| 1. |
- Dong, Yu, et al.
(författare)
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Observation of a Ubiquitous (π, π)-Type Nematic Superconducting Order in the Whole Superconducting Dome of Ultra-Thin BaFe2–xNixAs2 Single Crystals
- 2021
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Ingår i: Chinese Physics Letters. - : Institute of Physics Publishing (IOPP). - 0256-307X .- 1741-3540. ; 38:9
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Tidskriftsartikel (refereegranskat)abstract
- In iron-based superconductors, the (0, pi) or (pi, 0) nematicity, which describes an electronic anisotropy with a four-fold symmetry breaking, is well established and believed to be important for understanding the superconducting mechanism. However, how exactly such a nematic order observed in the normal state can be related to the superconducting pairing is still elusive. Here, by performing angular-dependent in-plane magnetoresistivity using ultra-thin flakes in the steep superconducting transition region, we unveil a nematic superconducting order along the (pi, pi) direction in electron-doped BaFe2 - x Ni x As2 from under-doped to heavily overdoped regimes with x = 0.065-0.18. It shows superconducting gap maxima along the (pi, pi) direction rotated by 45 degrees from the nematicity along (0, pi) or (pi, 0) direction observed in the normal state. A similar (pi, pi)-type nematicity is also observed in the under-doped and optimally doped hole-type Ba1 - y K y Fe2As2, with y = 0.2-0.5. These results suggest that the (pi, pi) nematic superconducting order is a universal feature that needs to be taken into account in the superconducting pairing mechanism in iron-based superconductors.
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| 2. |
- Andersson, Anna, et al.
(författare)
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The landscape of somatic mutations in infant MLL-rearranged acute lymphoblastic leukemias.
- 2015
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Ingår i: Nature Genetics. - : Springer Science and Business Media LLC. - 1546-1718 .- 1061-4036. ; 47:4, s. 192-330
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Tidskriftsartikel (refereegranskat)abstract
- Infant acute lymphoblastic leukemia (ALL) with MLL rearrangements (MLL-R) represents a distinct leukemia with a poor prognosis. To define its mutational landscape, we performed whole-genome, exome, RNA and targeted DNA sequencing on 65 infants (47 MLL-R and 18 non-MLL-R cases) and 20 older children (MLL-R cases) with leukemia. Our data show that infant MLL-R ALL has one of the lowest frequencies of somatic mutations of any sequenced cancer, with the predominant leukemic clone carrying a mean of 1.3 non-silent mutations. Despite this paucity of mutations, we detected activating mutations in kinase-PI3K-RAS signaling pathway components in 47% of cases. Surprisingly, these mutations were often subclonal and were frequently lost at relapse. In contrast to infant cases, MLL-R leukemia in older children had more somatic mutations (mean of 6.5 mutations/case versus 1.3 mutations/case, P = 7.15 × 10(-5)) and had frequent mutations (45%) in epigenetic regulators, a category of genes that, with the exception of MLL, was rarely mutated in infant MLL-R ALL.
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| 3. |
- Faber, Zachary J, et al.
(författare)
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The genomic landscape of core-binding factor acute myeloid leukemias
- 2016
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Ingår i: Nature Genetics. - : Springer Science and Business Media LLC. - 1546-1718 .- 1061-4036. ; 48, s. 1551-1556
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Tidskriftsartikel (refereegranskat)abstract
- Acute myeloid leukemia (AML) comprises a heterogeneous group of leukemias frequently defined by recurrent cytogenetic abnormalities, including rearrangements involving the core-binding factor (CBF) transcriptional complex. To better understand the genomic landscape of CBF-AMLs, we analyzed both pediatric (n = 87) and adult (n = 78) samples, including cases with RUNX1-RUNX1T1 (n = 85) or CBFB-MYH11 (n = 80) rearrangements, by whole-genome or whole-exome sequencing. In addition to known mutations in the Ras pathway, we identified recurrent stabilizing mutations in CCND2, suggesting a previously unappreciated cooperating pathway in CBF-AML. Outside of signaling alterations, RUNX1-RUNX1T1 and CBFB-MYH11 AMLs demonstrated remarkably different spectra of cooperating mutations, as RUNX1-RUNX1T1 cases harbored recurrent mutations in DHX15 and ZBTB7A, as well as an enrichment of mutations in epigenetic regulators, including ASXL2 and the cohesin complex. This detailed analysis provides insights into the pathogenesis and development of CBF-AML, while highlighting dramatic differences in the landscapes of cooperating mutations for these related AML subtypes.
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| 4. |
- Liu, Chang, et al.
(författare)
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Oligomer Dynamics of LL-37 Truncated Fragments Probed by α-Hemolysin Pore and Molecular Simulations
- 2023
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Ingår i: Small. - 1613-6810 .- 1613-6829. ; 19:37
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Tidskriftsartikel (refereegranskat)abstract
- Oligomerization of antimicrobial peptides (AMPs) is critical in their effects on pathogens. LL-37 and its truncated fragments are widely investigated regarding their structures, antimicrobial activities, and application, such as developing new antibiotics. Due to the small size and weak intermolecular interactions of LL-37 fragments, it is still elusive to establish the relationship between oligomeric states and antimicrobial activities. Here, an α-hemolysin nanopore, mass spectrometry (MS), and molecular dynamic (MD) simulations are used to characterize the oligomeric states of two LL-37 fragments. Nanopore studies provide evidence of trapping events related to the oligomer formation and provide further details on their stabilities, which are confirmed by MS and MD simulations. Furthermore, simulation results reveal the molecular basis of oligomer dynamics and states of LL-37 fragments. This work provides unique insights into the relationship between the oligomer dynamics of AMPs and their antimicrobial activities at the single-molecule level. The study demonstrates how integrating methods allows deciphering single molecule level understanding from nanopore sensing approaches.
