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  • 1.
    Hardy, Matthew P.
    et al.
    Center for Functional Genomics and Human Disease, Monash Institute of Reproduction and Development, Monash University, Monash Medical Centre, Clayton, Victoria, Australia / Department of Biochemistry and Biotechnology Institute, Trinity College, University of Dublin, Dublin 2, Ireland.
    Owczarek, Catherine M.
    Center for Functional Genomics and Human Disease, Monash Institute of Reproduction and Development, Monash University, Monash Medical Centre, Clayton, Victoria, Australia.
    Jermiin, Lars S.
    School of Biological Sciences and Sydney University Biological Informatics and Technology Center, University of Sydney, New South Wales 2006, Australia.
    Ejdebäck, Mikael
    Department of Biochemistry and Biotechnology Institute, Trinity College, University of Dublin, Dublin 2, Ireland.
    Hertzog, Paul J.
    Center for Functional Genomics and Human Disease, Monash Institute of Reproduction and Development, Monash University, Monash Medical Centre, Clayton, Victoria, Australia.
    Characterization of the type I interferon locus and identification of novel genes2004In: Genomics, ISSN 0888-7543, E-ISSN 1089-8646, Vol. 84, no 2, p. 331-345Article in journal (Refereed)
    Abstract [en]

    The human type I interferon (IFN) genes are clustered on human chromosome 9p21 and the mouse genes are located in the region of conserved synteny on mouse chromosome 4. We have identified two novel mouse Ifna genes (Ifna12, Ifna13) and Ifnl2 (IFN-like 2, a homologue of Limitin/IFN-like 1). Another type I IFN gene was designated Ifne1. Mouse Ifne1 was expressed in ovaries and uterus but not in tissues of hematopoietic origin. IFN-epsilon1 has general structural characteristics of a type I IFN. These studies represent the first detailed annotation of the mouse type I IFN locus, and the products of these novel genes may have important functions in reproduction and host defense.

  • 2.
    Olofsson, Peter
    et al.
    Section for Medical Inflammation Research, Lund University, Sweden.
    Johansson, Åsa
    Section for Medical Inflammation Research, Lund University, Sweden.
    Wedekind, Dirk
    Institute for Laboratory Animal Science and Central Animal Laboratory Medical School of Hannover, Hannover, Germany.
    Klöting, Ingrid
    Department of Laboratory Animal Science, Medical Faculty, University of Greifswald, Karlsburg, Germany.
    Klinga-Levan, Karin
    University of Skövde, School of Life Sciences.
    Lu, Shemin
    Section for Medical Inflammation Research, Lund University, Sweden.
    Holmdahl, Rikard
    Section for Medical Inflammation Research, Lund University, Sweden.
    Inconsistent susceptibility to autoimmunity in inbred LEW rats is due to genetic crossbreeding involving segregating of the arthritis-regulation gene Ncf12004In: Genomics, ISSN 0888-7543, E-ISSN 1089-8646, Vol. 83, no 5, p. 765-771Article in journal (Refereed)
    Abstract [en]

    We recently identified a single-nucleotide polymorphism in the Ncf1 gene, a component of the NADPH oxidase complex, to be the cause of one of the strongest identified loci for arthritis severity in rats. This polymorphism was found to be naturally occurring in a collection of inbred rat strains as well as in wild rats. Among the inbred strains we found that different LEW substrains (LEW/Ztm and LEW/Mol), originating from different breeders, showed an allelic discrepancy in Ncf1, suggesting an impact on arthritis susceptibility between these substrains. In fact, the LEW/Mol strain was completely resistant to pristane-induced arthritis, in contrast to the LEW/Ztm strain, which was susceptible. Moreover, the LEW/Mol strain had higher production of radical oxygen species in peripheral blood leukocytes, a phenomenon most likely regulated by the polymorphisms in the Ncf1 gene. However, the phenotypic difference between LEW/Mol and LEW/Ztm is most likely a combination of several genes, of which Ncf1 is suggested to be the major regulating gene. This has also been confirmed by previous linkage analyses involving the LEW/Ztm strain which shows that a QTL on chromosome 12, most likely caused by polymorphism of Ncf1, is the major regulatory gene but that other loci are contributing. That more genes are likely to contribute was shown by a complete genome comparison of the LEW/Ztm and the LEW/Mol rat strains that uncovered an introduction of approximately 37% non-LEW genome into the LEW/Mol strain, which probably was caused by past crossbreeding. Therefore, the LEW/Mol should be regarded as a recombinant inbred strain.

