selenoprotein/feber

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Computational genomic analysis of hemorrhagic fever viruses. Viral selenoproteins as a potential factor in pathogenesis.

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A number of distinct viruses are known as hemorrhagic fever viruses based on a shared ability to induce hemorrhage by poorly understood mechanisms, typically involving the formation of blood clots ("disseminated intravascular coagulation"). It is well documented that selenium plays a significant

The tick endosymbiont Candidatus Midichloria mitochondrii and selenoproteins are essential for the growth of Rickettsia parkeri in the Gulf Coast tick vector.

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BACKGROUND Pathogen colonization inside tick tissues is a significant aspect of the overall competence of a vector. Amblyomma maculatum is a competent vector of the spotted fever group rickettsiae, Rickettsia parkeri. When R. parkeri colonizes its tick host, it has the opportunity to dynamically

Genomic structures of viral agents in relation to the biosynthesis of selenoproteins.

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The genomes of both bacteria and eukaryotic organisms are known to encode selenoproteins, using the UGA codon for seleno-cysteine (SeC), and a complex cotranslational mechanism for SeC incorporation into polypeptide chains, involving RNA stem-loop structures. These common features and similar codon

Amblyomma maculatum SECIS binding protein 2 and putative selenoprotein P are indispensable for pathogen replication and tick fecundity.

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Selenium, a vital trace element, is incorporated into selenoproteins to produce selenocysteine. Our previous studies have revealed an adaptive co-evolutionary process that has enabled the spotted fever-causing tick-borne pathogen Rickettsia parkeri to survive by manipulating an antioxidant defense

Expression of Selenoprotein Genes Is Affected by Heat Stress in IPEC-J2 Cells.

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The aim of this study was to explore the impacts of heat stress (HS) on expressions of selenoprotein genes in IPEC-J2 cells. Cells were cultured with 5 % CO2-humidified chamber at 37 °C until the cells grew to complete confluence and then exposed to a mild hyperthermia at 41.5 °C (HS) or 37 °C

Damage to the myogenic differentiation of C2C12 cells by heat stress is associated with up-regulation of several selenoproteins.

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This study was conducted to profile the selenoprotein encoding genes or proteins in mouse C2C12 cells and integrate their roles in the skeletal cell damage induced by heat stress (HS). Cells were cultured at 37.0 °C or 41.5 °C for 4, 6 or 8 days. The mRNA expression of 24 selenoprotein encoding

[Congenital myopathies].

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BACKGROUND Congenital myopathies include many genetically distinct diseases which have in common the early appearance of symptoms and characteristic morphological findings. OBJECTIVE To resume clinical, pathological and genetic findings of the most frequent myopathies in this group. METHODS The most

[Structural congenital myopathies].

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BACKGROUND Congenital myopathies are a heterogeneous group of diseases that share clinical early onset and specific hystopathological alterations in muscle. Genetic studies allow to determine the causative mutation in most cases. Genotypic and phenotypic heterogeneity exists, which is illustrated by

Minicore myopathy with ophthalmoplegia caused by mutations in the ryanodine receptor type 1 gene.

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BACKGROUND Minicore myopathy (multi-minicore disease [MmD]) is a congenital myopathy characterized by multifocal areas with loss of oxidative activity on muscle biopsy. MmD is clinically heterogeneous and distinct phenotypes have been associated with recessive mutations in either the selenoprotein N

Multi-minicore Disease.

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Multi-minicore Disease (MmD) is a recessively inherited neuromuscular disorder characterized by multiple cores on muscle biopsy and clinical features of a congenital myopathy. Prevalence is unknown. Marked clinical variability corresponds to genetic heterogeneity: the most instantly recognizable

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