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1.
Int. microbiol ; 18(4): 235-244, dic. 2015. tab, ilus, graf
Artigo em Inglês | IBECS | ID: ibc-153127

RESUMO

Thermotolerant ethanologenic yeast Kluyveromyces marxianus is capable of fermenting various sugars including xylose but glucose represses to hamper the utilization of other sugars. To acquire glucose repression-defective strains, 33 isolates as 2-deoxyglucose (2-DOG)-resistant mutants were acquired from about 100 colonies grown on plates containing 2-DOG, which were derived from an efficient strain DMKU 3-1042. According to the characteristics of sugar consumption abilities and cell growth and ethanol accumulation along with cultivation time, they were classified into three groups. The first group (3 isolates) utilized glucose and xylose in similar patterns along with cultivation to those of the parental strain, presumably due to reduction of the uptake of 2-DOG or enhancement of its export. The second group (29 isolates) showed greatly delayed utilization of glucose, presumably by reduction of the uptake or initial catabolism of glucose. The last group, only one isolate, showed enhanced utilization ability of xylose in the presence of glucose. Further analysis revealed that the isolate had a single nucleotide mutation to cause amino acid substitution (G270S) in RAG5 encoding hexokinase and exhibited very low activity of the enzyme. The possible mechanism of defectiveness of glucose repression in the mutant is discussed in this paper (AU)


No disponible


Assuntos
Kluyveromyces/patogenicidade , Xilose/farmacocinética , Proteínas Repressoras/genética , Desoxiglucose/genética , Fermentação , Resposta ao Choque Térmico , Nucleotídeos/genética , Glucose/metabolismo
3.
Int. microbiol ; 16(3): 165-176, sept. 2013. ilus, tab
Artigo em Inglês | IBECS | ID: ibc-118207

RESUMO

Bacteria, fungi, and plants have metabolic pathways for the utilization of nitrogen present in purine bases. In Klebsiella pneumoniae, the genes responsible for the assimilation of purine ring nitrogen are distributed in three separated clusters. We characterized the gene cluster involved in the metabolism of allantoate (genes KPN_01761 to KPN_01771). The functional assignments of HpxK, as an allantoate amidohydrolase, and of HpxU, as a regulator involved in the control of allantoate metabolism, were assessed experimentally. Gene hpxU encodes a repressor of the RpiR family that mediates the regulation of this system by allantoate. In this study, the binding of HpxU to the hpxF promoter and to the hpxU-hpxW intergenic region containing the divergent promoter for these genes was evidenced by electrophoretic mobility shift assays. Allantoate released the HpxU repressor from its target operators whereas other purine intermediate metabolites, such as allantoin and oxamate, failed to induce complex dissociation. Sequence alignment of the four HpxU identified operators identified TGAA-N8-TTCA as the consensus motif recognized by the HpxU repressor (AU)


No disponible


Assuntos
Humanos , Klebsiella pneumoniae/genética , Elementos Reguladores de Transcrição/genética , Proteína Receptora de AMP Cíclico/genética , Amidoidrolases/análise , Proteínas Repressoras/análise , Mutagênese
4.
Int. microbiol ; 13(1): 33-39, mar. 2010. ilus, tab
Artigo em Inglês | IBECS | ID: ibc-87670

RESUMO

Anaerobic metabolism is controlled by several transcriptional regulators, including ArcA, Fnr, NarP, and NarL, with the Fnr and ArcA proteins sensitive to the cell's redox status. Specifically, the two-component ArcAB system is activated in response to the oxidation state of membrane-bound quinones, which are the central electron carriers of respiration. Fnr, by contrast, directly senses cellular oxidation status through the [4Fe-4S] cluster present in its own structure. In this study, a third additional redox-associated pathway that controls the nitrate respiration regulators NarL and NarP was identified. The results showed that, in Salmonella enterica, the expression of these two transcriptional regulators is under the control of Fur, a metalloregulator that senses the presence of Fe2+ and regulates the homeostasis of this cation inside the cell. Thus, the Fur- Fe2+ complex increases the expression of narL and represses that of narP. Furthermore, studies of S. enteric mutants defective in the Fur-regulated sRNA RfrA and RfrB showed that those sRNA control both narP and narL expression. These results confirm Fur as a global regulator based on its involvement not only in iron uptake and detoxification but also in the control of nitrate/nitrite respiration by sensing cellular redox status (AU)


