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- de Kock, M. O., et al.
(författare)
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The precambrian mafic magmatic record, including large igneous provinces of the kalahari craton and its constituents : A paleogeographic review
- 2019
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Ingår i: Springer Geology. - Singapore : Springer Singapore. - 2197-9545 .- 2197-9553. ; , s. 155-214
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Bokkapitel (refereegranskat)abstract
- The study of Precambrian dyke swarms, sill provinces and large igneous provinces on the Kalahari craton in southern Africa has expanded greatly since the pioneering work initiated almost four decades ago. The main contributors to this progress have been a large number of precise U–Pb crystallization ages of mafic rocks, published in a number of recent papers. This information is compiled here into a series of maps that provide a nearly 3 billion year intraplate magmatic record of the Kalahari craton and its earlier constituents, the proto-Kalahari, Kaapvaal and Zimbabwe cratons. We also review their possible paleogeographic relations to other cratons or supercontinents. This review provides a more accessible overview of individual magmatic events, and mostly includes precise U–Pb ages of mafic dykes and sills, some of which can be linked to stratigraphically well-constrained volcanic rocks. The extrusion ages of these volcanic units are also starting to be refined by, among others, in situ dating of baddeleyite. Some mafic dyke swarms, previously characterized entirely on similarity in dyke trends within a swarm, are found to be temporally composite and sometimes consist of up to three different generations. Other mafic dyke swarms, with different trends, can now be linked to protracted volcanic events like the stratigraphically well preserved Mesoarchean Nsuze Group (Pongola Supergroup) and Neoarchean Ventersdorp Supergroup. Following upon these Archean events, shorter-lived Proterozoic large igneous provinces also intrude the Transvaal Supergroup, Olifantshoek Supergroup and Umkondo Group, and include the world’s largest layered intrusion, the Bushveld Complex. Longer-lived late Paleoproterozoic magmatic events are also preserved as mafic intrusions and lava units within the Waterberg and Soutpansberg groups as well as the granitic basement. Many gaps in our knowledge of the Precambrian mafic record of the Kalahari craton remain, but further multi-disciplinary studies combining the latest advances in U–Pb geochronology and both paleomagnetism and geochemistry will help solve the Precambrian paleogeographic puzzle.
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- Nadeem, Aftab, et al.
(författare)
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Protein receptor-independent plasma membrane remodeling by HAMLET: a tumoricidal protein-lipid complex.
- 2015
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Ingår i: Scientific Reports. - : Springer Science and Business Media LLC. - 2045-2322. ; 5
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Tidskriftsartikel (refereegranskat)abstract
- A central tenet of signal transduction in eukaryotic cells is that extra-cellular ligands activate specific cell surface receptors, which orchestrate downstream responses. This ''protein-centric" view is increasingly challenged by evidence for the involvement of specialized membrane domains in signal transduction. Here, we propose that membrane perturbation may serve as an alternative mechanism to activate a conserved cell-death program in cancer cells. This view emerges from the extraordinary manner in which HAMLET (Human Alpha-lactalbumin Made LEthal to Tumor cells) kills a wide range of tumor cells in vitro and demonstrates therapeutic efficacy and selectivity in cancer models and clinical studies. We identify a ''receptor independent" transformation of vesicular motifs in model membranes, which is paralleled by gross remodeling of tumor cell membranes. Furthermore, we find that HAMLET accumulates within these de novo membrane conformations and define membrane blebs as cellular compartments for direct interactions of HAMLET with essential target proteins such as the Ras family of GTPases. Finally, we demonstrate lower sensitivity of healthy cell membranes to HAMLET challenge. These features suggest that HAMLET-induced curvature-dependent membrane conformations serve as surrogate receptors for initiating signal transduction cascades, ultimately leading to cell death.
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