Project description:RNA-seq analysis of Pseudomonas sp OST1909 exposed to various preparations of naphthenic acids samples led to the identiifcation of many NA-induced genes.
Project description:To confirm the mechanism of miR-29a in liver fibrosis healing, we have employed whole genome microarray expression profiling as a discovery platform to identify genes. CCl4 and TAA liver fibrosis model mouse were used for this experiment. After five weeks liver fibrosis induction period, mouse have been observed for one week (1w) or two weeks (2w) and negative control nucleotide (N.C) or miR-29a were injected every 3 days on this period. We used CCl4 1w N.C (n = 1), 1w miR-29a (n = 1), 2w N.C (n = 1), 2w miR-29a (n = 1), and also used TAA model mouse (total n = 8) liver samples for microarray analysis. We can get only one gene (PDGF-c) as a target of miR-29a which relate to liver fibrosis and down-regulated more than 1.5 times in common miR-29a injected group than N.C group.
Project description:To confirm the mechanism of miR-29a in liver fibrosis healing, we have employed whole genome microarray expression profiling as a discovery platform to identify genes. CCl4 and TAA liver fibrosis model mouse were used for this experiment. After five weeks liver fibrosis induction period, mouse have been observed for one week (1w) or two weeks (2w) and negative control nucleotide (N.C) or miR-29a were injected every 3 days on this period. We used CCl4 1w N.C (n = 1), 1w miR-29a (n = 1), 2w N.C (n = 1), 2w miR-29a (n = 1), and also used TAA model mouse (total n = 8) liver samples for microarray analysis. We can get only one gene (PDGF-c) as a target of miR-29a which relate to liver fibrosis and down-regulated more than 1.5 times in common miR-29a injected group than N.C group. CCl4 and TAA liver fibrosis model mouse were used for this experiment. After five weeks liver fibrosis induction period, mouse have been obserbed for one week (1w) or two weeks (2w) and negative control nucleotide (N.C) or miR-29a were injected every 3 days on this period. We used CCl4 1w N.C (n = 1), 1w miR-29a (n = 1), 2w N.C (n = 1), 2w miR-29a (n = 1), and also used TAA model mouse (total n = 8) liver samples for microarray analysis.
Project description:The whole proteome analysis of the Pseudomonas sp. FIP_A4 strain in presence and absence of fipronil was conducted to evaluate the differentially expressed enzymes that can play role in fipronil degradation.
Project description:miR-29a plays a critical role in neuronal development and is associated with neurodegenerative diseases, but its regulatory mechanisms remain unclear. To identify genes that influence miR-29a expression, we utilized the genetically diverse Collaborative Cross (CC) mouse strains and conducted expression profiling and Quantitative Trait Loci (QTL) analysis. A significant QTL on chromosome 7 was identified, and ten candidate genes were mapped within this region. RNAi-mediated knockdown experiments revealed that Psmd13 and Nap1l4 significantly increased miR-29a expression, implicating these genes as upstream regulators. Further investigation in mouse neural precursor cells (mNPCs) demonstrated that Psmd13 knockdown enhanced neuronal differentiation, as indicated by increased βIII-tubulin-positive cells, and miR-29a inhibition also promoted this process. Co-immunoprecipitation experiments showed that Psmd13 interacts with Dicer, modulating miR-29a levels through a differentiation-dependent mechanism. Chromatin immunoprecipitation sequencing (ChIP-seq) revealed co-binding of Psmd13 and Dicer at key genomic loci, including miR-29a, influencing chromatin accessibility and transcriptional regulation. Notably, proteasome inhibition using MG132 decreased Psmd13 and Dicer levels, leading to downregulation of miR-29a and impaired neuronal differentiation. These findings suggest that Psmd13 and Dicer coordinate to regulate miR-29a biogenesis and neuronal differentiation, highlighting the proteasome's essential role in maintaining neurodevelopmental homeostasis.
Project description:miR-29a plays a critical role in neuronal development and is associated with neurodegenerative diseases, but its regulatory mechanisms remain unclear. To identify genes that influence miR-29a expression, we utilized the genetically diverse Collaborative Cross (CC) mouse strains and conducted expression profiling and Quantitative Trait Loci (QTL) analysis. A significant QTL on chromosome 7 was identified, and ten candidate genes were mapped within this region. RNAi-mediated knockdown experiments revealed that Psmd13 and Nap1l4 significantly increased miR-29a expression, implicating these genes as upstream regulators. Further investigation in mouse neural precursor cells (mNPCs) demonstrated that Psmd13 knockdown enhanced neuronal differentiation, as indicated by increased βIII-tubulin-positive cells, and miR-29a inhibition also promoted this process. Co-immunoprecipitation experiments showed that Psmd13 interacts with Dicer, modulating miR-29a levels through a differentiation-dependent mechanism. Chromatin immunoprecipitation sequencing (ChIP-seq) revealed co-binding of Psmd13 and Dicer at key genomic loci, including miR-29a, influencing chromatin accessibility and transcriptional regulation. Notably, proteasome inhibition using MG132 decreased Psmd13 and Dicer levels, leading to downregulation of miR-29a and impaired neuronal differentiation. These findings suggest that Psmd13 and Dicer coordinate to regulate miR-29a biogenesis and neuronal differentiation, highlighting the proteasome's essential role in maintaining neurodevelopmental homeostasis.