Project description:In the present study, we disclose a new polypeptide corresponding to the sequence of human Talin-1 protein (named PDTLN1), which is highly expressed both in myocardial tissue and maternal peripheral blood of aborted fetuses with congenital heart disease (CHD). The results shown that PDTLN1, but not the scrambled version, caused cardiac developmental defects in zebrafish and inhibited cellular viability, proliferation and promoted apoptosis of P19 cells via the inhibition of PI3K/AKT signaling pathway. Our search may be helpful in gaining fresh perspective on the functions of human derived peptides and promote the detection of a novel class of diagnostic biomarkers in CHD. Further, to seek-and-find new targets for therapeutic intervention in CHD.
Project description:small RNA fractions were treated with either p19-WT or T111BpyAla to evaluate the catalytic ability of p19-T111BpyAla compared to the WT protein in degrading miRNAs
Project description:In order to found the target genes of ALV-miR-p19-01 which encoded by ALV-J, we used RNA-pull down and RNA-seq. The resulted showed there were 917 potential target genes of ALV-miRNA-p19-01 had been identified
Project description:We comprehensively investigated the neural-splicing using P19 cells, set up nine filtering conditions, and obtained 262 candidate exons (236 genes). Results of semi-quantitative RT-PCR in randomly selected 30 candidates suggested that 87% of the candidates were actually changed more than double compared with the undifferentiated and differentiated cells. GO analysis and pathway analysis also showed that these 236 candidate genes were highly involved in the neural events. These results suggested that our extraction of alternative exons was quite reasonable and successful.
Project description:As previously reported (Neuroscience letters 444(2008)127-131), we established embryonic carcinoma P19 cell line expressing the intracellular domain of APP (AICD). Although neurons could be differentiated from these cell lines with RA treatment, expression of AICD gave rise to neuron-specific apoptosis. To identify the genes that are involved in this cell death, we evaluated changes of gene expressions that was induced by AICD through this process of cell death. The expression profiles of almost forty thousands transcripts were monitored by DNA microarrays. AICD-expressing P19 cell lines (AICD/P19) and control P19 cell lines (pCDNA/P19) that carry vector alone were used and cultured. To induce neural differentiation of these P19 cell lines, cells were allowed to aggregate in culture medium with 5×10-7 M all-trans-retinoic acid (RA) for 4 days (aggregated state). After aggregation, cells were replated onto cell culture grade dishes or poly-L-Lysine coated cell-disks for two days (differentiated state). RNAs were isolated at each states.
Project description:SAGE identification of differentiation responsive genes in P19 embryonic cells induced to form cardiomyocytes in vitro. P19 embryonic carcinoma (EC) cells, induced to form cardiomyocytes in vitro - undifferentiated cells, day 3+0.5 and day 3+3.0 of differentiation protocol. Keywords = EC cells, P19, differentiation, cardiomyocytes Keywords: time-course
Project description:We comprehensively investigated the neural-splicing using P19 cells, set up nine filtering conditions, and obtained 262 candidate exons (236 genes). Results of semi-quantitative RT-PCR in randomly selected 30 candidates suggested that 87% of the candidates were actually changed more than double compared with the undifferentiated and differentiated cells. GO analysis and pathway analysis also showed that these 236 candidate genes were highly involved in the neural events. These results suggested that our extraction of alternative exons was quite reasonable and successful. We have biological duplicates in this project. We essentially compared Day 7 (neural-differentiated) against Day0 (Undifferentiated)
Project description:Analysis of senataxin effect on neuronal differentiation and neurite growth in RA-treated P19 cells by modulating senataxin expression levels. Senataxin silencing does not grossly affect the gene expression profiles of P19 cells