RESUMEN
The invertase mutant defective in the glucose signaling pathway of Schizosaccharomyces pombe (ird11) is resistant to glucose repression. This mutant is able to consume sucrose alongside glucose and grows in glucose-containing media with a generation time close to that of the wild type. Intracellular oxidation, protein carbonyl, and reduced glutathione levels and catalase, superoxide dismutase, and glutathione peroxidase activity were investigated in ird11, to determine the relationship between oxidative stress response and glucose signaling. The expression profiles of some genes involved in regulation of glucose repression (fbp1, fructose-1,6-bis-phosphatase; hxk2, hexokinase) and stress response (atf1 and pap1 transcription factors; ctt1, catalase; sod1, Cu,Zn superoxide dismutase) were analyzed using the quantitative real-time PCR technique. Oxidative stress response in ird11 seems to be affected by glucose signaling in a manner different from that caused by glucose deprivation.
Asunto(s)
Glucosa/metabolismo , Estrés Oxidativo , Proteínas de Schizosaccharomyces pombe/genética , Schizosaccharomyces/metabolismo , Transducción de Señal , Proteínas Asociadas a Pancreatitis , Reacción en Cadena en Tiempo Real de la Polimerasa , Schizosaccharomyces/genética , Proteínas de Schizosaccharomyces pombe/metabolismo , Superóxido Dismutasa/metabolismo , beta-Fructofuranosidasa/genética , beta-Fructofuranosidasa/metabolismoRESUMEN
We aim to ascertain the possible involvement of functional IL10 and TNF-α promoter polymorphisms on the susceptibility to Behçet's syndrome (BS), to examine whether IL10 and TNF-α genotypes might work synergistically influencing susceptibility to BS. IL10 -1082G/A, -819C/T and -592C/A and TNF -308G/A polymorphisms were analyzed in 102 Turkish patients with BS and 102 healthy subjects by using amplification refractory mutation system-polymerase chain reaction (ARMS-PCR). We have found no significant associations between IL10 -1082G/A, -819C/T, -592C/A, TNF-α -308G/A polymorphisms and BS. Also, no significant correlation was found between IL10 GCC, ACC, ATA haplotypes, GCC(+)/GCC(+), GCC(+)/GCC(-), GCC(-)/GCC(-) genotypes. There was no significant association between combined TNF-α/IL10 genotypes and BS. Our study indicates that functional TNF-α, IL10 genotypes or combined TNF-α, IL10 genotypes do not play a role in BS susceptibility in Turkish BS patients.
Asunto(s)
Síndrome de Behçet/genética , Interleucina-10/genética , Factor de Necrosis Tumoral alfa/genética , Adulto , Estudios de Casos y Controles , Demografía , Femenino , Genotipo , Humanos , Masculino , Persona de Mediana Edad , Polimorfismo de Nucleótido Simple/genéticaRESUMEN
Natural resistance associated macrophage protein 1 (NRAMP1), also named as solute carrier family 11 member A1 gene (SLC11A1), has multiple pleiotropic effects on macrophage activation pathways such as up-regulation of the CXC chemokine KC, tumor necrosis factor alpha (TNF-alpha), interleukin-1 b (IL-1 b), inducible nitric oxide syntase (iNOS), and major histocompatibility complex (MHC) class II expression. Since NRAMP1 plays a role in the up-regulation of the TNF-alpha, iNOS and MHC expression, it may also be a candidate gene for Behçet's syndrome (BS). We analyzed the association of NRAMP1 polymorphisms [(GT)( n ), INT4, 3'UTR and D543N] in 102 Turkish patients with BS and 102 healthy subjects by using amplification refractory mutation system-polymerase chain reaction (ARMS-PCR). We found a significant association between BS and NRAMP1 INT4 G/C allele frequency (p = 0.004, OR = 1.88, 95% CI = 1.21-2.93). However, there were no significant differences in the distribution of allele frequencies of NRAMP1 (GT)( n ), 3'UTR, D543N polymorphisms between BS patients and healthy controls. There was also no correlation between NRAMP1 polymorphisms and clinical manifestations of BS. Our study suggests that NRAMP1 may be one of the plausible candidate genes for BS. However, it is likely that INT4 polymorphism is not disease-specific and seems to be common to immune-mediated diseases.