Project description:Purpose : to decipher the role a newly identified protein, RNF219, we performed a knock down of this protein and try to determine how it affect the global mRNA expression of the cells.
Project description:Using microarray, we compared miRNAs expression profiles of MDA-MB-231 cells transfected with myocardin and empty vector (pcDNA3.1) and found that 25 miRNAs were significantly changed in myocardin-transfected groups (17 up-regulated and 9 down-regulated miRNAs). Moreover, we showed that 18 of 25 miRNAs significantly regulated by myocardin were inhibited by ERα in MDA-MB-231 cells. In addition,through a microarray approach, we identify the subset of miRNAs modulated by ERα in MDA-MB-231 cells. Our results determined that ERα may function as tumor-promoter through down-regulating expression of 3 miRNAs (miR-26b, miR-146a and miR-331-3p) in MDA-MB-231 cells.
Project description:The investigators aim to assess the procedure time and miss rate of polyps when performing polypectomy in the colon on the way up* and down** or only on the way down**.
(* advancing the scope to the cecum, ** pulling back the scope after intubation of the cecum). Our hypothesis is that using the strategy to remove all visible polyps firstly on the way up and secondly on the way down is less time consuming and misses less polyps as with the strategy to remove polyps only on the way down.
Project description:Using microarray, we compared miRNAs expression profiles of MDA-MB-231 cells transfected with myocardin and empty vector (pcDNA3.1) and found that 25 miRNAs were significantly changed in myocardin-transfected groups (17 up-regulated and 9 down-regulated miRNAs). Moreover, we showed that 18 of 25 miRNAs significantly regulated by myocardin were inhibited by ERM-NM-1 in MDA-MB-231 cells. In addition,through a microarray approach, we identify the subset of miRNAs modulated by ERM-NM-1 in MDA-MB-231 cells. Our results determined that ERM-NM-1 may function as tumor-promoter through down-regulating expression of 3 miRNAs (miR-26b, miR-146a and miR-331-3p) in MDA-MB-231 cells. There are 4 samples in this experiment (pcDNA3.1-transfected, myocardin-transfected, ERM-NM-1-transfected, myocardin plus ERM-NM-1 co-transfecteded groups) and each sample was replicated 3 times. The vector-pcDNA3.1 was used as control.
Project description:We performed a zebrafish forward genetic screen by Tol2 mediated gene-trap approach and uncovered one mutant stac (The number of the transgenic line: B55) that showed severe cell-death distributed in the various brain and trunk in the homozygote embryos. Analysis of stac homozygous embryos demonstrates typical apoptosis. So it is necessary to analyze whether the apoptosis and cell cycle regulated signaling transductions are changed in the mutant, in order to provide valuable clues to some other species. And the up-regulated and down-regulated genes in the mutant compared to the WT were examined by zebrafish cDNA microarray.
Project description:down/up regulation of nad biosynthesis in arabidopsis and role of l-aspartate oxidase-Down/up regulation of NAD biosynthesis in Arabidopsis : role of L-Aspartate oxidase
Project description:The evolutionarily conserved CCR4-NOT complex acts as a central player in the control of mRNA turnover and mediates accelerated mRNA degradation upon histone deacetylase (HDAC) inhibition. Here, we explored acetylation-induced changes in the composition of the CCR4-NOT complex by purification of the endogenously tagged scaffold subunit NOT1 and identified ring finger protein 219 (RNF219) as an acetylation-regulated cofactor. We provide evidence that RNF219 is an active RING-type E3 ubiquitin ligase which stably associates with the CCR4-NOT complex via the NOT9 module through a short linear motif located in the C-terminal low-complexity region of RNF219. Using a reconstituted six-subunit human CCR4-NOT complex, we demonstrate that RNF219 acts as an inhibitor of deadenylation. Accordingly, our transcriptome-wide mRNA half-life measurements reveal that RNF219 attenuates global mRNA turnover in cells, independently of its E3 ligase activity. Our results establish RNF219 as a negative regulator of CCR4-NOT-mediated mRNA deadenylation, whose loss upon HDAC inhibition contributes to accelerated mRNA turnover.