Notably, during UVB radiation‑induced apoptosis, the overexpression of Calb1 inhibited cell death, resulting in the decreased expression of Bad and caspase‑12, and in the upregulated expression of Bcl‑2. These results suggested that Calb1 inhibited the upregulation of genes involved in apoptosis. The siRNA‑mediated knockdown of Calb1 resulted in increased rates of UVB radiation‑induced apoptosis, the increased expression of Bad and caspase‑12, and the decreased expression of Bcl‑2, further demonstrating that Calb1 may mediate UVB radiation‑mediated apoptosis by regulating Ca2+. On the whole, the findings of the present study indicate that UVB exposure can lead to an imbalance in the intracellular Ca2+ homeostasis in HLECs and that Calb1 protein exerts a negative effect on the expression of pro‑apoptotic genes in HLECs. https://www.selleckchem.com/products/zidesamtinib.html Calb1 may thus inhibit the UVB radiation‑induced apoptosis of HLECs by regulating Ca2+.Polyphenols are increasingly investigated for the treatment of periodontitis and research on their use in dental biomaterials is currently being conducted. Grape pomace extracts are a rich source of polyphenols. In the present study, the polyphenols of two different types of grape pomace were characterized and identified by high‑performance liquid chromatography‑diode array detector, and the effect of polyphenol‑rich grape pomace extracts on mesenchymal stem cell (MSC) osteogenic differentiation was investigated. Solid‑liquid extraction was used to recover polyphenols from red and white grape pomace. The two extracts have been characterized through the phenolic content and antioxidant power. Human MSCs (hMSCs) from the bone marrow were cultured both with and without given amounts (10 or 20 µg/ml) of the obtained pomace extracts. Their effects on cell differentiation were evaluated by reverse transcription‑quantitative polymerase chain reaction, compared with relevant controls. Results showed that both pomace extracts, albeit different in phenolic composition and concentration, induced multiple effects on hMSC gene expression, such as a decreased receptor activator of nuclear factor κ‑Β ligand/osteoprotegerin ratio and an enhanced expression of genes involved in osteoblast differentiation, thus suggesting a shift of hMSCs towards osteoblast differentiation. The obtained results provided data in favor of the exploitation of polyphenol properties from grape pomace extracts as complementary active molecules for dental materials and devices for bone regeneration in periodontal defects.A long noncoding RNA called small nucleolar RNA host gene 14 (SNHG14) has been validated as a key regulator of cellular processes in multiple types of human cancer. However, to the best of our knowledge, the expression status and specific roles of SNHG14 in retinoblastoma (RB) have not been studied. The aims of the present study were to determine the expression status of SNHG14 in RB, assess the effects of SNHG14 on malignant characteristics of RB cells and investigate the mechanisms of action of SNHG14 in RB. SNHG14 expression levels in RB tissue samples and cell lines were measured by reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR). Cell proliferation, apoptosis, migration and invasion in vitro, and tumor growth in vivo were quantitated by the Cell Counting Kit‑8 assay, flow cytometry, migration and invasion assays, and mouse tumor xenograft experiments, respectively. The target microRNA (miRNA) of SNHG14 was predicted by bioinformatics analysis and was subsequently validated by a lucte STAT3 by sponging miR‑124. Therefore, targeting the SNHG14/miR‑124/STAT3 pathway may be an effective therapeutic strategy against RB.Understanding the development, regeneration, and disorders of the liver is the major goal in liver biology. Current mechanistic knowledge of human livers has been largely derived from mouse models and cell lines, which fall short in recapitulating the features of human liver cells or the structures and functions of human livers. Organoids as an in vitro system hold the promise to generate organ-like tissues in a dish. Recent advances in human liver organoids also facilitate the understanding of the biology and diseases in this complex organ. Here we review the progress in human liver organoids, mainly focusing on the methods to generate liver organoids, their applications, and possible future directions. © The Author(s) 2020. Published by Oxford University Press on behalf of Journal of Molecular Cell Biology, IBCB, SIBS, CAS.In dairy plants, clean-in-place (CIP) apparatus cannot be disassembled and, therefore, it is not easy to clean the inner surface of their pipes. In this study, the inhibitory effects of chemical agents on biofilms formed by three foodborne pathogens, Bacillus cereus , Escherichia coli , and Staphylococcus aureus , were evaluated in a dairy CIP system. First, the experiment was conducted on a laboratory scale, and after inoculating each of the three bacteria (200 μl) on stainless steel (SS) chips (25 × 25 mm) the effect of single cleaning agents was confirmed. Individual treatments such as NaClO (30, 50, 100, and 200 ppm), NaOH (0.005, 0.01, 0.05, and 0.1%), citric acid (1, 3, 5, and 7%), and nisin (5, 10, 25, 50, 100, and 200 ppm) were used to clean the SS chip for 10 min. The best concentration was selected for each solution. The optimal concentration was then tested in a commercial plant. Simultaneous cleaning with 200 ppm NaClO (10 min) and 7% citric acid (10 min) reduced the biofilms of B. cereus , E. coli , and S. aureus by 6.9, 7.0, and 8.0 log CFU/cm 2 , respectively. Further, 7% citric acid and 0.1% NaOH was optimal for E. coli . Moreover, NaClO and citric acid are legally approved for use as food additives in Korea. Our results demonstrated that combined treatment with NaClO and citric acid was the most effective approach for reducing the biofilm formed by foodborne pathogens on CIP apparatuses. Consequently, these findings can contribute to the production of safe dairy products.Mutations of epigenetic regulators are pervasive in human tumors. ASXL1 is frequently mutated in myeloid malignancies. We previously found that ASXL1 forms together with BAP1 a complex that can deubiquitinylate mono-ubiquitinylated lysine 119 on Histone H2A (H2AK119ub1), a Polycomb repressive mark. However, a complete mechanistic understanding of ASXL1 in transcriptional regulation and tumor suppression remains to be defined. Here we find that depletion of Asxl1 confers murine 32D cells to IL3-independent growth at least partly due to sustained activation of PI3K/AKT signaling. Consistently, Asxl1 is critical for the transcriptional activation of Pten, a key negative regulator of AKT activity. Then we confirm that Asxl1 is specifically enriched and required for H2AK119 deubiquitylation at the Pten promoter. Interestingly, ASXL1 and PTEN expression levels are positively correlated in human blood cells and ASXL1 mutations are associated with lower expression levels of PTEN in human myeloid malignancies. Furthermore, malignant cells with ASXL1 downregulation or mutations exhibit higher sensitivity to the AKT inhibitor MK2206.