hh.sePublikationer
Ändra sökning
Avgränsa sökresultatet
1 - 7 av 7
RefereraExporteraLänk till träfflistan
Permanent länk
Referera
Referensformat
  • apa
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • Annat format
Fler format
Språk
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Annat språk
Fler språk
Utmatningsformat
  • html
  • text
  • asciidoc
  • rtf
Träffar per sida
  • 5
  • 10
  • 20
  • 50
  • 100
  • 250
Sortering
  • Standard (Relevans)
  • Författare A-Ö
  • Författare Ö-A
  • Titel A-Ö
  • Titel Ö-A
  • Publikationstyp A-Ö
  • Publikationstyp Ö-A
  • Äldst först
  • Nyast först
  • Skapad (Äldst först)
  • Skapad (Nyast först)
  • Senast uppdaterad (Äldst först)
  • Senast uppdaterad (Nyast först)
  • Disputationsdatum (tidigaste först)
  • Disputationsdatum (senaste först)
  • Standard (Relevans)
  • Författare A-Ö
  • Författare Ö-A
  • Titel A-Ö
  • Titel Ö-A
  • Publikationstyp A-Ö
  • Publikationstyp Ö-A
  • Äldst först
  • Nyast först
  • Skapad (Äldst först)
  • Skapad (Nyast först)
  • Senast uppdaterad (Äldst först)
  • Senast uppdaterad (Nyast först)
  • Disputationsdatum (tidigaste först)
  • Disputationsdatum (senaste först)
Markera
Maxantalet träffar du kan exportera från sökgränssnittet är 250. Vid större uttag använd dig av utsökningar.
  • 1.
    Ahlqvist, Emma
    et al.
    Lund University, Lund, Sweden; Department of Clinical Sciences, Lund University, Malmö, Sweden.
    Ekman, Diana
    Karolinska Institute, Stockholm, Sweden.
    Lindvall, Therese
    Lund University, Lund, Sweden.
    Popovic, Marjan
    Karolinska Institute, Stockholm, Sweden; Lund University, Lund, Sweden.
    Förster, Michael
    Karolinska Institute, Stockholm, Sweden; Lund University, Lund, Sweden.
    Hultqvist, Malin
    Lund University, Lund, Sweden.
    Klaczkowska, Dorota
    Karolinska Institute, Stockholm, Sweden; Lund University, Lund, Sweden.
    Teneva, Ivanka
    Lund University, Lund, Sweden.
    Johannesson, Martina
    Lund University, Lund, Sweden; Wellcome Trust Centre for Human Genetics, Oxford, United Kingdom.
    Flint, Jonathan
    Wellcome Trust Centre for Human Genetics, Oxford, United Kingdom.
    Valdar, William
    University of North Carolina, Chapel Hill, NC, United States.
    Nandakumar, Kutty Selva
    Karolinska Institute, Stockholm, Sweden; Lund University, Lund, Sweden.
    Holmdahl, Rikard
    Karolinska Institute, Stockholm, Sweden; Lund University, Lund, Sweden.
    High-resolution mapping of a complex disease, a model for rheumatoid arthritis, using heterogeneous stock mice2011Ingår i: Human Molecular Genetics, ISSN 0964-6906, E-ISSN 1460-2083, Vol. 20, nr 15, s. 3031-3041Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Resolving the genetic basis of complex diseases like rheumatoid arthritis will require knowledge of the corresponding diseases in experimental animals to enable translational functional studies. Mapping of quantitative trait loci in mouse models of arthritis, such as collagen-induced arthritis (CIA), using F(2) crosses has been successful, but can resolve loci only to large chromosomal regions. Using an inbred-outbred cross design, we identified and fine-mapped CIA loci on a genome-wide scale. Heterogeneous stock mice were first intercrossed with an inbred strain, B10.Q, to introduce an arthritis permitting MHCII haplotype. Homozygous H2(q) mice were then selected to set up an F(3) generation with fixed major histocompatibility complex that was used for arthritis experiments. We identified 26 loci, 18 of which are novel, controlling arthritis traits such as incidence of disease, severity and time of onset and fine-mapped a number of previously mapped loci. © The Author 2011. Published by Oxford University Press. All rights reserved.