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| 5. |
- Loch, Rolf Antonie, et al.
(författare)
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Cross interactions between Apolipoprotein E and amyloid proteins in neurodegenerative diseases
- 2023
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Ingår i: Computational and Structural Biotechnology Journal. - : Elsevier BV. - 2001-0370. ; 21, s. 1189-1204
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Tidskriftsartikel (refereegranskat)abstract
- Three common Apolipoprotein E isoforms, ApoE2, ApoE3, and ApoE4, are key regulators of lipid homeostasis, among other functions. Apolipoprotein E can interact with amyloid proteins. The isoforms differ by one or two residues at positions 112 and 158, and possess distinct structural conformations and functions, leading to isoform-specific roles in amyloid-based neurodegenerative diseases. Over 30 different amyloid proteins have been found to share similar characteristics of structure and toxicity, suggesting a common interactome. The molecular and genetic interactions of ApoE with amyloid proteins have been extensively studied in neurodegenerative diseases, but have not yet been well connected and clarified. Here we summarize essential features of the interactions between ApoE and different amyloid proteins, identify gaps in the understanding of the interactome and propose the general interaction mechanism between ApoE isoforms and amyloid proteins. Perhaps more importantly, this review outlines what we can learn from the interactome of ApoE and amyloid proteins; that is the need to see both ApoE and amyloid proteins as a basis to understand neurodegenerative diseases.
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| 6. |
- Wang, Hongzhi, et al.
(författare)
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ATP Impedes the Inhibitory Effect of Hsp90 on Aβ(40) Fibrillation
- 2021
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Ingår i: Journal of Molecular Biology. - : Elsevier BV. - 0022-2836 .- 1089-8638. ; 433:2
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Tidskriftsartikel (refereegranskat)abstract
- Heat shock protein 90 (Hsp90) is a molecular chaperone that assists protein folding in an Adenosine triphosphate (ATP)-dependent way. Hsp90 has been reported to interact with Alzheimer's disease associated amyloid-beta (A beta) peptides and to suppress toxic oligomer- and fibril formation. However, the mechanism remains largely unclear. Here we use a combination of atomic force microscopy (AFM) imaging, circular dichroism (CD) spectroscopy and biochemical analysis to quantify this interaction and put forward a microscopic picture including rate constants for the different transitions towards fibrillation. We show that Hsp90 binds to A beta(40) monomers weakly but inhibits A beta(40) from growing into fibrils at substoichiometric concentrations. ATP impedes this interaction, presumably by modulating Hsp90's conformational dynamics and reducing its hydrophobic surface. Altogether, these results might indicate alternative ways to prevent A beta(40) fibrillation by manipulating chaperones that are already abundant in the brain.
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| 7. |
- Wu, Jinming, et al.
(författare)
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Identifying the role of co-aggregation of Alzheimer's amyloid-beta with amorphous protein aggregates of non-amyloid proteins
- 2022
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Ingår i: Cell Reports Physical Science. - : Elsevier BV. - 2666-3864. ; 3:9
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Tidskriftsartikel (refereegranskat)abstract
- Protein homeostasis collapse typically leads to protein aggregation into amyloid fibrils and diffuse amorphous aggregates, which both occur in Alzheimer’s and other neurodegenerative diseases, but their relationship remains to be clarified. Here we examine the interactions between the amorphously aggregated non-chaperone proteins (albumin, β-lactoglobulin, and superoxide dismutase 1) and Alzheimer’s amyloid-β (Aβ) peptides. Amorphous aggregates suppress the primary nucleation and elongation of Aβ fibrillation and modulate Aβ toxicity. The higher inhibitory efficiency of intermediately sized molten globular aggregates (20–300 nm) on Aβ fibrillation is hypothesized to be due to the higher amount of exposed hydrophobic residues and higher free energy. The formed co-aggregates are off-pathway species that favor formation of the amorphous end state instead of fibrillar amyloid structures normally formed by Aβ. Our findings expand our knowledge of how the native and aggregated cellular proteins modulate Aβ aggregation at the molecular and mesoscopic level and point out the major conclusions.
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| 8. |
- Zhang, Qing, et al.
(författare)
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Andersson-Magnéli Phases TinO2n-1 : Recent Progress Inspired by Swedish Scientists
- 2021
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Ingår i: Zeitschrift für Anorganische und Allgemeines Chemie. - : Wiley. - 0044-2313 .- 1521-3749. ; 647:2-3, s. 126-133
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Tidskriftsartikel (refereegranskat)abstract
- Among homologous series of metal oxides, Andersson-Magneli phases TinO2n-1 (n=4-10) have attracted renewed scientific attention because of their behaviour in electrical conductivity and chemical/thermal stability. Various applications have also been reported for the phases with different values of n, or slightly reduced rutile (TiO2). The characteristic properties of these materials depend strongly on the compositional deviation from TiO2 and the way in which the structure accommodates the deviation. Thus, an urgent requirement is to overcome difficulties in characterizing such materials at atomic resolution. Here, we trace the discovery of the Andersson-Magneli phases, and report the application of recent developments in electron microscopy to reveal the relation, at the local level, between structural characteristics and electronic states, specifically for the materials TinO2n-1 with n=4-8. The electrical conductivity of Ti4O7 has been reported previously to show three clearly distinct states on decreasing temperature from 300 K. For this reason, we focus on Ti4O7 as a representative example of the TinO2n-1 phases and report structural characteristics at temperatures corresponding to each of the three different phases, focusing on the distribution of Ti3+ and Ti4+ cations from analysis of single-crystal XRD data. Electron diffraction experiments and electrical conductivity measurements are also reported.
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