| 1. |
- Miao, Fengjuan, et al.
(författare)
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Inkjet printing of electrochemically-exfoliated graphene nano-platelets
- 2016
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Ingår i: Synthetic metals. - : Elsevier. - 0379-6779 .- 1879-3290. ; 220, s. 318-322
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Tidskriftsartikel (refereegranskat)abstract
- In this study, we report on a facile method of inkjet printing of graphene nano-platelets (GNPs). The GNPs are exfoliated from graphite by means of an electrochemical process in an inorganic salt based electrolyte. The electrochemically exfoliated GNPs with oxygen-bearing functional groups exhibit spectroscopic features similar to those of reduced graphene oxides. As a result, ink formulation with such GNPs for inkjet printing readily accomplishes without using stabilizer and various conductive objects are easily fabricated on different substrates by inkjet printing. The as-printed films of the electrochemically exfoliated GNPs deliver an electrical conductivity of 44 S/m, a typical value for as-printed pristine GNP films in the literature. A simple thermal treatment results in an improved DC conductivity by two orders of magnitude to ~2.5 × 103 S/m.
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| 2. |
- Zhang, Xiao-Jie, et al.
(författare)
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Auto-suppression of Tet dioxygenases protects the mouse oocyte genome from oxidative demethylation
- 2024
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Ingår i: Nature Structural & Molecular Biology. - : NATURE PORTFOLIO. - 1545-9993 .- 1545-9985. ; 31:1
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Tidskriftsartikel (refereegranskat)abstract
- DNA cytosine methylation plays a vital role in repressing retrotransposons, and such derepression is linked with developmental failure, tumorigenesis and aging. DNA methylation patterns are formed by precisely regulated actions of DNA methylation writers (DNA methyltransferases) and erasers (TET, ten-eleven translocation dioxygenases). However, the mechanisms underlying target-specific oxidation of 5mC by TET dioxygenases remain largely unexplored. Here we show that a large low-complexity domain (LCD), located in the catalytic part of Tet enzymes, negatively regulates the dioxygenase activity. Recombinant Tet3 lacking LCD is shown to be hyperactive in converting 5mC into oxidized species in vitro. Endogenous expression of the hyperactive Tet3 mutant in mouse oocytes results in genome-wide 5mC oxidation. Notably, the occurrence of aberrant 5mC oxidation correlates with a consequent loss of the repressive histone mark H3K9me3 at ERVK retrotransposons. The erosion of both 5mC and H3K9me3 causes ERVK derepression along with upregulation of their neighboring genes, potentially leading to the impairment of oocyte development. These findings suggest that Tet dioxygenases use an intrinsic auto-regulatory mechanism to tightly regulate their enzymatic activity, thus achieving spatiotemporal specificity of methylome reprogramming, and highlight the importance of methylome integrity for development. Here the authors show that TET dioxygenases, the erasers of DNA methylation, use a self-limiting mechanism via their LCD domain to ensure adaptable methylome status and protect the genome from excessive oxidative methylation.
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| 3. |
- Tao, Bairui, et al.
(författare)
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Three-dimensional graphene nanosheets supported by NiO/Si-MCP as electrode materials for high-performance supercapacitors
- 2017
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Ingår i: Ionics (Kiel). - : Springer Science and Business Media LLC. - 0947-7047 .- 1862-0760. ; 23:8, s. 2185-2191
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Tidskriftsartikel (refereegranskat)abstract
- A three-dimensional (3D) graphene/NiO/Si-microchannel (MCP) composite electrode is synthesized by the conventional microelectronic machining process and electrochemical exfoliation technology for electrochemical capacitors. SEM, AFM, and Raman scattering are used to investigate the morphology and structure, and electrochemical characterization reveals that the 3D graphene/NiO/Si-MCP has a high specific capacitance of 833 Fg-1 at a current density of 5 Ag-1 in 6 mol L-1 KOH. Moreover, good cycling performance with 92% capacitance retention after 1000 cycles is observed indicating the novel electrode has large potential in high-performance supercapacitors.
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| 4. |
- Wang, Yangyang, et al.
(författare)
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UHRF2 promotes DNA damage response by decreasing p21 via RING finger domain
- 2018
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Ingår i: Biotechnology letters. - : SPRINGER. - 0141-5492 .- 1573-6776. ; 40:8, s. 1181-1188
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Tidskriftsartikel (refereegranskat)abstract
- To investigate the interaction of E3 ubiquitin ligase UHRF2 with p21 and the mechanism of UHRF2 in repairing DNA damage caused by hydroxyurea (HU) in HEK293 cells. Western blotting indicated that the overexpression of UHRF2 reduced the level of p21, particularly in HEK293 cells. Immunoprecipitation and immunofluorescence staining reveled that UHRF2 combined with p21 in the nucleus. In addition, UHRF2 degraded p21 through ubiquitination and shortened the half-life of p21. UHRF2 could repair DNA damage caused by HU treatment, which was impaired by the inhibition of p21 in HEK293 cells. UHRF2 may negatively modulate p21 to regulate DNA damage response, suggesting a novel pathway of UHRF2 repairing DNA damage through the partial regulation of p21.
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