| 1. |
- Bernard-Marissal, N, et al.
(författare)
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Altered interplay between endoplasmic reticulum and mitochondria in Charcot-Marie-Tooth type 2A neuropathy
- 2019
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Ingår i: Proceedings of the National Academy of Sciences of the United States of America. - : Proceedings of the National Academy of Sciences. - 1091-6490. ; 116:6, s. 2328-2337
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Tidskriftsartikel (refereegranskat)abstract
- Interactions between mitochondria and the endoplasmic reticulum (ER) at the level of mitochondria-associated membranes (MAM) constitute a key signaling hub, emerging as a shared target altered in multiple neurodegenerative diseases. We use both in vivo and in vitro models of Charcot–Marie–Tooth type 2A, an axonal form of neuropathy, to demonstrate that the presence of mutated Mitofusin 2 leads to altered MAM. In neurons, these modifications occur concomitantly with activation of ER stress response, dysregulated calcium handling, and alterations in mitochondrial morphology and transport, collectively contributing to axonopathy. Importantly, the reported results indicate that the pathological consequences of mutated Mitofusin 2 may be targeted with drugs reinforcing the ER–mitochondria cross-talk and/or reducing ER stress.
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| 5. |
- Zhang, SB, et al.
(författare)
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GIT1 protects against breast cancer growth through negative regulation of Notch
- 2022
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Ingår i: Nature communications. - : Springer Science and Business Media LLC. - 2041-1723. ; 13:1, s. 1537-
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Tidskriftsartikel (refereegranskat)abstract
- Hyperactive Notch signalling is frequently observed in breast cancer and correlates with poor prognosis. However, relatively few mutations in the core Notch signalling pathway have been identified in breast cancer, suggesting that as yet unknown mechanisms increase Notch activity. Here we show that increased expression levels of GIT1 correlate with high relapse-free survival in oestrogen receptor-negative (ER(-)) breast cancer patients and that GIT1 mediates negative regulation of Notch. GIT1 knockdown in ER(-) breast tumour cells increased signalling downstream of Notch and activity of aldehyde dehydrogenase, a predictor of poor clinical outcome. GIT1 interacts with the Notch intracellular domain (ICD) and influences signalling by inhibiting the cytoplasm-to-nucleus transport of the Notch ICD. In xenograft experiments, overexpression of GIT1 in ER(-) cells prevented or reduced Notch-driven tumour formation. These results identify GIT1 as a modulator of Notch signalling and a guardian against breast cancer growth.
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| 6. |
- Lee, MD, et al.
(författare)
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Small-world connectivity dictates collective endothelial cell signaling
- 2022
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Ingår i: Proceedings of the National Academy of Sciences of the United States of America. - : Proceedings of the National Academy of Sciences. - 1091-6490. ; 119:18, s. e2118927119-
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Tidskriftsartikel (refereegranskat)abstract
- The endothelium is the single layer of cells lining all blood vessels and acts as a central control hub to regulate multiple cardiovascular functions in response to hundreds of physiological stimuli. The detection of various physiological stimuli is distributed in spatially separated sites across the endothelium. Distributed sensing is difficult to reconcile with the requirement for coordinated cell activity across large regions of the endothelium. Here, we show that the endothelium resolves the issue by using a network with scale-free and small-world properties. The organization confers a high signal-propagation speed and a high degree of synchronizability across the endothelium. The network organization also explains the robust nature of endothelial communication and its resistance to damage or failure.
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| 7. |
- Louhivuori, L, et al.
(författare)
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Predicting a tumour's drug uptake
- 2018
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Ingår i: Nature biomedical engineering. - : Springer Science and Business Media LLC. - 2157-846X. ; 2:10, s. 717-718
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Tidskriftsartikel (refereegranskat)
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