Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA290331 | ENA |
REPOSITORIES: ENA
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Project description:Expression data from isogenic Pten WT or KO mouse T-ALLs treated with DBZ or DMSO
| PRJNA290332 | ENA
Project description:To explore the mechanisms downstream of NOTCH1 and PTEN in the control of leukemia cell growth, we performed expression profiling on NOTCH1 induced and Pten-positive T-ALL tumor cells infected with constitutively active AKT (myristoylated-AKT). Constitutive activation of AKT rescues the transcriptional programs induced by NOTCH1 inhibition in Pten-positive T-ALL cells We performed microarray gene expression analysis of GSI treatment in Pten WT NOTCH1 induced leukemias infected with constitutively active AKT (myristoylated-AKT) or empty vector.
2015-08-31 | E-GEOD-71089 | biostudies-arrayexpress
Project description:To investigate the underlying mechanisms mediating resistance to NOTCH inhibition in Pten-null T-ALL tumor cells we performed gene expression profiling of isogenic Pten-positive and Pten-deleted leukemia lymphoblasts after acute treatment with DBZ in vivo. This analysis revealed that, while direct NOTCH1 target genes (such as Hes1, Dtx1, PtcrA, HeyL and Notch3) are effectively downregulated in both Pten-positive and Pten-deleted tumors, genetic ablation of Pten elicits a global reversal of much of the transcriptional effects of NOTCH inhibition. We performed microarray gene expression analysis of GSI treatment in isogenic Pten KO or WT NOTCH1 induced leukemias
2015-08-31 | E-GEOD-71087 | biostudies-arrayexpress
Project description:Approximately 50% of melanomas harbor an activating BRAFV600E mutation. Standard of care involves a combination of inhibitors targeting mutant BRAF and MEK1/2, the substrate for BRAF in the MAPK pathway. PTEN loss of function mutations occur in 40% of BRAFV600E melanomas, resulting in increased PI3K/AKT activity that enhances resistance to BRAF/MEK combination inhibitor therapy. To compare the response of PTEN null to PTEN wild type cells in an isogenic background, CRISPR was used to knock out PTEN in the A375 melanoma cell line that harbors a BRAFV600E mutation. Kinome profiling was performed using the parental line and two PTEN KO clones (5 and 11), treated with DMSO, or treated with 100nM dabrafenib and 10nM trametinib for 1 day or for 7 days. PTEN KO cells showed dramatically increased binding of HER3 and AKT3 compared to wild type. The activation of the SOX10-FOXD3-HER3-AKT axis in PTEN KO cells could be targeted with the ERBB/HER inhibitor neratinib.
2024-04-23 | PXD033921 | Pride
Project description:To investigate the underlying mechanisms mediating resistance to NOTCH inhibition in Pten-null T-ALL tumor cells we performed gene expression profiling of isogenic Pten-positive and Pten-deleted leukemia lymphoblasts after acute treatment with DBZ in vivo. This analysis revealed that, while direct NOTCH1 target genes (such as Hes1, Dtx1, PtcrA, HeyL and Notch3) are effectively downregulated in both Pten-positive and Pten-deleted tumors, genetic ablation of Pten elicits a global reversal of much of the transcriptional effects of NOTCH inhibition.
2015-08-31 | GSE71087 | GEO
Project description:AF10 is a cofactor of the H3K79 methyltransferase DOT1L. To uncover the role of H3K79me in reprogramming to induced pluripotent stem cells (iPSCs), we bred reprogrammable mice encoding doxycycline inducible Oct4-2A-Klf4-2A-IRES-Sox2-2A-c-Myc (OKSM) transgene with conditional flox (fl)-AF10 (Mllt10). We isolated mouse embryonic fibroblasts (MEFs), deleted AF10 with CRE-recombinase or treated cells with empty vector control, and initiated reprogramming in DOT1L chemical inhibitor SGC0946 or DMSO control. Gene expression was assessed using RNA-Seq and genome wide localization of H3K79me1 and H3K79me2 was determined by ChIP-Seq on day 4 of reprogramming.
2023-04-01 | GSE214139 | GEO
Project description:Nuclear localization of PTEN is essential for its tumor suppressive role, and loss of nuclear PTEN is more prominent than cytoplasmic PTEN in many kinds of cancers. However, nuclear PTEN-specific regulatory mechanisms were rarely reported. Based on the finding that nuclear PTEN is more unstable than cytoplasmic PTEN. Thus, 293T cells were transiently transfected with plasmid encoding Flag-tagged PTEN along with empty vector, followed by affinity purification using an anti-Flag antibody, and the bound proteins were analyzed by liquid chromatography with tandem mass spectrometry (LC−MS/MS). Here we identify that F-box only protein 22 (FBXO22) induces ubiquitylation of nuclear but not cytoplasmic PTEN at lysine 221, which is responsible for the degradation of nuclear PTEN.
2020-04-22 | PXD017983 | Pride
Project description:AF10 is a cofactor of the H3K79 methyltransferase DOT1L. To uncover the role of H3K79me in reprogramming to induced pluripotent stem cells (iPSCs), we bred reprogrammable mice encoding doxycycline inducible Oct4-2A-Klf4-2A-IRES-Sox2-2A-c-Myc (OKSM) transgene with conditional flox (fl)-AF10 (Mllt10). We isolated mouse embryonic fibroblasts (MEFs), deleted AF10 with CRE-recombinase or treated cells with empty vector control, and initiated reprogramming in DOT1L chemical inhibitor SGC0946 or DMSO control. Gene expression was assessed using RNA-Seq and genome wide localization of H3K79me1, H3K79me2, and RNA Polymerase II (RNAPII) was determined by ChIP-Seq on day 4 of reprogramming.
2023-04-01 | GSE214141 | GEO
Project description:We report the genome wide distribution of the three states of H3K79 methylation (H3K79me1/me2/me3) and H3K27me3 in mouse lineage negative Sca-1 positive Kit positive cells (LSKs), granulocyte macrophage progenitors (GMPs) and LSK derived MLL-AF9 leukemias in the presence or absence of the Af10 OM-LZ domain. Legend- MIT:MSCV-IRES-tdTomato (Empty vector control) and CRE (MIT vector with the Cre recombinase).
2014-09-08 | GSE55038 | GEO