| 1. |
- Johnson, Magnus S.C. 1969, et al.
(författare)
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Interaction of scavenger receptor class B type I with peroxisomal targeting receptor Pex5p.
- 2003
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Ingår i: Biochemical and biophysical research communications. - 0006-291X. ; 312:4, s. 1325-34
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Tidskriftsartikel (refereegranskat)abstract
- Scavenger receptor class B type I (SR-BI) is an HDL receptor that mediates selective HDL lipid uptake. Peroxisomes play an important role in lipid metabolism and peroxisomal targeting signal type 1 (PTS1)-containing proteins are translocated to peroxisomes by the peroxisomal targeting import receptor, Pex5p. We have previously identified a PTS1 motif in the intracellular domain of rat SR-BI. Here, we examine the possible interaction between Pex5p and SR-BI. Expression of a Flag-tagged intracellular domain of SR-BI resulted in translocation to the peroxisome as demonstrated by double labeling with anti-Flag IgG and anti-catalase IgG analyzed by confocal microscopy. Immunoprecipitation experiments with anti-SR-BI antibody showed that Pex5p co-precipitated with SR-BI. However, when an antibody against Pex5p was used for immunoprecipitation, only the 57kDa, non-glycosylated form, of SR-BI co-precipitated. We conclude that the PTS1 domain of SR-BI is functional and can mediate peroxisomal interaction via Pex5p, in vitro.
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| 2. |
- Eriksson, Maria, 1969-
(författare)
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En fråga om heder
- 2004
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Ingår i: Kvinnovetenskaplig tidskrift. - 0348-8365. ; :3, s. 97-99
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Recension (övrigt vetenskapligt/konstnärligt)
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| 3. |
- Eriksson, Maria, 1969-
(författare)
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En fråga om heder, av Unni Wikan
- 2004
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Ingår i: Kvinnovetenskaplig tidskrift. - 0348-8365. ; :3, s. 97-99
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Recension (övrigt vetenskapligt/konstnärligt)
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| 4. |
- Eriksson, Maria, 1969-
(författare)
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I skuggan av Pappa : familjerätten och hanteringen av fäders våld
- 2003
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Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- The aims of this thesis are to shed light on the handling of fathers’ violence in the context of separation and divorce in Sweden today; and to analytically and empirically relate age, gender and kinship to each other. The aims are fulfilled by three interlinked studies of what constructions and the constructing of age, gender and kinship mean for the handling of fathers’ violence against mothers/co-parents and children: in social policy; by separated mothers; and finally by family law secretaries. Each study builds upon a separate set of qualitative material: public documents from three policy areas; thematically structured interviews with abused, separated mothers and family law secretaries. The empirical results make visible some unintended consequences of current attempts in Sweden to create gender equality, shared parenting, a “new father” and to promote children’s interests. Study one demonstrates that when the politics and policy regarding parenthood, separation and divorce are taken as the point of departure, the contemporary age-, gender-, and kinship-order stands out as patriarchal: as marked by father-power based upon ties of blood to not yet adult children. Furthermore, violent fathers neither exist as a concept nor as a policy problem. The interviewed mothers narrate how they have tried to deal with the co-parent’s/ex-partners’ behaviour as violence but have encountered hindrances; the interviewed family law secretaries’ handling fathers’ violence stands out as more of a non-handling, especially in the case of violence against children. When the everyday constructions and constructing of age, gender and kinship discussed in study two and three are taken together, the contours of the patriarchal order seen through the lens of policy are also made visible: fathers’ space for action is vast; children’ and mothers’ more limited. The analysis shows how political and professional handling of fathers’ violence through a non-handling is made possible by well-established notions of heterosexual relationships, fatherhood, motherhood, age- and kinship-relations, as well as family law secretary-professionalism. However, the two studies based upon interviews demonstrate not just how the everyday constructions and constructing mentioned above can be used to reproduce father-power, but also how this power can be challenged.
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| 5. |
- Eriksson, Maria, 1969-
(författare)
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Unni Wikan : En fråga om heder
- 2004
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Ingår i: Kvinnovetenskaplig tidskrift. - 0348-8365. ; :3, s. 97-99
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Recension (övrigt vetenskapligt/konstnärligt)
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| 6. |
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| 7. |
- Åberg, N David, 1970, et al.
(författare)
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Insulin-like growth factor-I increases astrocyte intercellular gap junctional communication and connexin43 expression in vitro.
- 2003
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Ingår i: Journal of neuroscience research. - : Wiley. - 0360-4012. ; 74:1, s. 12-22
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Tidskriftsartikel (refereegranskat)abstract
- Connexin43 (cx43) forms gap junctions in astrocytes, and these gap junctions mediate intercellular communication by providing transport of low-molecular-weight metabolites and ions. We have recently shown that systemic growth hormone increases cx43 in the brain. One possibility was that local brain insulin-like growth factor-I (IGF-I) could mediate the effect by acting directly on astrocytes. In the present study, we examined the effects of direct application of recombinant human IGF-I (rhIGF-I) on astrocytes in primary culture concerning cx43 protein expression and gap junctional communication (GJC). After 24 hr of stimulation with rhIGF-I under serum-free conditions, the GJC and cx43 protein were analyzed. Administration of 30 ng/ml rhIGF-I increased the GJC and the abundance of cx43 protein. Cell proliferation of the astrocytes was not significantly increased by rhIGF-I at this concentration. However, a higher concentration of rhIGF-I (150 ng/ml) had no effect on GJC/cx43 but increased cell proliferation. Because of the important modulatory role of IGF binding proteins (IGFBPs) on IGF-I action, we analyzed IGFBPs in conditioned media. In cultures with a low abundance of IGFBPs (especially IGFBP-2), the GJC response to 30 ng/ml rhIGF-I was 81%, compared with the average of 25%. Finally, as a control, insulin was given in equimolar concentrations. However, GJC was not affected, which suggests that rhIGF-I acted via IGF-I receptors. In summary, the data show that rhIGF-I may increase GJC/cx43, whereas a higher concentration of rhIGF-I--at which stimulation of proliferation occurred--did not affect GJC/cx43. Furthermore, IGFBP-2 appeared to modulate the action of rhIGF-I on GJC in astrocytes by a paracrine mechanism.
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