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Nanoarmor strengthens the structure and function of single cells by coating and encapsulating nanomaterials on single cells. It has tremendous potential for environmental, energy, and medical applications.Nanoarmor can isolate cells from their environment, endowing them with catalytic functions and photoelectric properties, and protecting the patient when used for medical applications.Nanoarmor can endow cells with self-driving capability, which has good prospects for applications in disease treatments.Nanoarmor can form heterojunctions on cells to facilitate electron transfer.Nanoarmor can be formed through biomineralization or biomimetic mineralization, with different involvements of the cell. Single cell modification or hybridization technology has become a popular direction in bioengineering in recent years, with applications in clean energy, environmental stewardship, and sustainable human development. Here, we draw attention to nanoarmor, a representative achievement of cytoprotection and functionalization technology. The fundamental principles of nanoarmor need to be studied with input from multiple disciplines, including biology, chemistry, and material science. In this review, we explain the role of nanoarmor and review progress in its applications. We also discuss three main challenges associated with its development: self-driving ability, heterojunction characteristics, and mineralization formation. Finally, we propose a preliminary classification system for nanoarmor. Single cell modification or hybridization technology has become a popular direction in bioengineering in recent years, with applications in clean energy, environmental stewardship, and sustainable human development. Here, we draw attention to nanoarmor, a representative achievement of cytoprotection and functionalization technology. The fundamental principles of nanoarmor need to be studied with input from multiple disciplines, including biology, chemistry, and material science. In this review, we explain the role of nanoarmor and review progress in its applications. We also discuss three main challenges associated with its development: self-driving ability, heterojunction characteristics, and mineralization formation. Finally, we propose a preliminary classification system for nanoarmor.

Soil heavy metals pollution can cause many serious environment problems because of involving a very complex pollution process for soil health. Therefore, it is very important to explore methods that can effectively evaluate heavy metal pollution. Researchers were actively looking for new ideas and new methods for evaluating and predicting levels of soil heavy metal pollution. The study on microbial communities is one of the effective methods using gene chip technology. Gene chip technology, as a high-throughput metagenomics analysis technique, has been widely used for studying the structure and function of complex microbial communities in different polluted environments from different pollutants, including the soil polluted by heavy metals. However, there is still a lack of a systematic summarization for the polluted soil by heavy metals. This paper systematically analyzed soil heavy metals pollution via reviewing previous studies on applying gene chip technology, including single species, tolerance mechanisms, enrichment mechanisms, anticipation and evaluation of soil remediation, and multi-directional analysis. The latest gene chip technologies and corresponding application cases for discovering critical species and functional genes via analyzing microbial communities and evaluating heavy metal pollution of soil were also introduced in this paper. This article can provide scientific guidance for researchers actively investigating the soil polluted by heavy metals.

The mechanism of action of artemisinin and its derivatives, the most potent of the anti-malarial drugs, is not completely understood. Here we present an unbiased chemical proteomics analysis to directly explore this mechanism in Plasmodium falciparum . We use an alkyne-tagged artemisinin analogue coupled with biotin to identify 124 artemisinin covalent binding protein targets, many of which are involved in the essential biological processes of the parasite. Such a broad targeting spectrum disrupts the biochemical landscape of the parasite and causes its death. Furthermore, using alkyne-tagged artemisinin coupled with a fluorescent dye to monitor protein binding, we show that haem, rather than free ferrous iron, is predominantly responsible for artemisinin activation. The haem derives primarily from the parasite’s haem biosynthesis pathway at the early ring stage and from haemoglobin digestion at the latter stages. Our results support a unifying model to explain the action and specificity of artemisinin in parasite killing. The mechanism of action of artemisinin, an antimalarial drug, is not well understood. Here, the authors use a labelled artemisinin analogue to show that the drug is mainly activated by haem and then binds covalently to over 120 proteins in the malaria parasite, affecting many of its cellular processes.

There is growing concern about the potential ecological risks posed by pharmaceutical residues in the aquatic environment. However, our understanding of the toxic effects of antiepileptic pharmaceuticals, such as carbamazepine (CBZ), on aquatic animal larvae is still limited. In this study, the tadpoles of the black-spotted pond frog (Pelophylax nigromaculatus) were exposed to environmentally relevant concentrations of CBZ (0.3 and 3.0 μg/L) for 30 days, and their growth, intestinal microbial composition, and metabolites were investigated to assess the potential toxic effects of CBZ in non-targeted aquatic organisms. Some tadpoles died during exposure, but there was no significant among-group difference in the survival and growth rates. CBZ exposure significantly altered the composition of tadpole intestinal microbiota. Relative abundances of some bacterial genera (e.g., Blautia, Prevotella, Bacillus, Microbacterium, etc.) decreased, while others (e.g., Paucibacter, etc.) increased in CBZ-exposed tadpoles. Interestingly, CBZ-induced alterations in some bacteria might not necessarily lead to adverse outcomes for animals. Meanwhile, small molecular intestinal metabolites related to energy metabolism, and antioxidant and anti-inflammatory activities were also altered after exposure. Taken together, environmentally relevant levels of CBZ might alter the metabolic and immune performances of amphibian larvae by modifying the abundance of some specific bacteria and the level of metabolites in their intestines, thereby potentially causing a long-term effect on their fitness.

