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| 5. |
- Almet, A, et al.
(författare)
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A roadmap for the human skin cell atlas
- 2023
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Ingår i: JOURNAL OF INVESTIGATIVE DERMATOLOGY. - 0022-202X. ; 143:9, s. B10-B10
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Konferensbidrag (övrigt vetenskapligt/konstnärligt)
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| 6. |
- Apostolou, E, et al.
(författare)
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Progress and challenges in stem cell biology
- 2023
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Ingår i: Nature cell biology. - : Springer Science and Business Media LLC. - 1476-4679 .- 1465-7392. ; 25:2, s. 203-206
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Tidskriftsartikel (refereegranskat)
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| 7. |
- Apostolou, E, et al.
(författare)
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Progress and challenges in stem cell biology
- 2023
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Ingår i: Nature cell biology. - : Springer Science and Business Media LLC. - 1476-4679 .- 1465-7392. ; 25:2, s. 203-206
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Tidskriftsartikel (refereegranskat)
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| 8. |
- Grose, R, et al.
(författare)
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A crucial role of beta 1 integrins for keratinocyte migration in vitro and during cutaneous wound repair
- 2002
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Ingår i: Development: For advances in developmental biology and stem cells. - 1477-9129. ; 129:9, s. 2303-2315
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Tidskriftsartikel (refereegranskat)abstract
- Integrins are ubiquitous transmembrane receptors that play crucial roles in cell-cell and cell-matrix interactions. In this study, we have determined the effects of the loss of beta1 integrins in keratinocytes in vitro and during cutaneous wound repair. Flow cytometry of cultured beta1-deficient keratinocytes confirmed the absence of beta1 integrins and showed downregulation of alpha6beta4 but not of alphanu integrins. beta1-null keratinocytes were characterised by poor adhesion to various substrates, by a reduced proliferation rate and by a strongly impaired migratory capacity. In vivo, the loss of 01 integrins in keratinocytes caused a severe defect in wound healing. beta1-null keratinocytes showed impaired migration and were more densely packed in the hyperproliferative epithelium. Surprisingly, their proliferation rate was not reduced in early wounds and even increased in late wounds. The failure in re-epithelialisation resulted in a prolonged inflammatory response, leading to dramatic alterations in the expression of important wound-regulated genes. Ultimately, beta1-deficient epidermis did cover the wound bed, but the epithelial architecture was abnormal. These findings demonstrate a crucial role of beta1 integrins in keratinocyte migration and wound re-epithelialisation.
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| 9. |
- Petrova, V, et al.
(författare)
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Protrudin functions from the endoplasmic reticulum to support axon regeneration in the adult CNS
- 2020
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Ingår i: Nature communications. - : Springer Science and Business Media LLC. - 2041-1723. ; 11:1, s. 5614-
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Tidskriftsartikel (refereegranskat)abstract
- Adult mammalian central nervous system axons have intrinsically poor regenerative capacity, so axonal injury has permanent consequences. One approach to enhancing regeneration is to increase the axonal supply of growth molecules and organelles. We achieved this by expressing the adaptor molecule Protrudin which is normally found at low levels in non-regenerative neurons. Elevated Protrudin expression enabled robust central nervous system regeneration both in vitro in primary cortical neurons and in vivo in the injured adult optic nerve. Protrudin overexpression facilitated the accumulation of endoplasmic reticulum, integrins and Rab11 endosomes in the distal axon, whilst removing Protrudin’s endoplasmic reticulum localization, kinesin-binding or phosphoinositide-binding properties abrogated the regenerative effects. These results demonstrate that Protrudin promotes regeneration by functioning as a scaffold to link axonal organelles, motors and membranes, establishing important roles for these cellular components in mediating regeneration in the adult central nervous system.
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