No disponible


Assuntos
Proteínas de Bactérias/metabolismo , Proteínas de Ligação a DNA/biossíntese , Regulação Bacteriana da Expressão Gênica , Nitratos/metabolismo , Proteínas Repressoras/metabolismo , Salmonella enterica/fisiologia , Fatores de Transcrição/biossíntese , Proteínas de Bactérias/biossíntese , Ferro/metabolismo , Oxirredução , Salmonella enterica/metabolismo
6.
Eur. j. anat ; 6(3): 161-165, dic. 2002. ilus
Artigo em Inglês | IBECS | ID: ibc-17925

RESUMO

Endomyocardial biopsies from patients with dilated cardiomyopathy were obtained by cardiac catheterization. Tissue samples were embedded in epoxy resin and sectioned into serial semithin sections for immunohistochemical visualization of either the apoptosis repressor protein or the FLICE inhibitory protein. Colocalization of apoptosis repressor protein and FLICE inhibitory protein was observed in cardiac myocytes, with nuclear DNA fragmentation and myofibrillary degradation. Intact myocytes were devoid of FLICE inhibitory protein and apoptosis repressor protein staining. FLICE (Fas-associated death-domain-like IL-1-converting enzyme) inhibitory protein and apoptosis repressor protein were localized in the perinuclear cytoplasm, mainly in areas that showed myofibrillary degradation as visualized by fluorescence microscopy. FLICE inhibitory and apoptosis repressor proteins may be intracellular markers for monitoring myocardial damage in several cardiac diseases in humans (AU)


Se obtuvieron biopsias endomiocárdicas de pacientes con cardiomiopatía prolongada mediante cateterización cardíaca. Las muestras de tejido fueron incluidas en resina epoxi y se hicieron cortes semifinos seriados para la visualización inmunohistoquímica de la proteína represora de apoptosis o la proteína inhibidota FLICE. Se observó la colocalización de la proteína represora de apoptosis y la proteína inhibidora FLICE en los miocitos cardíacos, con fragmentación nuclear del DNA y degradación miofibrilar. Los miocitos intactos carecieron de tinción para la proteína inhibidora FLICE y la proteína represora de apoptosis. La proteína inhibidora FLICE (Fas-associated death-domain-like IL-1 -converting enzyme) y la proteína represora de apoptosis se localizaron en el citoplasma perinuclear, principalmente en áreas que mostraban degradación miofibrilar, según se observó mediante microscopía de fluorescencia. Ambas proteínas pueden ser marcadores intracelulares para vigilar y valorar el daño miocárdico en diversas enfermedades cardíacas en humanos (AU)


Assuntos
Humanos , Apoptose , Endocárdio/patologia , Proteínas Repressoras/análise , Cardiomiopatias/patologia , Biópsia , Imuno-Histoquímica , Microscopia de Fluorescência , Biomarcadores
7.
Rev. neurol. (Ed. impr.) ; 34(supl.1): 54-58, 28 feb., 2002.
Artigo em Espanhol | IBECS | ID: ibc-27816

RESUMO

Introducción. El síndrome de Rett (SR), una enfermedad neurológica del desarrollo que constituye la segunda causa de retraso mental profundo en el sexo femenino, es provocada en la mayoría de los casos por mutaciones de novo en un gen situado en el cromosoma X, gen que codifica la proteína de unión a las metil-CpG (MECP2); se han descubierto mutaciones en este gen en aproximadamente un 80 por ciento de los casos comprobados que presentan la forma clásica del SR. También se encontraron mutaciones en el gen MECP2 en aproximadamente un tercio de los casos de SR no clásicos e incluso en otras enfermedades: mujeres con retraso mental leve o profundo, niños con autismo e incluso niños con encefalopatía neonatal o con un cuadro clínico similar al del SR. Desarrollo. Los estudios de correlación genotipo-fenotipo en el SR clásico sugieren que el patrón de inactivación del cromosoma X tiene un efecto más importante en la determinación de la gravedad de la enfermedad que el tipo o la localización de la mutación. Sin embargo, cuando se considera la totalidad de los fenotipos asociados a las mutaciones MECP2, se comprueba que el tipo de mutación tiene alguna correlación con la presentación clínica o la gravedad de la enfermedad. Conclusión. Los recientes avances en la genética del SR presentan, por lo tanto, aplicaciones concretas en el panorama clínico, y proporcionan marcadores auxiliares de diagnóstico y posibles indicadores de pronóstico, así como para el consejo genético a las familias de pacientes con SR (AU)


Assuntos
Feminino , Criança , Humanos , Proteínas Repressoras , Fenótipo , Cromossomos Humanos X , Proteínas Cromossômicas não Histona , Marcadores Genéticos , Mutação , Genótipo , Síndrome de Rett , Proteínas de Ligação a DNA
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