  • 2.
    Atteia, A.
    et al.
    Depto. de Genética Molecular, Inst. de Fisiología Celular, Univ. Nacl. Auton. de Mex., Mexico.
    van Lis, R.
    Depto. de Genética Molecular, Inst. de Fisiología Celular, Univ. Nacl. Auton. de Mex., Mexico.
    Wetterskog, Daniel
    Department of Plant Physiology, Göteborg University, Göteborg, Sweden.
    Gutiérrez-Cirlos, E.-B.
    Department of Biochemistry, Dartmouth Medical School, Hanover, United States.
    Ongay-Larios, L.
    Unidad de Biología Molecular, Inst. de Fisiología Celular, Univ. Nacl. Auton. de Mex., Mexico.
    Franzén, Lars-Gunnar
    Högskolan i Halmstad, Sektionen för ekonomi och teknik (SET), Bio- och miljösystemforskning (BLESS), Växtcellbiologi: Energiomvandling i växtceller.
    González-Halphen, D.
    Depto. de Genética Molecular, Inst. de Fisiología Celular, Univ. Nacl. Auton. de Mex., Mexico.
    Structure, organization and expression of the genes encoding mitochondrial cytochrome c1 and the Rieske iron-sulfur protein in Chlamydomonas reinhardtii2003Ingår i: Molecular Genetics and Genomics, ISSN 1617-4615, E-ISSN 1617-4623, Vol. 268, nr 5, s. 637-644Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    The sequence and organization of the Chlamydomonas reinhardtii genes encoding cytochrome c 1 ( Cyc1) and the Rieske-type iron-sulfur protein ( Isp), two key nucleus-encoded subunits of the mitochondrial cytochrome bc 1 complex, are presented. Southern hybridization analysis indicates that both Cyc1 and Isp are present as single-copy genes in C. reinhardtii. The Cyc1 gene spans 6404 bp and contains six introns, ranging from 178 to 1134 bp in size. The Isp gene spans 1238 bp and contains four smaller introns, ranging in length from 83 to 167 bp. In both genes, the intron/exon junctions follow the GT/AG rule. Internal conserved sequences were identified in only some of the introns in the Cyc1 gene. The levels of expression of Isp and Cyc1 genes are comparable in wild-type C. reinhardtii cells and in a mutant strain carrying a deletion in the mitochondrial gene for cytochrome b (dum-1). Nevertheless, no accumulation of the nucleus-encoded cytochrome c 1 or of core proteins I and II was observed in the membranes of the respiratory mutant. These data show that, in the green alga C. reinhardtii, the subunits of the cytochrome bc1 complex fail to assemble properly in the absence of cytochrome b.

  • 3.
    Fernandez Lahore, Gonzalo
    et al.
    Karolinska Institute, Solna, Sweden.
    Nandakumar, Kutty Selva
    Karolinska Institute, Solna, Sweden; Southern Medical University, Guangzhou, China.
    Polymorphic estrogen receptor binding site causes Cd2-dependent sex bias in the susceptibility to autoimmune diseases2021Ingår i: Nature Communications, E-ISSN 2041-1723, Vol. 12, nr 1, artikel-id 5565Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Complex autoimmune diseases are sexually dimorphic. An interplay between predisposing genetics and sex-related factors probably controls the sex discrepancy in the immune response, but the underlying mechanisms are unclear. Here we positionally identify a polymorphic estrogen receptor binding site that regulates Cd2 expression, leading to female-specific differences in T cell-dependent mouse models of autoimmunity. Female mice with reduced Cd2 expression have impaired autoreactive T cell responses. T cells lacking Cd2 costimulation upregulate inhibitory Lag-3. These findings help explain sexual dimorphism in human autoimmunity, as we find that CD2 polymorphisms are associated with rheumatoid arthritis and 17-β-estradiol-regulation of CD2 is conserved in human T cells. Hormonal regulation of CD2 might have implications for CD2-targeted therapy, as anti-Cd2 treatment more potently affects T cells in female mice. These results demonstrate the relevance of sex-genotype interactions, providing strong evidence for CD2 as a sex-sensitive predisposing factor in autoimmunity.