  • 3.
    Rahman, Aminur
    et al.
    University of Skövde, School of Bioscience. University of Skövde, The Systems Biology Research Centre. Örebro University.
    Nahar, Noor
    University of Skövde, School of Bioscience. University of Skövde, The Systems Biology Research Centre.
    Nawani, Neelu N.
    Dr. D. Y. Patil Biotechnology and Bioinformatics Institute, India.
    Jass, Jana
    Örebro University.
    Ghosh, Sibdas
    Iona College, New Rochelle, NY, USA.
    Olsson, Björn
    University of Skövde, School of Bioscience. University of Skövde, The Systems Biology Research Centre.
    Mandal, Abul
    University of Skövde, School of Bioscience. University of Skövde, The Systems Biology Research Centre.
    Comparative genome analysis of Lysinibacillus B1-CDA, a bacterium that accumulates arsenics2015In: Genomics, ISSN 0888-7543, E-ISSN 1089-8646, Vol. 106, no 6, p. 384-392Article in journal (Refereed)
    Abstract [en]

    Previously, we reported an arsenic resistant bacterium Lysinibacillus sphaericus B1-CDA, isolated from an arsenic contaminated lands. Here, we have investigated its genetic composition and evolutionary history by using massively parallel sequencing and comparative analysis with other known Lysinibacillus genomes. Assembly of the sequencing reads revealed a genome of ~ 4.5 Mb in size encompassing ~ 80% of the chromosomal DNA. We found that the set of ordered contigs contains abundant regions of similarity with other Lysinibacillus genomes and clearly identifiable genome rearrangements. Furthermore, all genes of B1-CDA that were predicted be involved in its resistance to arsenic and/or other heavy metals were annotated. The presence of arsenic responsive genes was verified by PCR in vitro conditions. The findings of this study highlight the significance of this bacterium in removing arsenics and other toxic metals from the contaminated sources. The genetic mechanisms of the isolate could be used to cope with arsenic toxicity.

  • 4.
    Rahman, Aminur
    et al.
    University of Skövde, School of Bioscience. University of Skövde, The Systems Biology Research Centre. Örebro universitet, Institutionen för naturvetenskap och teknik.
    Nahar, Noor
    University of Skövde, School of Bioscience. University of Skövde, The Systems Biology Research Centre.
    Olsson, Björn
    University of Skövde, School of Bioscience. University of Skövde, The Systems Biology Research Centre.
    Jass, Jana
    Örebro universitet, Institutionen för naturvetenskap och teknik.
    Nawani, Neelu N.
    Dr. D. Y. Patil Biotechnology and Bioinformatics Institute, Dr. D. Y. Patil Vidyapeeth, Tathawade, Pune-411033, India.
    Ghosh, Sibdas
    Iona College, New Rochelle, NY, USA.
    Saha, Ananda K.
    University of Rajshahi, Rajshahi, Bangladesh.
    Hossain, Khaled
    University of Rajshahi, Bangladesh.
    Mandal, Abul
    University of Skövde, School of Bioscience. University of Skövde, The Systems Biology Research Centre.
    Genome analysis of Enterobacter cloacae B2-DHA: A bacterium resistant to chromium and/or other heavy metalsIn: Genomics, ISSN 0888-7543, E-ISSN 1089-8646Article in journal (Other academic)
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