Poly[bis­[μ2-2-(1H-1,2,4-triazol-1-yl)acetato]zinc(II)]

In the title compound, [Zn(C4H4N3O2)2]n, the ZnII atom is coordinated by two O atoms [Zn—O = 1.969 (2) and 1.997 (2) Å] and two N atoms [Zn—N = 2.046 (2) and 2.001 (2) Å] in a distorted tetra­hedral geometry. Non-classical inter­molecular C—H⋯O hydrogen bonds link the complex into a three-dimensional supra­molecular framework

Independent modulation of individual genomic component transcription and a cis-acting element related to high transcriptional activity in a multipartite DNA virus

Background: The genome of Banana bunchy top virus (BBTV) consists of at least six circular, single-stranded DNA components of 1kb in length. Some BBTV isolates may also carry satellite DNA molecules that are not essential for BBTV infection. The relation between multipartite DNA virus replication and their transcriptional levels and the underlying mechanism remain unclear. Results: To understand the coordinated replication and transcription of the multiple genomic components, the absolute amounts of each BBTV DNA component were measured by real-time PCR (qPCR), and their transcriptional levels were determined by RNAseq and reverse transcription-qPCR (qRT-PCR). Significant differences were found in the absolute amounts of individual BBTV genomic components. Transcriptional levels of each BBTV genomic component obtained from the RNAseq data matched closely to those obtained from qRT-PCR, but did not correspond to the absolute amount of each DNA component. The ratio of transcript over DNA copies ranged from 46.21 to 1059.44%, which was possibly regulated by the promoter region in the intergenic region of each component. To further determine this speculation, the promoter region of the DNA-S, -M or -N was constructed to the upstream of green fluorescent protein (GFP) gene for transient expression by agrobacterium-mediated transformation method. The qRT-PCR showed the highest transcriptional activity was promoted by DNA-N promoter, about 386.58% activity comparing with CaMV 35S promoter. Confocal microscopy observation showed that the intensity of green fluorescence was corresponding to that of qRT-PCR. Conclusions: Our data clearly showed that BBTV was able to control the transcriptional level of each DNA component independently by through the promoter sequences in the intergenic region. Moreover, a cis-acting element from DNA-N component had a high transcriptional activity.National Natural Science Foundation of China [31401709]; Hainan Provincial Natural Science Foundation [20153130]; Central Public-interest Scientific Institution Basal Research Fund for Chinese Academy of Tropical Agricultural Sciences [19CXTD-33]; Young Elite Scientists Sponsorship Program, CSTC [CSTC-QN201704]Open access journalThis item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at [email protected]

Interface-Engineered Ni-Coated CdTe Heterojunction Photocathode for Enhanced Photoelectrochemical Hydrogen Evolution.

Photoelectrochemical (PEC) water splitting for hydrogen production using the CdTe photocathode has attracted much interest due to its excellent sunlight absorption property and energy band structure. This work presents a study of engineered interfacial energetics of CdTe photocathodes by deposition of CdS, TiO2, and Ni layers. A heterostructure CdTe/CdS/TiO2/Ni photocathode was fabricated by depositing a 100-nm n-type CdS layer on a p-type CdTe surface, with 50 nm TiO2 as a protective layer and a 10 nm Ni layer as a co-catalyst. The CdTe/CdS/TiO2/Ni photocathode exhibits a high photocurrent density (Jph) of 8.16 mA/cm2 at 0 V versus reversible hydrogen electrode (VRHE) and a positive-shifted onset potential (Eonset) of 0.70 VRHE for PEC hydrogen evolution under 100 mW/cm2 AM1.5G illumination. We further demonstrate that the CdTe/CdS p-n junction promotes the separation of photogenerated carriers, the TiO2 layer protects the electrode from corrosion, and the Ni catalyst improves the charge transfer across the electrode/electrolyte interface. This work provides new insights for designing noble metal-free photocathodes toward solar hydrogen development

Antitumor Effects of Berberine on Gliomas via Inactivation of Caspase-1-Mediated IL-1β and IL-18 Release

Gliomas arise in the glial cells of the brain or spine and are the most prevalent and devastating type of brain tumors. Studies of tumor immunology have established the importance of the tumor micro-environment as a driver of oncogenesis. Inflammatory mediators such as IL-1β and IL-18 released by monocytes regulate transcriptional networks that are required for malignant cell growth. Berberine is a natural botanical alkaloid that is widely found in the Berberis species. Although it has been widely used as an anti-diarrheal treatment in North America for several decades, our study is the first to investigate berberine as an anti-tumor agent in glioma cells. In this study, we demonstrate that berberine significantly inhibits inflammatory cytokine Caspase-1 activation via ERK1/2 signaling and subsequent production of IL-1β and IL-18 by glioma cells. Moreover, we found that berberine treatment led to decreased motility and subsequently cell death in U251 and U87 cells. In addition, our study is the first to indicate that berberine can reverse the process of epithelial-mesenchymal transition, a marker of tumor invasion. Taken together, our work supports berberine as a putative anti-tumor agent targeting glioma cells

