ZNF143, a human homolog of the transcriptional activator Staf, is a C2H2-type protein consisting of seven zinc finger domains. As a transcription factor (TF), ZNF143 is sequence specifically binding to chromatin and activates the expression of protein-coding and non-coding genes on a genome scale. Although it is ubiquitous expressed, its expression in cancer cells and tissues is usually higher than that in normal cells and tissues. Therefore, abnormal expression of ZNF143 is related to cancer cell survival, proliferation, differentiation, migration, and invasion, suggesting that new small molecules can be designed by targeting ZNF143 as it may be a good potential biomarker and therapeutic target for related cancers. However, the mechanism on how ZNF143 regulates its targeting gene remains unclear. Recently, with the development of chromatin conformation capture (3C) and its derivatives, and high-throughput sequencing technology, new findings have been obtained in the study of ZNF143. Pioneering studies have showed that ZNF143 binds directly to promoters and contributes to chromatin interactions connecting promoters to distal regulatory elements, such as enhancers. Further, it has proved that ZNF143 is involved in CCCTCbinding factor (CTCF) in establishing the conserved chromatin loops by cooperating with cohesin and other partners. These results indicate that ZNF143 is a key loop formation factor. In addition, we report ZNF143 is dynamically bound to chromatin during the cell cycle demonstrated that it is a potential mitotic bookmarking factor. It may be associated with CTCF for mitosis-to-G1 phase transition and chromatin loop re-establishment in early G1 phase. In the future, researchers could further clarify the fine mechanism of ZNF143 in mediating chromatin loops with the help of CUT&RUN (CUT&Tag) and Cut-C technology. Thus, in this review, we summarize the research progress of TF ZNF143 in detail and also predict the potential functions of ZNF143 in cell fate and identity based on our recent discoveries.

CBLB502, a Toll-like receptor (TLR)5 agonist derived from Salmonella flagellin, was shown to protect mammalian hematopoietic and gastrointestinal systems from acute irradiation syndrome and to stimulate regeneration. To explore whether CBLB502 can improve testicular injuries caused by irradiation, mice were intraperitoneally injected with 0.2 mg/kg CBLB502 or vehicle control 30 min prior to applying 5.0 Gy ionizing radiation (IR). We observed these mice for the following 120 days and determined that CBLB502 pretreatment alleviated IR-induced oxidative stress, alleviated the distorted architecture of seminiferous tubules, reversed the decline of sperm quantity and quality, and helped recover male mouse fertility. Additionally, CBLB502 efficiently reduced DNA damage and chromosomal aberrations in IR-treated mice and their offspring. Due to the suppression of p53-dependent apoptosis, in IR-treated mice, CBLB502 was shown to significantly activate the nuclear factor kappa B (NFκB) pathway and reduce the apoptotic rate in association with an increase in anti-apoptotic B-cell lymphoma (BCL)2 levels and a decrease in the levels of DNA repair protein and proliferating cell nuclear antigen (PCNA). Moreover, an IR-induced reduction in serum testosterone and superoxide dismutase (SOD) levels and an increase in malondialdehyde (MDA) levels were considerably reversed in CBLB502-pretreated mice. No significant reverse effects were found in Tlr5 knockout mice, suggesting that protection of the testis against IR by CBLB502 is primarily dependent on the TLR5 signaling pathway. Our results may help further investigations into potential CBLB502 applications for the protection of the male reproductive system during radiotherapy.

Vascular endothelial growth inhibitor (VEGI), also known as tumor necrosis factor superfamily member 15 or TNF ligand-related molecule 1, is identified as one kind of antiangiogenic cytokine that belongs to the tumor necrosis factor superfamily. VEGI includes three isoforms: VEGI-174, VEGI-192, and VEGI-251. VEGI can activate multiple signaling pathways including nuclear factor-kappaB, c-Jun N-terminal kinase, and p38 mitogen-activated protein kinase. Moreover, it suppresses endothelial cell proliferation, angiopoiesis, and tumor growth. Genetic engineering techniques have been used to produce recombinant human vascular endothelial growth inhibitor, and great progress has been made in its application for curing cancer. VEGI could serve as a potential target in the development of angiogenesis-based cancer therapy, and this paper briefly summarizes the progress of the research on VEGI.

As an important pro-inflammatory cytokine, interleukin-1beta (IL-1β) participates in a variety of physiological and pathological responses. In order to obtain higher yielded recombinant human interleukin-1 beta (rhIL-1β), we cloned hIL-1β cDNA sequences based on the coding sequence of human mature IL-1β. After recombinant pPICZαA/hIL-1β was separated and sequenced, we transformed recombinant pPICZαA/hIL-1β into Pichia pastoris GS115, SMD1168 and X-33 strain via electroporation. The results showed that recombinant pPICZαA/ hIL-1β had the highest expression level in X-33 Pichia pastoris. Subsequently, rhIL-1β was purified by sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE), and identified by Western blot. Then the fermentation process was optimized to increase product yield. Under the fermentation conditions of the absorption value of fermentation liquor before induction of 600, oxygen concentration of 20%, methanol concentration of 0.25% with pH 5.0, the yield of rhIL-1β reached to 250 mg/L after 72 h induction at 26°C. After aqueous two-phase extraction combined with chromatography, the purity of rhIL-1β was 95% and the yield was up to 85%. The biological activity of rhIL-1β was detected by MTT assay, and the result showed that rhIL-1β significantly inhibited the growth and proliferation of B16 melanoma cells.

In recent years, functional magnetic resonance technology has discovered that abnormal connections in different brain regions of the brain may serve as the pathophysiological mechanism of mental illness. Exploring the mechanism of information flow and integration between different brain regions is of great significance for understanding the pathophysiological mechanism of mental illness. This article aims to analyze the mechanism of depression by comparing human brain images of normal people and patients with depression and conduct research. Fluoxetine, a selective 5-HT reuptake inhibitor (SSRI) widely used in clinical practice, can selectively inhibit 5-HT transporter and block the reuptake of 5-HT by the presynaptic membrane. The effect of 5-HT is prolonged and increased, thereby producing antidepressant effects. It has low affinity for adrenergic, histaminergic, and cholinergic receptors and has a weaker effect, resulting in fewer adverse reactions. This paper uses the comparative experiment method and the Welch method and uses the average shortest path length L to describe the average value of the shortest path length between two nodes in the network. Attention refers to the ability of a person’s mental activity to point and to concentrate on something. Sustained attention means that attention is kept on a certain cognitive object or activity for a certain period of time, which is also called the stability of attention. The research on attention of depression patients generally focuses on continuous attention, and the results obtained show inconsistencies. Most studies have shown that the sustained attention of the depression group is significantly worse than that of the healthy control group. An overview of magnetic resonance imaging technology and an analysis of depression based on resting state were carried out. The key brain areas of the sample core network were scanned, and the ALFF results were analyzed. The data showed that the severity of depression in the depression group was negatively correlated with the ReHo value in the posterior left cerebellum ( P = 0.010 ). The sense of despair was negatively correlated with the ReHo value in the posterior right cerebellum ( P = 0.013 ). The diurnal variation was negatively correlated with the ReHo value of the left ring ( P = 0.014 ). It was positively correlated with the ReHo value of the left ventricle ( P = 0.048 ). This experiment has better completed the research on the mechanism of depression by analyzing the functional images of patients with depression and normal human brain.