| 1. |
- Dzierzanowska-Fangrat, Katarzyna, et al.
(author)
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Lack of an association between Helicobacter infection and autoimmune hepatitis in children
- 2006
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In: Polish Journal of Microbiology. - 1733-1331. ; 55:2, s. 157-159
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Journal article (peer-reviewed)abstract
- An association between Helicobacter infection and autoimmune hepatitis (AIH) in children was investigated. The prevalence of antibodies to H. pylori did not differ between the AIH and the control group, (22% versus 14%), and antibodies to non-gastric Helicobacter were not detected in either group. H. pylori DNA was found in two AIH liver tissues, but Helicobacter was not cultured from any sample.
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| 2. |
- Golec, Ewelina, et al.
(author)
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Alternative splicing encodes functional intracellular CD59 isoforms that mediate insulin secretion and are down-regulated in diabetic islets
- 2022
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In: Proceedings of the National Academy of Sciences of the United States of America. - : Proceedings of the National Academy of Sciences (PNAS). - 0027-8424 .- 1091-6490. ; 119:24
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Journal article (peer-reviewed)abstract
- Human pancreatic islets highly express CD59, which is a glycosylphosphatidylinositol (GPI)-anchored cell-surface protein and is required for insulin secretion. How cell-surface CD59 could interact with intracellular exocytotic machinery has so far not been described. We now demonstrate the existence of CD59 splice variants in human pancreatic islets, which have unique C-terminal domains replacing the GPI-anchoring signal sequence. These isoforms are found in the cytosol of beta-cells, interact with SNARE proteins VAMP2 and SNAP25, colocalize with insulin granules, and rescue insulin secretion in CD59-knockout (KO) cells. We therefore named these isoforms IRIS-1 and IRIS-2 (Isoforms Rescuing Insulin Secretion 1 and 2). Antibodies raised against each isoform revealed that expression of both IRIS-1 and IRIS-2 is significantly lower in islets isolated from human type 2 diabetes (T2D) patients, as compared to healthy controls. Further, glucotoxicity induced in primary, healthy human islets led to a significant decrease of IRIS-1 expression, suggesting that hyperglycemia (raised glucose levels) and subsequent decreased IRIS-1 expression may contribute to relative insulin deficiency in T2D patients. Similar isoforms were also identified in the mouse CD59B gene, and targeted CRISPR/Cas9-mediated knockout showed that these intracellular isoforms, but not canonical CD59B, are involved in insulin secretion from mouse beta-cells. Mouse IRIS-2 is also down-regulated in diabetic db/db mouse islets. These findings establish the endogenous existence of previously undescribed non-GPI-anchored intracellular isoforms of human CD59 and mouse CD59B, which are required for normal insulin secretion.
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| 3. |
- Herd, Katarzyna, et al.
(author)
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Folktale patterns and memory-building processes in Swedish football : Transfer me a hero
- 2024
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In: Football, Fandom and Collective Memory : Global Perspectives - Global Perspectives. - 9781003374527 ; , s. 240-256
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Book chapter (peer-reviewed)abstract
- In this chapter, I problematise how “heroes” can be constructed in modern football clubs in spite of constant change and short stays. Narratives from the transfer system in Sweden are juxtaposed with media stories about players’ rationale for staying, transferring or choosing a certain club. The analysis suggests that the persistence of the hero-story and emotional connections are possible to forge because of the well-established narrative patterns that are easily applicable in the football context through collective memories. Supporters and players can engage in exchanges beneficial for both groups: fans can build collective memories and group identities, whereas footballers count on a lasting emotional space in a club. Their hero status does not need to be contested because it is not unique, and instead falls into a well-known, easily relatable structure.
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| 4. |
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| 5. |
- Kremlitzka, Mariann, et al.
(author)
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Alternative translation and retrotranslocation of cytosolic C3 that detects cytoinvasive bacteria
- 2022
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In: Cellular and Molecular Life Sciences. - : Springer Science and Business Media LLC. - 1420-682X .- 1420-9071. ; 79:6
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Journal article (peer-reviewed)abstract
- Complement C3 was originally regarded as a serum effector protein, although recent data has emerged suggesting that intracellular C3 can also regulate basic cellular processes. Despite the growing interest in intracellular C3 functions, the mechanism behind its generation has not been demonstrated. In this study we show that C3 can be expressed from an alternative translational start site, resulting in C3 lacking the signal peptide, which is therefore translated in the cytosol. In contrast to the secreted form, alternatively translated cytosolic C3 is not glycosylated, is present mainly in a reduced state, and is turned over by the ubiquitin–proteasome system. C3 can also be retrotranslocated from the endoplasmic reticulum into the cytosol, structurally resembling secreted C3. Finally, we demonstrate that intracellular cytosolic C3 can opsonize invasive Staphylococcus aureus within epithelial cell, slowing vacuolar escape as well as impacting bacterial survival on subsequent exposure to phagocytes. Our work therefore reveals the existence and origin of intracellular, cytosolic C3, and demonstrates functions for cytosolic C3 in intracellular detection of cytoinvasive pathogens.
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