Abstract The transcription factor forkhead box K1 (FOXK1) has recently been recognized to mediate a wide range of biological progresses, including cell proliferation, differentiation, cell cycle progression, apoptosis, DNA damage, and tumorigenesis. However, the role and molecular mechanisms of FOXK1 in esophageal squamous cell carcinoma (ESCC) progression and in the response to ionizing radiation (IR) have not been well characterized. In this study, we investigated the expression level, clinical significance, biological role, and molecular mechanism of FOXK1 in ESCC. High expression level of FOXK1 was observed in ESCC cell lines and tissues, which was correlated with TNM stage, invasion depth, and lymph node metastasis. In addition, overexpression of FOXK1 promoted ESCC cells proliferation, migration, and invasion, whereas silencing FOXK1 showed the opposite effect. Moreover, Silencing FOXK1 enhanced radiosensitivity by inhibiting DNA damage repair, inducing G1 arrest and apoptosis. Further studies revealed that FOXK1 activated transcription of CDC25A and CDK4 in ESCC cells by directly binding to their promoter regions. Furthermore, knockdown of CDC25A or CDK4 reversed those biological processes mediated by overexpression of FOXK1. Collectively, FOXK1, as well as its downstream target genes CDC25A and CDK4, may be potential therapeutic and radiosensitizing targets for ESCC.
Objective To detect mutations of the ADAR1 gene in three Chinese families with dyschromatosis symmetrica hereditaria (DSH).Methods DNA was extracted from the blood samples of seven patients with DSH and their 33 relatives in three families with DSH as well as from 50 unrelated healthy controls.PCR and direct sequencing were performed to detect mutations in the ADAR1 gene.Results All the patients carried mutations in the ADAR1 gene.Three mutations were identified,including one frameshift mutation c.2433-2434delAG in family 2 and two missense mutations,i.e.,c.1760A ＞ G (p.Y587C) in family 1 and c.3620G ＞ T (p.G1207V) in family 3.No mutations were found in the ADAR1 gene in unaffected individuals in these families or the healthy controls.Conclusion Two novel missense mutations are found in the ADAR1 gene of two Chinese families,which may represent a molecular mechanism underlying the development of DSH.
A novel bacterium, designated strain L28T, was isolated from the rhizosphere soil of a mangrove plant in Hong Kong. Cells of strain L28T are Gram-stain-positive, rod-shaped and endospore-forming. Optimum growth occurs at 37 °C (range, 20–45 °C), 0.5 % (w/v) NaCl (range, 0–5.0 %) and pH 7.5 (range, 6.5–9.0). The major fatty acids are iso-C15 : 0 and C16 : 1ω7c alcohol. The major respiratory quinone is MK-7. The polar lipid profile comprises phospholipid, phosphatidylglycerol, phosphatidylethanolamine, diphosphatidylglycerol and two unidentified lipids. The 16S rRNA gene sequence analyses indicated that strain L28T exhibited the highest similarity of 96.7 % to Bacillus asahii MA001T. The genome size of strain L28T was 4 063 863 bp with a 36.9 mol% DNA G+C content. Based on the phenotypic and chemotaxonomic properties, along with the phylogenic distinctiveness, it was concluded that this strain represents a novel species of the genus Bacillus , for which the name Bacillus acanthi sp. nov. is proposed. The type strain of this novel species is L28T (=DSM 104296T=MCCC 1K03287T).
As an important part of electronic products and systems, the fault prediction and health management of board-level circuits has attracted wide attention and the testability design is the basis of the related studies. In this paper, a new method of testability design based on the correlation of circuit nodes is proposed and used to realize the selection of test points in a high-voltage power supply. First of all, all nodes in the circuit are grouped based on correlation analysis, and then calculate the distance between the fault class according to the existing fault data to select the test points of the circuit. Finally, extract the fault features of the selected test points and diagnose the fault. The results verifies the effectiveness of the proposed method in this paper.
'/%3e%3cuse xlink:href='%23a' transform='rotate(23.036 .093 25.536)'/%3e%3cuse xlink:href='%23a' transform='rotate(45.87 1.273 16.18)'/%3e%3cuse xlink:href='%23a' transform='rotate(69.945 .996 12.078)'/%3e%3cuse xlink:href='%23a' transform='rotate(20.66 -19.689 31.932)'/%3e%3c/svg%3e)