ATR/Chk1 signaling induces autophagy through sumoylated RhoB-mediated lysosomal translocation of TSC2 after DNA damage

RhoB作为抑癌蛋白通过诱导肿瘤细胞的凋亡在抑制肿瘤的发生发展中发挥着重要作用，并且与肿瘤耐药性密切相关，但关于RhoB如何促进细胞死亡的分子机理的研究仍不清楚。在本研究中，该团队发现在DNA单链损伤情况下，ATR-Chk1信号通路的激活，会使RhoB被Chk1磷酸化，该磷酸化修饰会使RhoB从细胞质膜解离下来进入细胞质中，进而被SUMO化修饰。SUMO化修饰后的RhoB会与TSC2形成复合物，并将TSC2复合物带到溶酶体上，引起细胞自噬的发生。 该文共同第一作者为刘明冬、曾涛玲和张新，通讯作者为王洪睿教授和赵同金教授。【Abstract】DNA damage can induce autophagy; however, the underlying mechanism remains largely unknown. Here we report that DNA damage leads to autophagy through ATR/Chk1/RhoB-mediated lysosomal recruitment of TSC complex and subsequent mTORC1 inhibition. DNA damage caused by ultraviolet light (UV) or alkylating agent methyl methanesulphonate (MMS) results in phosphorylation of small GTPase RhoB by Chk1. Phosphorylation of RhoB enhances its interaction with the TSC2, and promotes its sumoylation by PIAS1, which is required for RhoB/TSC complex to translocate to lysosomes. As a result, mTORC1 is inhibited, and autophagy is activated. Knockout of RhoB severely attenuates lysosomal translocation of TSC complex and the DNA damage-induced autophagy. Reintroducing wild-type but not sumoylation-resistant RhoB into RhoB−/− cells restores the onset of autophagy. Hence, our study identifies a molecular mechanism for translocation of TSC complex to lysosomes in response to DNA damage, which depends on ATR/Chk1-mediated RhoB phosphorylation and sumoylation.This work was supported by the National Natural Science Foundation of China (U1605222, 81472459, 31671223), the National Key Research and Development Project of China (2016YFC1302400, 2016YFA0502003), the Fundamental Research Funds for the Central Universities (20720140550, 20720160070), the National Science Foundation for Fostering Talents in Basic Research of the National Natural Science Foundation of China (J1310027), the Project 111 sponsored by the State Bureau of Foreign Experts and Ministry of Education (B12001), the National Natural Science Foundation of China (31601132) to T.Z., the National Natural Science Foundation of China (81402290) to Q.L., and the National Natural Science Foundation of China (U1405223) to X.D

Inhibition of Necroptosis Rescues SAH-Induced Synaptic Impairments in Hippocampus via CREB-BDNF Pathway

Subarachnoid hemorrhage (SAH) is a devastating form of stroke that leads to incurable outcomes. Increasing evidence has proved that early brain injury (EBI) contributes mostly to unfavorable outcomes after SAH. A previously unknown mechanism of regulated cell death known as necroptosis has recently been reported. Necrostatin-1 (nec-1), a specific and potent inhibitor of necroptosis, can attenuate brain impairments after SAH. However, the effect of nec-1 on the hippocampus and its neuroprotective impact on synapses after SAH is not well understood. Our present study was designed to investigate the potential effects of nec-1 administration on synapses and its relevant signal pathway in EBI after SAH. Nec-1 was administrated in a rat model via intracerebroventricular injection after SAH. Neurobehavior scores and brain edema were detected at 24 h after SAH occurred. The expression of the receptor-interacting proteins 1 and 3 (RIP1and3) was examined as a marker of necroptosis. We used hematoxylin and eosin staining, Nissl staining, silver staining and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) to observe the morphological changes in hippocampus. The protective effect of nec-1 on synapses was evaluated using western blotting and electron microscopy and Western blotting was used to detect the cAMP responsive element binding (CREB) protein and brain-derived neurotrophic factor (BDNF), and we used transmission electron microscopy and TUNEL to detect the protective effects of nec-1 when a specific inhibitor of CREB, known as 666-15, was used. Our results showed that in the SAH group, RIP1, and RIP3 significantly increased in the hippocampus. Additionally, injection of nec-1 alleviated brain edema and improved neurobehavior scores, compared with those in the SAH group. The damage to neurons was attenuated, and synaptic structure also improved in the Sham+nec-1 group. Furthermore, nec-1 treatment significantly enhanced the levels of phospho-CREB and BDNF compared with those in the SAH group. The protective effect of nec-1 could hindered by 666-15. Thus, nec-1 mitigated SAH-induced synaptic impairments in the hippocampus through the inhibition of necroptosis in connection with the CREB-BDNF pathway. This study may provide a new strategy for SAH patients in clinical practice