    Ladda ner fulltext (pdf)
    fulltext
  • 4.
    Li, Xi
    et al.
    Oriflame Cosmetics AB, Skin Research Institute, Stockholm, Sweden.
    Ponandai-Srinivasan, Sakthi
    Division of Obstetrics and Gynecology, Department of Women's and Children's Health, Karolinska Institute, Stockholm, Sweden; Karolinska University Hospital, Stockholm, Sweden.
    Nandakumar, Kutty Selva
    Southern Medical University, School of Pharmaceutical Sciences, Guangzhou, China; Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden.
    Fabre, Susanne
    Oriflame Cosmetics AB, Skin Research Institute, Stockholm, Sweden.
    Xu Landén, Ning
    Department of Medicine, Solna, Dermatology and Venereology, Centre of Molecular Medicine, Karolinska Institutet, Stockholm, Sweden.
    Mavon, Alain
    Oriflame Cosmetics AB, Skin Research Institute, Stockholm, Sweden.
    Khmaladze, Ia
    Oriflame Cosmetics AB, Skin Research Institute, Stockholm, Sweden.
    Targeting microRNA for improved skin health2021Ingår i: Health Science Reports, E-ISSN 2398-8835, Vol. 4, nr 4, artikel-id e374Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    BACKGROUND: In human skin, miRNAs have important regulatory roles and are involved in the development, morphogenesis, and maintenance by influencing cell proliferation, differentiation, immune regulation, and wound healing. MiRNAs have been investigated for many years in various skin disorders such as atopic dermatitis, psoriasis, as well as malignant tumors. Only during recent times, cosmeceutical use of molecules/natural active ingredients to regulate miRNA expression for significant advances in skin health/care product development was recognized.

    AIM: To review miRNAs with the potential to maintain and boost skin health and avoid premature aging by improving barrier function, preventing photoaging, hyperpigmentation, and chronological aging/senescence.

    METHODS: Most of the cited articles were found through literature search on PubMed. The main search criteria was a keyword "skin" in combination with the following words: miRNA, photoaging, UV, barrier, aging, exposome, acne, wound healing, pigmentation, pollution, and senescence. Most of the articles reviewed for relevancy were published during the past 10 years.

    RESULTS: All results are summarized in Figure 1, and they are based on cited references.

    CONCLUSIONS: Thus, regulating miRNAs expression is a promising approach for novel therapy not only for targeting skin diseases but also for cosmeceutical interventions aiming to boost skin health.

  • 5.
    Nandakumar, Kutty Selva
    et al.
    Lund University, Lund, Sweden.
    Holmdahl, R.
    Lund University, Lund, Sweden.
    A genetic contamination in MHC-congenic mouse strains reveals a locus on chromosome 10 that determines autoimmunity and arthritis susceptibility2005Ingår i: European Journal of Immunology, ISSN 0014-2980, E-ISSN 1521-4141, Vol. 35, nr 4, s. 1275-1282Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Among the arthritis-susceptible MHC (H-2)-congenic mouse strains, B10.RIII mice are highly susceptible to collagen-induced arthritis. Surprisingly, the B10.RIII strain was also more susceptible to the T cell independent model CAIA (collagen-antibody-induced arthritis). Through genome-wide genotyping, we found that the B10.RIII and B10.Q strains differed not only in chromosome 17 (MHC) but also in a region on chromosome 10, which contained a fragment from the MHC donor RIIIS/J. We isolated the chromosome 10 as well as the chromosome 17 segments on the B10.RIII and B10.Q backgrounds. Congenic mice containing the RIIIS/J-derived chromosome 10 segment showed significantly higher susceptibility and severity of arthritis with an enhanced autoimmune response to type II collagen. Furthermore, this chromosomal segment significantly promoted CAIA. Similarly, the RIIIS/J segment in chromosome 17 also promoted CAIA independently of other gene segments. These data show that other gene regions, apart from MHC class II, may explain effects both at the priming and effector level of arthritis observed in widely used MHC congenic strains. These new congenic fragments, on both chromosome 10 and 17, provide new mouse strains suitable for studies aiming at positional cloning of new genes associated with arthritis.

