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Immobilizing of attapulgite into phthalocyanine not only enhanced the catalytic efficiency of metal phthalocyanine compound materials but also prevented the aggregation of phthalocyanines. Therefore, a novel isoamoxyphthalocyanine-attapulgite (ZnPc(3-iso-PeO)4-ATP) composites were fabricated by the ultrasonic impregnation menthod. The as-prepared ZnPc(3-iso-PeO)4-ATP composites were characterized by powder X-ray diffraction, Fourier transform infrared spectra, scanning electron microscopy (SEM), transmission electron microscopy, thermogravimetric analysis and UV–Vis diffuse reflectance spectroscopy spectra. The photocatalytic activities of as-obtained photocatalysts were measured by the degradation of malachite green (MG) under visible-light irradiation. The optimal conditions for the degradation of MG were determined with changing kind of catalysts and the ratio of phthalocyanine to attapulgite. In the ZnPc(3-iso-PeO)4-ATP system, it was demonstrated that preventing the aggregation of phthalocyanines was helpful to enhance the photocatalytic property. It was found that the degradation efficiency of MG reached 70% after 50 min when the ratio of ZnPc(3-iso-PeO)4 to ATP was up to 2:1. Furthermore, the possible visible-light photocatalytic mechanism of ZnPc(3-iso-PeO)4-ATP composites for the photodegradation of MG was also discussed. The excellent activity is mainly attributed to its more effective separation of electron–hole pairs. [ABSTRACT FROM AUTHOR]

etylcholinesterase inhibitors played significant roles in treatment of Alzheimer's disease. Based on the research foundation of our previous work and molecular modeling, twelve 3,6-diaryl-7 H-thiazolo[3,2- b][1,2,4]triazin-7-one derivatives were synthesized and characterized by mass spectra, infrared spectra, NMR and elemental analyses. The study of AChE inhibitory activity was carried out using the Ellman colorimetric assay with huperzine-A as the positive control. All target compounds exhibited more than 40% inhibition at 10 μM. Some target compounds showed good inhibition against AChE. The preliminary structure-activity relationships were the halogen atoms at the phenyl ring at the C6 position, the hydroxy groups and the long side chains at the phenyl ring at the C3 position of the parent nucleus played significant roles in the AChE inhibitory activity of the target compounds. [ABSTRACT FROM AUTHOR]

2'-O-methylation is one of the most prevalent RNA modifications found in different RNA types. However, the identities of enzymes participating in the transfer of methyl groups are not well defined. To date, fibrillarin (FBL) is the only known small nucleolar ribonucleoprotein (snoRNP) 2'-O-methyltransferase. Whether other snoRNP 2'-O-methyltransferases exist and their functions in targeting RNAs to determine cell differentiation and function need to be elucidated. Here, we identify FBL-like protein 1 (FBLL1) as a 2'-O-methyltransferase and find its function in promoting neuronal differentiation. We show that FBLL1 is a key snoRNP complex enzyme that transfers methyl groups to substrate RNAs both in vitro and in vivo. Moreover, FBLL1 exhibits different 2'-O-methyltransferase site selectivity from FBL and tissue-specific distribution. FBLL1 is preferentially expressed in the brain, especially in human neuron cells, and promotes neuronal differentiation through 2'-O-methylation of GAP43 messenger RNA (mRNA). Knockdown of FBLL1, but not FBL, reduced 2'-O-methylation levels in GAP43 mRNA, decreased expression of GAP43 proteins, and eventually repressed neuronal differentiation. Our finding of neuron-specific FBLL1 adds insights into RNA modification in neurobiology and provides clues for understanding 2'-O-methylation in health and disease., Competing Interests: Competing interests statement:The authors declare no competing interest.

The innate immune system initiates innate immune responses by recognizing pathogen-related molecular patterns on the surface of pathogenic microorganisms through pattern recognition receptors. Through cascade signal transduction, it activates downstream transcription factors NF-κB and interferon regulatory factors (IRFs), and then leads to the production of inflammatory cytokines and type Ⅰ interferon, which resists the infection of pathogenic microorganism. TBK1 is a central adapter protein of innate immune signaling pathway and can activate both NF-κB and IRFs. It is a key protein kinase in the process of anti-infection. The finetuning regulation of TBK1 is essential to maintain immune homeostasis and resist pathogen invasion. This paper reviews the biological functions and ubiquitin modification of TBK1 in innate immunity, to provide theoretical basis for clinical treatment of pathogenic infections and autoimmune diseases.

MicroRNAs (miRNAs/miRs) are small, non-coding RNAs that are reported to serve numerous important regulatory functions; however, the role of miRNAs in regulating breast cancer cell biology remains poorly understood. Accumulating evidence has demonstrated that miRNAs orchestrate multiple cellular functions and serve crucial roles in cell differentiation and cancer development, either by acting as tumor suppressors or oncogenes. In particular, miR-155-5p expression levels have been found to be upregulated and serve as a prognostic marker in numerous types of solid cancer, including human breast cancer. More than half of patients with breast cancer benefit from treatment with adjuvant paclitaxel chemotherapy following the early postoperative period. Despite the initial response to intensive combination chemotherapy, the majority of most patients will eventually acquire resistance to the drug and succumb to their disease. Therefore, further investigations into the association between miRNAs and the mechanism of paclitaxel resistance are required. The results of the present study revealed a strong positive association between miR-155-5p expression levels and the paclitaxel resistance, as the expression levels of miR-155-5p were upregulated in resistant cells. MiR-155-5p was further validated to regulate paclitaxel resistance using gain- and loss-of-function experiments. TP53INP1 was identified as a direct target gene of miR-155-5p by combining the results from the prediction algorithm based on free energy minimization and reverse transcription-quantitative PCR (qRT-PCR) analysis. Also, miR-155-5p was suggested to be a key regulator of paclitaxel resistance in tumor cells, as it increased cell viability and motility, and promoted resistance to paclitaxel-induced apoptosis. The transfection with miR-155-5p inhibitors re-sensitized the paclitaxel-resistant breast cancer cells, while the overexpression of miR-155-5p led to an increase in the resistance to paclitaxel. Furthermore, the overexpression of the target gene, TP53INP1, contributed to the re-sensitivity of drug-resistant cells to paclitaxel. The subsequent combination of the knockdown of miR-155-5p and the overexpression of TP53INP1 conferred paclitaxel sensitivity in resistant cells. These results may enhance the understanding of the molecular mechanisms underlying breast cancer progression and resistance to chemotherapy, and suggested that miR-155-5p or TP53INP1 may serve as novel therapeutic approaches to combat resistance to therapy, as well as the proliferation and evasion of apoptosis in breast cancer., (Copyright © 2021 Elsevier GmbH. All rights reserved.)