Furthermore, miR-30d-5p depletion inhibited the proliferation, reduced apoptosis and decreased the expression of cle-caspase 3 in H9c2 cells with hypoxia treatment. Luciferase reporter, RIP, and western blot assays further confirmed that miR-30d-5p negatively regulated the expression of SIRT1. Interestingly, the rescue-of-function experiments further indicated that knockdown of SIRT1 attenuated the effect of miR-30d-5p depletion on proliferation, apoptosis NF-κB signaling pathway inH9c2 cells with hypoxia treatment. In addition, the suppression of NF-κB signaling pathway increased cell viability while decreased cell apoptosis in hypoxia-mediatedH9c2 cells. Our data suggested Res mayprotectH9c2 cells against hypoxia-induced apoptosis through miR-30d-5p/SIRT1/NF-κB axis.miRNAs are important regulatory components involving in many biological processes, including plant development, vegetative and reproductive growth, and stress response. However, identification and characterization of miRNAs still remain limited for conifer species. In this study, with deep sequencing, we obtained 1,314,450 unique reads with 18-30 nt length from a stress-tolerant conifer, Sabina chinensis. We identified 37 conserved and 103 novel miRNAs, their unique characteristics were further analyzed, and 10 randomly selected were validated by qRT-PCR. Through miRNA target predictions and annotations, we found miRNA may have several targets as well a target could be regulated by several miRNAs, and a total of 2,397 mRNAs were predicted to be targets of the 140 miRNAs. These targets included not only important transcription factors such as auxin response factors, but also indispensable non-transcriptional factor proteins. Pathway-based analysis showed that S. chinensis miRNAs are involved in 172 metabolic pathways, of which 3 were discovered in adaptation-related pathways, indicating their possible relevance to the species’ stress-tolerance characteristics. This study is expected to lay the foundation for exploring the regulative roles of miRNAs in development, growth, and response to environmental stresses of S. chinensis.The Homeobox B9 (HOXB9) is a homeodomain-containing transcription factor that participates in the progression of various malignancies. Nevertheless, the functional role of HOXB9 in prostate cancer cells is largely unknown. Hence, we aimed to address the effect of HOXB9 on the progression of prostate cancer cells. Small interfering RNA (siRNA) against HOXB9 was used to downregulate HOXB9 expression in PC3 and DU145 cells. Western blotting was performed to detect the expression levels of HOXB9 and other related proteins. Cell proliferation was tested by the Cell Counting Kit-8 (CCK-8) and cell cycle and apoptosis were investigated by flow cytometry. Angiogenesis was examined using tube formation assays The Transwell assays were carried out to assess the migratory and invasive capacities of cells. Here, we found that HOXB9 knockdown significantly reduced cell proliferation via inducing cell cycle arrest at G1 phase. This treatment also reduced angiogenesis, migration and invasion abilities of PC3 and DU145 cells in vitro. We also found that HOXB9 knockdown inhibits the activation of the PI3K/AKT signaling pathway in prostate cancer cells. In conclusion, our findings revealed that HOXB9 promotes prostate cancer progression and might be a novel and effective therapeutic target for human prostate cancer.The adenine biosynthetic mutants ade1 and ade2 of Saccharomyces cerevisiae accumulate a characteristic red pigment in their vacuoles under adenine limiting conditions. This red pigmentation phenotype, widely used in a variety of genetic screens and assays, is the end product of a glutathione-mediated detoxification pathway, where the glutathione conjugates are transported into the vacuole. The glutathione conjugation step, however, has still remained unsolved. We show here, following a detailed analysis of all the members of the thioredoxinfold superfamily, the involvement of the monothiol glutaredoxin GRX4 as essential for pigmentation. GRX4 plays multiple roles in the cell, and we show that the role in ade pigmentation does not derive from its regulatory role of the iron transcription factor, Aft1p, but a newly identified GST activity of the protein that we could demonstrate using purified Grx4p. Further, we demonstrate that the GRX domain of GRX4 and its active site cysteine C171 is critical for this activity. The findings thus solve a decades old enigma on a critical step in the formation of this red pigmentation.GAGA associated factor (GAF) is a sequence-specific DNA binding transcription factor that is evolutionarily conserved from flies to humans. Emerging evidence shows a context-dependent function of vertebrate GAF (vGAF, a.k.a. ThPOK) in multiple processes like gene activation, repression, and enhancer-blocking. We hypothesize that context-dependent interaction of vGAF with a diverse set of proteins forms the basis for the multifunctional nature of vGAF. To this end, we deciphered the protein-protein interactome of vGAF and show that vGAF interacts with chromatin remodelers, RNA metabolic machinery, transcriptional activators/ repressors, and components of DNA repair machinery. We further validated the biological significance of our protein-protein interaction data with functional studies and established a novel role of vGAF in DNA repair and cell-survival after UV-induced DNA damage. One of the major risk factors for skin cutaneous melanoma is prolonged exposure of UV and subsequent DNA damage. vGAF is highly expressed in normal skin tissue. Interestingly, our analysis of high-throughput RNA-sequencing data shows that vGAF is heavily downregulated across all major stages of skin cutaneous melanoma suggesting its potential as a diagnostic biomarker. Taken together, our study provides a plausible explanation for the diverse gene regulatory functions of vGAF and unravels its novel role in DNA repair.This paper explores the potential mechanism of microRNA-143-5p regulation effects on pulmonary artery smooth muscle cells (PASMCs) functions