Expression data of reprogrammed miR-302/367-iPS cells
ABSTRACT: Pluripotent marker correlation between miR-302/367-iPS, ES and fibroblast cells Mouse fibroblast were reprogrammed with miR-302/367 lentiviral vector, total RNA was extracted by trizol and microarray assay was performed
Project description:Pluripotent marker correlation between miR-302/367-iPS, ES and fibroblast cells Overall design: Mouse fibroblast were reprogrammed with miR-302/367 lentiviral vector, total RNA was extracted by trizol and microarray assay was performed
Project description:To define the role of miR-302-367 cluster in cardiac development, we overexpressed miR-302-367 cluster in mouse heart by using R26R-miR-302-367; Nkx2.5-Cre mice. This data set contains the microarrays examining gene expression in the hearts of R26R-miR-302-367; Nkx2.5-Cre mice at postnatal day 14. We overexpressed miR-302-367 cluster in developing mouse heart using Nkx2.5-Cre mouse line
Project description:MEFs were infected with Oct4, Sox2, Klf4 (+/- Sall4), sorted for miR-290/302 reporter expression at day 9 (OSK) or 12 (Sall4+OSK), and then profiled. Resulting iPSCs were also profiled. Mouse ES cells were differentiated and sorted for miR-290/302 reporter expression during Fgf/Activin differentiation (day 4 or day 7). Performed in biological triplicate. Biological triplicate samples represent three independent lines. Total RNA collected with Trizol. All processing conducted at the UCLA Neuroscience Genomics Core. MouseRef-8 v2.0 Expression BeadChips.
Project description:Wild-type or miR-302 knockout tissue was isolated from embryos during neurulation in replicate Performed in biological triplicate except for E7.5 WT which was in duplicate and E9.5 timepoints which were in quadruplicate. Biological replicate samples represent independent embryos. Total RNA collected with Trizol. All processing conducted at the UCLA Neuroscience Genomics Core. MouseRef-8 v2.0 Expression BeadChips.
Project description:Baseline gene expression of adipose stem cell derived iPSCs generated by lentiviral Yamanaka 4 factors. We used microarrays to analyze the global gene expression of hACS derived iPSCs with KMOS and KMOS+miR-302. Compare the global gene expression of iPSCs with hESCs and adipose stem cells.
Project description:Upon RNA profiling of WT and Dgcr8-/- mESCs in 2iL and differentiation for 48 hours, miRNAs are proved to be important for the transcriptional changes during ESC exiting from pluripotency. Further miRNA sequencing of WT ESCs in different timepoints revealed that miRNAs expression changes dynamically during ESC to EpiLC transition and identified miR-290/302 as key miRNAs facilitating the dismantling of naive pluripotency. Overall design: Total RNA was analyzed from WT and Dgcr8-/- mESCs and Dgcr8 in 2iL and differentiation for 48 hours. Small RNA was sequenced for WT mESCs in 4 timepoints during exiting from pluripotency.Two biological replicates were sequenced for each sample.
Project description:The PI3K pathway is a major driver of cancer progression. However, clinical resistance to PI3K inhibition is common. IBL-302 is a novel highly specific triple PIM, PI3K and mTOR inhibitor. Screening IBL-302 in over 700 cell lines representing 47 tumor types identified neuroblastoma as a strong candidate for PIM/PI3K/mTOR inhibition. IBL-302 was more effective than single PI3K inhibition in vitro and IBL-302 treatment of neuroblastoma patient-derived xenograft (PDX) cells induced apoptosis, differentiated tumor cells, and decreased N-Myc protein levels. IBL-302 further enhanced the effect of the common cytotoxic chemotherapies cisplatin, doxorubicin, and etoposide. Global genome, proteome and phospho-proteome analyses identified crucial biological processes, including cell motility and apoptosis, targeted by IBL-302 treatment. While IBL-302 treatment alone reduced tumor growth in vivo, combination therapy with low-dose cisplatin inhibited neuroblastoma PDX growth. Complementing conventional chemotherapy treatment with PIM/PI3K/mTOR inhibition has the potential to improve clinical outcomes and reduce severe late effects in children with high-risk neuroblastoma.