Project description:To study the transcriptome differences of tumor transplanted into WT and KO host, E0771 tumors harvested from WT and KO host were extracted for total RNA and mRNA sequencing was performed. To study the transcriptome differences of WT and KO fat tissue, visceral fat tissue were harvested from obese WT and KO mice and total RNA was extracted and sequenced.
Project description:We sequenced mRNA of three dual perturbation experiments of E. coli K12 MG1655 changing both genetic and environmental conditions. Each dual perturbation experiment consists of four RNA-seq samples (WT, WT+nutrient supplementation, transcription factor KO, transcription factor KO+nutrient supplementation). The three conditions are: 1) adenine supplementation/nac KO, 2) L-tryptophan supplementation/cra KO, 3) anaerobic/mntR KO.
Project description:mRNA was sequenced from HCT116 MYC 3' TBE1 (WT) and KO cells to identify genes differentially expressed after deletion of the MYC 3' TBE1
Project description:We sequenced mRNA of WT, p35S:AtBBD1 (OX) and atbbd1 (KO) plants. Plants were grown in soil for three weeks at 23 ℃ with 60% relative humidity. mRNA was isolated 6 hours after threating with 20% PEG.
Project description:Nogo-A is an important axonal growth inhibitor in the adult and developing CNS. In vitro, Nogo-A has been shown to inhibit migration and cell spreading of neuronal and nonneuronal cell types. Here, we studied in vivo and in vitro effects of Nogo-A on vascular endothelial cells during angiogenesis of the early postnatal brain and retina in which Nogo-A is expressed by many types of neurons. Genetic ablation or virus-mediated knock down of Nogo-A or neutralization of Nogo-A with an antibody caused a marked increase in the blood vessel density in vivo. In culture, Nogo-A inhibited spreading, migration, and sprouting of primary brain microvascular endothelial cells (MVECs) in a dose-dependent manner and induced the retraction of MVEC lamellipodia and filopodia. Mechanistically, we show that only the Nogo-A-specific Delta 20 domain exerts inhibitory effects on MVECs, but the Nogo-66 fragment, an inhibitory domain common to Nogo-A, -B, and -C, does not. Furthermore, the action of Nogo-A Delta 20 on MVECs required the intracellular activation of the Ras homolog gene family, member A (Rho-A)-associated, coiled-coil containing protein kinase (ROCK)-Myosin II pathway. The inhibitory effects of early postnatal brain membranes or cultured neurons on MVECs were relieved significantly by anti-Nogo-A antibodies. These findings identify Nogo-A as an important negative regulator of developmental angiogenesis in the CNS. They may have important implications in CNS pathologies involving angiogenesis such as stroke, brain tumors, and retinopathies.
Project description:Circular RNAs (circRNA) are a novel class of widespread non-coding RNAs (ncRNAs) that regulate gene expression in mammals. Recent studies demonstrate that functional peptides can be encoded by short open reading frames (sORFs) in ncRNAs, including circRNAs. In this study, through deep RNA sequencing on human endometrial cancer (EC) samples and their paired adjacent normal tissues, we uncovered that the circRNA hsa-circ-0000437 is significantly reduced in EC compared to matched paracancerous tissue. The hsa-circ-0000437 contains a sORF encoding a functional peptide termed as CORO1C-47aa. Overexpression of CORO1C-47aa is capable of inhibiting angiogenesis at the initiation stage by suppressing endothelial cell proliferation, migration, and differentiation through competing with TACC3 to bind to ARNT and suppress VEGF. The anti-tumor effects of CORO1C-47aa on EC progression suggest that CORO1C-47aa has a potential value in anti-carcinoma therapies and deserves further investigation.
Project description:Negative feedback is a crucial physiological regulatory mechanism, but no such regulator of angiogenesis has been established. Here we report a novel angiogenesis inhibitor that is induced in endothelial cells (ECs) by angiogenic factors and inhibits angiogenesis in an autocrine manner. We have performed cDNA microarray analysis to survey VEGF-inducible genes in human ECs. We characterized one such gene, KIAA1036, whose function had been uncharacterized. The recombinant protein inhibited migration, proliferation, and network formation by ECs as well as angiogenesis in vivo. This inhibitory effect was selective to ECs, as the protein did not affect the migration of smooth muscle cells or fibroblasts. Specific elimination of the expression of KIAA1036 in ECs restored their responsiveness to a higher concentration of VEGF. The expression of KIAA1036 was selective to ECs, and hypoxia or TNF-alpha abrogated its inducible expression. As this molecule is preferentially expressed in ECs, we designated it "vasohibin." Transfection of Lewis lung carcinoma cells with the vasohibin gene did not affect the proliferation of cancer cells in vitro, but did inhibit tumor growth and tumor angiogenesis in vivo. We propose vasohibin to be an endothelium-derived negative feedback regulator of angiogenesis.
Project description:We sequenced mRNA of three dual perturbation experiments of E. coli K12 MG1655 changing both genetic and environmental conditions. Each dual perturbation experiment consists of four RNA-seq samples (WT, WT+nutrient supplementation, transcription factor KO, transcription factor KO+nutrient supplementation). The three conditions are: 1) adenine supplementation/nac KO, 2) L-tryptophan supplementation/cra KO, 3) anaerobic/mntR KO. Determination of whether a transcription factor plays a regulatory role in a particular environmental shift by examining differential expression of mRNA levels.