  • 6.
    Vaartjes, Daniëlle
    et al.
    Karolinska Institute, Stockholm, Sweden.
    Klaczkowska, Dorota
    Karolinska Institute, Stockholm, Sweden.
    Cragg, Mark S.
    University of Southampton Faculty of Medicine, Southampton, United Kingdom.
    Nandakumar, Kutty Selva
    Karolinska Institute, Stockholm, Sweden; Southern Medical University, Guangzhou, China.
    Bäckdahl, Liselotte
    Karolinska Institute, Stockholm, Sweden.
    Holmdahl, Rikard
    Karolinska Institute, Stockholm, Sweden; Southern Medical University, Guangzhou, China.
    Genetic dissection of a major haplotype associated with arthritis reveal FcγR2b and FcγR3 to act additively2021Ingår i: European Journal of Immunology, ISSN 0014-2980, E-ISSN 1521-4141, Vol. 51, nr 3, s. 682-693Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    A haplotype with tightly linked Fc gamma receptor (FcγR) genes is known as a major locus controlling immune responses and autoimmune diseases, including arthritis. Here, we split a congenic fragment derived from the NOD mouse (Cia9) to study its effect on immune response and arthritis in mice. We found that arthritis susceptibility was indeed controlled by the FcγR gene cluster and a recombination between the FcγR2b and FcγR3 loci gave us the opportunity to separately study their impact. We identified the NOD-derived FcγR2b and FcγR3 alleles as disease-promoting for arthritis development without impact on antibody secretion. We further found that macrophage-mediated phagocytosis was directly correlated to FcγR3 expression in the congenic mice. In conclusion, we positioned FcγR2b and FcγR3 alleles as disease regulatory and showed that their genetic polymorphisms independently and additively control innate immune cell activation and arthritis.

    Ladda ner fulltext (pdf)
    fulltext
  • 7.
    Xu, Yanting
    et al.
    Southern Medical University, Guangzhou, China.
    Tan, Huijing
    Southern Medical University, Guangzhou, China.
    Liu, Kaifei
    Southern Medical University, Guangzhou, China.
    Wen, Cailing
    Southern Medical University, Guangzhou, China.
    Pang, Caixia
    Southern Medical University, Guangzhou, China.
    Liu, Haiqian
    Southern Medical University, Guangzhou, China.
    Xu, Rui
    Southern Medical University, Guangzhou, China.
    Li, Qixing
    Southern Medical University, Guangzhou, China.
    He, Chonghua
    Southern Medical University, Guangzhou, China.
    Nandakumar, Kutty Selva
    Southern Medical University, Guangzhou, China.
    Zhou, Chun
    Southern Medical University, Guangzhou, China.
    Targeted inhibition of ATP5B gene prevents bone erosion in collagen-induced arthritis by inhibiting osteoclastogenesis.2021Ingår i: Pharmacological Research, ISSN 1043-6618, E-ISSN 1096-1186, Vol. 165, artikel-id 105458Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Bone resorption by osteoclasts is an energy consuming activity, which depends on mitochondrial ATP. ATP5B, a mitochondrial ATP synthase beta subunit, is a catalytic core involved in producing ATP. Here, we investigated the contribution of ATP5B in osteoclast differentiation and joint destruction. ATP5B (LV-ATP5B) targeting or non-targeting (LV-NC) siRNA containing lentivirus particles were transduced into bone marrow macrophage derived osteoclasts or locally administered to arthritic mouse joints. Inhibition of ATP5B reduced the expression of osteoclast related genes and proteins, suppressed bone resorption by significantly impairing F-actin formation and decreased the levels of adhesion-associated proteins. In addition, ATP5B deficiency caused osteoclast mitochondrial dysfunction and, impaired the secretion of vacuole protons and MMP9. Importantly, inhibition of ATP5B expression, protected arthritis mice from joint destructions although serum levels of inflammatory mediators (TNF-α, IL-1β) and IgG2α antibodies were unaffected. These results demonstrate an essential function of ATP5B in osteoclast differentiation and bone resorption, and suggest it as a potential therapeutic target for protecting bones in RA.

1 - 7 av 7
RefereraExporteraLänk till träfflistan
Permanent länk
Referera
Referensformat
  • apa
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • Annat format
Fler format
Språk
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Annat språk
Fler språk
Utmatningsformat
  • html
  • text
  • asciidoc
  • rtf