Ceruloplasmin is a serum ferroxidase that carries more than 90% of the copper in plasma and has documented roles in iron homeostasis as well as antioxidative functions. In our previous studies, it has been shown that the ceruloplasmin gene is strongly up-regulated in catfish during challenge with Edwardsiella ictaluri. However, little is known about the function of this gene in teleost fish. The objective of this study, therefore, was to characterize the ceruloplasmin gene from channel catfish, determine its genomic organization, profile its patterns of tissue expression, and establish its potential for physiological antioxidant responses in catfish after bacterial infection with E. ictaluri and iron treatment. The genomic organization suggested that the catfish ceruloplasmin gene had 20 exons and 19 introns, encoding 1074 amino acids. Exon sizes of the catfish ceruloplasmin gene were close to or identical with mammalian and zebrafish homologs. Further phylogenetic analyses suggested that the gene was highly conserved through evolution. The catfish ceruloplasmin gene was mapped to both the catfish physical map and linkage map. The catfish ceruloplasmin gene was mainly expressed in liver with limited expression in other tissues, and it was significantly up-regulated in the liver after bacterial infection alone or after co-injection with bacteria and iron-dextran, while expression was not significantly induced with iron-dextran treatment alone.
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http://dx.doi.org/10.1016/j.fsi.2010.12.033 | DOI Listing |
Eur J Hum Genet
December 2024
Estonian Genome Center, Institute of Genomics, University of Tartu, Tartu, Estonia.
Population-based biobanks enable genomic screening to support initiatives that prevent disease onset or slow its progression and to estimate the prevalence of genetic diseases in the population. Wilson's disease (WD) is a rare genetic copper-accumulation disorder for which timely intervention is crucial, as treatment is readily available. We studied WD in the Estonian Biobank population to advance patient screening, swift diagnosis, and subsequent treatment.
View Article and Find Full Text PDFJ Dairy Sci
December 2024
Department of Dairy and Food Sciences, South Dakota State University, Brookings, South Dakota 57007; School of Animal Sciences, Virginia Tech, Blacksburg, VA. Electronic address:
The objective of this study was to evaluate the effects of a rumen-derived direct-fed microbial (DFM) product on performance, blood biomarkers, ruminal fermentation, and bacterial abundance in dairy cows during the transition period until 100 DIM. Fifty-six Holstein cows were enrolled in a randomized complete block design from -21 to 100 DIM. Cows were blocked based on expected calving date, parity, and previous lactation milk yield for multiparous or genetic merit for primiparous cows.
View Article and Find Full Text PDFCase Reports Hepatol
November 2024
Paediatric Gastroenterology and Digestive Endoscopy Unit, IRCCS Istituto Giannina Gaslini, Genoa, Italy.
Wilson's disease (WD) is a rare autosomal recessive disorder caused by mutations in the ATP7B gene, resulting in copper accumulation. Symptoms rarely appear before the age of 5, almost never before 3. The phenotypic variability of WD suggests the presence of modifying factors, making early diagnosis challenging.
View Article and Find Full Text PDFJ Dairy Sci
December 2024
School of Animal Science, Virginia Tech, Blacksburg, VA 24061. Electronic address:
This study aimed to evaluate the effects of rumen-protected Met on lactation performance, inflammation, and immune response, and liver glutathione of lactating dairy cows during a subclinical mastitis challenge (SMC). Thirty-two Holstein cows (145 ± 51 DIM) were enrolled in a randomized complete block design. At -21 d relative to the SMC, cows were assigned to dietary treatments, and data were collected before and during the SMC.
View Article and Find Full Text PDFInt J Mol Sci
November 2024
Second Department of Neurology, Institute of Psychiatry and Neurology, Sobieskiego Street 9, 02-957 Warsaw, Poland.
Wilson's disease (WD) is an autosomal recessive disorder of copper metabolism. The genetic defect in WD affects the gene, which encodes the ATP7B transmembrane protein, which is essential for maintaining normal copper homeostasis in the body. It is primarily expressed in the liver and acts by incorporating copper into ceruloplasmin (Cp), the major copper transport protein in the blood.
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