Effect of Ro 08-2750 treatment on gene expression of human leukemia cell lines MOLM13 and K562
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE114320 | GEO | 2019/05/09
REPOSITORIES: GEO
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Project description:Effect of Ro 08-2750 treatment on gene expression of human leukemia cell lines MOLM13 and K562
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Project description:Hepatic fibrosis is a dynamic process characterized by the net accumulation of extracellular matrix resulting from chronic liver injury such as nonalcoholic steatohepatitis. During the pathogenesis of hepatic fibrosis, activation of hepatic stellate cells (HSCs) causes transdifferentiation of quiescent cells into proliferative and fibrogenic myofibroblasts. In the present study, we developed a novel RORα-selective ligand, ODH-08, based on the modification of JC1-40, a previously reported N-methylthiourea analog. Administration of ODH-08 to Western diet (WD)-fed mice improved the signs of hepatic fibrosis: decreased hepatic collagen deposition and suppression of the expression of fibrogenic markers. ODH-08 inhibits the TGF1-induced fibrogenic activation of HSCs through suppression of the TGFβ1–SMAD signaling pathway, which represents a novel mechanism for the antifibrogenic effect of RORα. Thus, ODH-08 appears to be a promising antifibrotic agent to treat hepatic fibrosis. We performed a microarray analysis in the liver tissue of ODH-08-treated WD-fed mice to anlyse differentially expressed genes under ODH-08 administration. The control group was vehicle-treated WD-fed mice.
2024-03-01 | GSE250531 | GEO
Project description:RNA binding proteins (RBPs) are key regulators of normal and pathological gene expression. Small molecules targeting RBP-RNA interactions are a rapidly emerging class of therapeutics. Ro-08-2750 (Ro) was previously identified as a competitive inhibitor of Musashi-RNA interactions. Here we show Ro potently inhibits steroidogenesis and viability independent of Musashi-2 in multiple cell lines. We identified Ro-interacting proteins using an unbiased proteome-wide approach. Other RBPs were a prominent class of Ro-interacting proteins and leveraging large-scale ENCODE data we found a subset of these phenocopy Ro inhibition. We provide a general framework for validating the specificity and identifying targets of RBP inhibitors in a cellular context.
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Project description:To assess how the miR-142 deficit affected the BM LSC-enriched LSK landscape, we conducted a single cell RNA-seq analysis of BM miR-142+/+ BCR-ABL (CP CML) and miR-142−/− BCR-ABL (BC CML) LSKs which were harvested from the respective mice, 2 weeks after BCR-ABL induction.
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Project description:Using BCR-ABL-induced chronic myeloid leukemia (CML) as a disease model for leukemia stem cells (LSCs), we showed that BCR-ABL down-regulates the B lymphoid kinase (Blk) gene in leukemia stem cells in CML mice and that Blk functions as a tumor suppressor in LSCs and suppresses LSC function. Inhibition of this Blk pathway accelerates CML development, whereas increased activity of the Blk pathway delays CML development. To identify the pathways in which Blk regulates function of LSCs, we performed a comparative DNA microarray analysis using total RNA isolated from non-BCR-ABL-expressing Lin-Sca-1+c-Kit+, BCR-ABL- and BCR-ABL-Blk expressing LSCs. This analysis revealed a large group of candidate genes that exhibited changes in the levels of transcription in the Blk expressing LSCs, and uncovered the molecular mechanisms by which Blk suppresses LSCs and CML development.
2012-07-06 | GSE36096 | GEO
Project description:We studied the following conditions: m6A RNA methylation in MOLM13 AML cells; METTL3 deficiency on gene expression and translational efficiency
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Project description:Indian rhesus macaques are arguably the most reliable animal models in AIDS research. In this species the MHC class I allele Mamu-B*08, among others, is associated with elite control of SIV replication. A similar scenario is observed in humans where the expression of HLA-B*27 or HLA-B*57 has been linked to slow or no progression to AIDS after HIV infection. Despite having large differences in their primary structure, it has been reported that HLA-B*27 and Mamu-B*08 display peptides with sequence similarity. To fine-map the Mamu-B*08 binding motif and assess its similarities with that of HLA-B*27 we affinity purified the peptidomes bound to these MHC class I molecules and analyzed them by LC-MS/MS identifying several thousands of endogenous ligands. Sequence analysis of both sets of peptides revealed a degree of similarity in their binding motifs, especially at peptide position 2 (P2) where arginine was present in the vast majority of ligands of both allotypes. In addition, several differences emerged from this analysis: (i) ligands displayed by Mamu-B*08 tended to be shorter and to have lower molecular weight, (ii) Mamu-B*08 showed a higher preference for glutamine at P2 as a suboptimal binding motif and (iii) the second major anchor position, found at P-omega, was much more restrictive in Mamu-B*08. In this regard, HLA-B*27 bound efficiently peptides with aliphatic, aromatic (including tyrosine) and basic C-terminal residues while Mamu-B*08 preferred peptides with leucine and phenylalanine in this position. These results deepen our understanding of the molecular basis of the presentation of peptides by Mamu-B*08 and can contribute to the detection of novel SIV epitopes restricted by this allotype.
2016-10-07 | PXD004964 | Pride
Project description:We previously demonstrated that Alox5 deficiency impairs the function of LSCs and prevents the initiation of BCR-ABL-induced CML. To identify the pathways in which Alox5 gene regulates function of LSCs, we performed a comparative DNA microarray analysis using total RNA isolated from non-BCR-ABL-expressing Lin-Sca-1+c-Kit+, BCR-ABL-expressing wild type LSCs and BCR-ABL-expressing Alox5-/- LSCs. The result was validated by quantitative real-time PCR analysis of non-BCR-ABL-expressing Lin-Sca-1+c-Kit+, BCR-ABL-expressing wild type LSCs and BCR-ABL-expressing Alox5-/- LSCs. We have shown that Alox5 is a critical regulator of leukemia stem cells (LSCs) in a BCR-ABL-induced chronic myeloid leukemia (CML) mouse model, and we hypothesize that the Alox5 pathway represents a major molecular network that regulates LSC function. Therefore, we sought to further dissect this pathway by comparing the gene expression profiles of wild type and Alox5-/- LSCs derived from our mouse model for BCR-ABL-induced CML. DNA microarray analysis revealed a small group of candidate genes that exhibited changes in the levels of transcription in the absence of Alox5 expression. In particular, we noted that the expression of the Msr1 gene was up-regulated in Alox5-/- LSCs, suggesting that Msr1 might suppress the proliferation of LSCs. Using our CML mouse model, we show that Msr1 is down-regulated by BCR-ABL and this down-regulation is partially restored by Alox5 deletion, and that Msr1 deletion causes acceleration of CML development. Moreover, Msr1 deletion markedly increases LSC function through its effects on cell cycle progression and apoptosis. We also show that Msr1 affects CML development by regulating the PI3K-AKT pathway and ?-Catenin. Together, these results demonstrate that Msr1 suppresses LSCs and CML development. The enhancement of Msr1 function may be of significance in the development of novel therapeutic strategies targeting CML. To identify genes that are regulated by BCR-ABL in LSCs and LSCs without Alox5 gene, we compared the gene profile between wild type(WT) LSCs or Alox5-/- LSCs.
2011-05-17 | E-GEOD-29347 | biostudies-arrayexpress