·030) and HFS/F was associated with higher insulin (P=0·016) and lower glucose (P=0·025). Maternal HFS diet alters offspring insulin sensitivity and de novo hepatic lipogenesis via altered gene and protein expression, which appears to be potentiated by folate supplementation.
[Mh] Termos MeSH primário: Dieta Hiperlipídica
Resistência à Insulina
Insulina/sangue
Metabolismo dos Lipídeos
Fenômenos Fisiológicos da Nutrição Materna
[Mh] Termos MeSH secundário: Acetil-CoA Carboxilase/genética
Acetil-CoA Carboxilase/metabolismo
Animais
Animais Recém-Nascidos
Glicemia/metabolismo
Regulação para Baixo
Ácido Graxo Sintases/genética
Ácido Graxo Sintases/metabolismo
Feminino
Ácido Fólico/administração & dosagem
Fígado/metabolismo
Masculino
Fosfotransferases (Aceptor do Grupo Álcool)/genética
Fosfotransferases (Aceptor do Grupo Álcool)/metabolismo
Gravidez
Efeitos Tardios da Exposição Pré-Natal
Proteínas Proto-Oncogênicas c-akt/genética
Proteínas Proto-Oncogênicas c-akt/metabolismo
Proteínas Proto-Oncogênicas c-raf/genética
Proteínas Proto-Oncogênicas c-raf/metabolismo
Ratos
Ratos Sprague-Dawley
Resistina/genética
Resistina/metabolismo
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Blood Glucose); 0 (Insulin); 0 (Resistin); 0 (Retn protein, rat); 935E97BOY8 (Folic Acid); EC 2.3.1.85 (Fatty Acid Synthases); EC 2.7.1.- (Phosphotransferases (Alcohol Group Acceptor)); EC 2.7.1.- (phosphatidylinositol 4,5-biphosphate kinase); EC 2.7.11.1 (Akt2 protein, rat); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); EC 2.7.11.1 (Proto-Oncogene Proteins c-raf); EC 2.7.11.1 (Raf1 protein, rat); EC 6.4.1.2 (Acetyl-CoA Carboxylase)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171030
[Lr] Data última revisão:
171030
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171024
[St] Status:MEDLINE
[do] DOI:10.1017/S0007114517002501



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