in hypoxic pulmonary hypertension (HPH) via targeting HIF-1a, which may offer a new idea for HPH therapy. PASMCs were transfected with mimics control/miR-143-5p mimics or inhibitor control/miR-143-5p inhibitor. We used Western blotting and RT-qPCR to detect the protein and mRNA expressions, CCK-8 assay to detect cellular viability, Annexin V-FITC/PI staining and caspase- 3/cleaved caspase-3 protein to evaluate cellular apoptosis, transwell migration experiment for cellular migration measurement and Dual luciferase reporter gene assay to prove the target of miR-143-5p. Cells under hypoxic condition presented the decreased protein and mRNA expressions of α-smooth muscle actin (SM-α-actin), Myocardin, smooth muscle myosin heavy chain (SMMHC), and smooth muscle-22α (SM22α), Calponin1 and Hypoxia-inducible factor-1α(HIF-1α), the increased cell viability and miR-143-5p level; Overexpression of miR-143-5p obviously reduced vascular smooth muscle-specific contraction marker protein levels and cellular apoptosis, increased cellular migration of PASMCs with hypoxia stimulation; Low-expression of miR-143-5p caused the opposite changes, while co-transfected with Si HIF-1 α blocked the beneficial effects of miR-143-5p inhibition on PASMCs under hypoxia. MicroRNA-143-5p can promote the phenotype conversion, proliferation and migration of pulmonary artery smooth muscle cells under hypoxic condition through direct targeting of HIF-1α.Solanum whitefly, Aleurothrixus trachoides (Back). (Hemiptera Aleyrodidae) was considered as a non-virus vector by European and Mediterranean Plant Protection Organization (EPPO) reports. However, in the present study it was found to transmit Duranta leaf curl virus (DLCV) to tomato, bell pepper and potato. A. trachoides infested field samples of Duranta sp (100%) and tomato (20%) tested positive for begomovirus by PCR using begomovirus degenerate primers and primers specific to Tomato leaf curl New Delhi virus showing amplicon of 520 bp and 2.7 Kb respectively. The DNA samples of A. trachoides collected from virus positive duranta and tomato plants also tested positive for the virus. Virulent whiteflies from duranta could successfully transmit DLCV to bell pepper (26%) and tomato (13 %) plants as confirmed by Rolling Circle Amplification. The rate of virus transmission by A. trachoides from DLCV inoculated tomato to bell pepper and tomato to potato was 100% and tomato to tomato was 80%. The results suggest whitefly A. trachoides as the vector for DLCVand to the best of our knowledge, this is the first report for A. trachoides as vector of begomovirus. These findings suggest need for reconsideration of A. trachoides as a virus-vector. This will have great impact on solanaceous vegetable cultivation in India and other parts of the world.Ischemia-reperfusion (IR) injury is a major cause of clinical emergencies during and after surgical procedures. Propofol protects the heart from cardiovascular IR injury by inhibiting autophagy. MicroRNAs (miRNAs) participate in anesthetic-regulated cardiovascular injury. MiR-20b-5p targets unc-51-like autophagy activating kinase 1 (ULK1). Its role in propofol-modulated cardiovascular IR injury remains unclear, however. In this study, we used an in vitro model of hypoxia-reoxygenation (HR)-induced injury to human umbilical vein endothelial cells (HUVECs) to determine the protective effect of miR-20b-5p in cells preconditioned with propofol. We found that miR-20b-5p was significantly higher and ULK1 was lower in propofol-preconditioned HUVECs with HR injury than in HUVECs with HR injury only. Additionally, miR-20b-5p overexpression increased cell viability and repressed autophagy and apoptosis more in propofol-preconditioned HUVECs with HR injury than in HUVECs with HR injury only. A luciferase reporter assay confirmed the target reaction between miR-20b-5p and ULK1. Overexpression of ULK1 restrained the protective effect of miR-20b-5p in propofol-preconditioned HUVECs with HR injury. In conclusion, our results indicate that propofol inhibits autophagic cell death via the miR-20b-5p-ULKI axis and that ULK1 may be a therapeutic target for cardiovascular IR injury.As a tumor suppressor, p53 preserves genomic integrity in eukaryotes. However, limited evidence is available for the p53 shuttling between the cytoplasm and nucleus. Previous studies have shown that β-actin polymerization negatively regulates p53 nuclear import through its interaction with p53. In this study, we found that DNA damage induces both β-actin and p53 accumulation in the nucleus. β-actin knockdown impaired the nuclear transport of p53. Additionally, β-actin could interact with p53 which was enhanced in response to genotoxic stress. Furthermore, N terminal deletion mutants of p53 shows reduced levels of association with β-actin. We further identified Ser15, Thr18 and Ser20 of p53 are critical to the β-actin p53 interaction, which upon mutation into alanine abrogates the binding. Taken together, this study reveals that β-actin regulates the nuclear import of p53 through protein-protein interaction.A gene co-expression network (CEN) is of biological interest, since co-expressed genes share common functions and biological processes or pathways. Finding relationships among modules can reveal inter-modular preservation, and similarity in transcriptome, functional, and biological behaviors among modules of the same or two different datasets. There is no method which explores the one-to-one relationships and one-to-many relationships among modules extracted from control and disease samples based on both topological and semantic similarity using both microarray and RNA seq data. In this work, we propose a novel fusion measure to detect mapping between modules from two sets of co-expressed modules extracted from control and disease stages of Alzheimer’s disease (AD) and Parkinson’s disease (PD) datasets. Our measure considers both topological and biological information of a module and is an estimation of four parameters, namely, semantic similarity, eigengene correlation, degree difference, and the number of common genes.