A template-free strategy was designed to prepare hierarchical porous carbons (HPCs) using fluid catalytic cracking oil modified a coal tar pitch (CTP). The resulting HPCs possess large specific surface areas, reasonable pore size distributions, and wrinkled structures, which could improve the overall electrochemical performance. They exhibit a specific capacitance value of 329 F g −1 at 0.5 A g −1 and still maintain 220 F g −1 at 20 A g −1 , manifesting the remarkable rate capability. Additionally, the assembled symmetrical supercapacitor delivers a highest energy density of 23.6 Wh kg −1 at a power density of 500 W kg −1 and outstanding cycle stability of 92.8% capacitance retention after 10000 cycles. This work paves a new way to fabricate advanced carbon materials from low-cost CTP and provides a promising approach for value-added utilization of CTP. Graphical abstract

Hydrogen sulfide (H 2 S) is now widely considered the third endogenous gasotransmitter and plays critical roles in cancer biological processes. In this study, we demonstrate that 5-(4-hydroxyphenyl)-3H-1,2-dithiole-3-thione (ADT-OH), the most widely used moiety for synthesising slow-releasing H 2 S donors, induces melanoma cell death in vitro and in vivo. Consistent with previous reports, ADT-OH inhibited IκBɑ degradation, resulting in reduced NF-κB activation and subsequent downregulation of the NF-κB-targeted anti-apoptotic proteins XIAP and Bcl-2. More importantly, we found that ADT-OH suppressed the ubiquitin-induced degradation of FADD by downregulating the expression of MKRN1, an E3 ubiquitin ligase of FADD. In addition, ADT-OH had no significant therapeutic effect on FADD-knockout B16F0 cells or FADD-knockdown A375 cells. Based on these findings, we evaluated the combined effects of ADT-OH treatment and FADD overexpression on melanoma cell death in vivo using a mouse xenograft model. As expected, tumour-specific delivery of FADD through a recombinant Salmonella strain, VNP-FADD, combined with low-dose ADT-OH treatment significantly inhibited tumour growth and induced cancer cell apoptosis. Taken together, our data suggest that ADT-OH is a promising cancer therapeutic drug that warrants further investigation into its potential clinical applications.

This study was designed to evaluate ERK5 expression in lung cancer and malignant melanoma progression and to ascertain the involvement of ERK5 signaling in lung cancer and melanoma. We show that ERK5 expression is abundant in human lung cancer samples, and elevated ERK5 expression in lung cancer was linked to the acquisition of increased metastatic and invasive potential. Importantly, we observed a significant correlation between ERK5 activity and FAK expression and its phosphorylation at the Ser910 site. Mechanistically, ERK5 increased the expression of the transcription factor USF1, which could transcriptionally upregulate FAK expression, resulting in FAK signaling activation to promote cell migration. We also provided evidence that the phosphorylation of FAK at Ser910 was due to ERK5 but not ERK1/2, and we then suggested a role for Ser910 in the control of cell motility. In addition, ERK5 had targets in addition to FAK that regulate epithelial-to-mesenchymal transition and cell motility in cancer cells. Taken together, our findings uncover a cancer metastasis-promoting role for ERK5 and provide the rationale for targeting ERK5 as a potential therapeutic approach.

. is described, which is the fourth species distributed in the Ailao Mountains in Yunnan, China. Detailed illustrations of the habitus and diagnostic characters of the new species are provided. Furthermore, an identification key to all four species recorded in the Ailao Mountains is presented, supplemented by geographical and altitudinal distribution maps.

Adenylate kinase 2 (AK2) is a wide-spread and highly conserved protein kinase whose main function is to catalyze the exchange of nucleotide phosphate groups. In this study, we showed that AK2 regulated tumor cell metastasis in lung adenocarcinoma. Positive expression of AK2 is related to lung adenocarcinoma progression and poor survival of patients. Knockdown or knockout of AK2 inhibited, while overexpression of AK2 promoted, human lung adenocarcinoma cell migration and invasion ability. Differential proteomics results showed that AK2 might be closely related to epithelial-mesenchymal transition (EMT). Further research indicated that AK2 regulated EMT occurrence through the Smad-dependent classical signaling pathways as measured by western blot and qPCR assays. Additionally, in vivo experiments showed that AK2-knockout in human lung tumor cells reduced their EMT-like features and formed fewer metastatic nodules both in liver and in lung tissues. In conclusion, we uncover a cancer metastasis-promoting role for AK2 and provide a rationale for targeting AK2 as a potential therapeutic approach for lung cancer.

Chinese hamster ovary (CHO) cells serve as the predominant mammalian expression system for recombinant protein production. However, clonal heterogeneity and instability in recombinant protein expression remain significant challenges. SET domain bifurcated histone lysine methyltransferase 1 (SETDB1) catalyzes histone 3 lysine 9 trimethylation (H3K9me3), a critical epigenetic modification regulating gene expression. Despite its functional importance, the dynamics of SETDB1 expression and its regulatory impacts in CHO cells remain poorly characterised. Through transcriptomic analysis of high- and low monoclonal antibody (mAb)-producing CHO clones, we identified SETDB1 as a key modulator of mAb expression. Notably, SETDB1 expression exhibited an inverse correlation with recombinant protein levels in transfected CHO cells. SETDB1-knockdown (SETDB1-KD) CHO cells demonstrated significantly enhanced recombinant antibody-specific productivity. The use of small-molecule SETDB1 inhibitors resulted in a comparable enhancement of transgene expression to that observed with SETDB1 silencing. During extended cultivation, recombinant protein production progressively diminished concurrent with declining SETDB1-KD efficacy. This temporal correlation demonstrates that SETDB1-mediated epigenetic regulation is essential for maintaining both recombinant protein titers and chromosomal stability in industrial biomanufacturing processes. Transcriptome dynamics analysis revealed that SETDB1 silencing induces transcriptional pattern remodeling in transfected cells. These findings elucidate SETDB1's regulatory role in CHO cells and provide actionable insights for the optimisation of recombinant protein production through cell engineering strategies.