Gene expression of human hematopoietic stem cells (CD34+) stimulated with native & mutant (244) form of myeloid stem-cell transcription factor PU.1 alone & in combination with myeloid specific cytokines (IL3+GMCSF+Flt2+MCSF+SCF)
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PROVIDER: PRJNA428367 | ENA |
REPOSITORIES: ENA
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Project description:Human CD34+ hematopoietic stem cells gives rise to complete blood lineages through the process of hematopoiesis. Here we tried to differentiate a particular lineage i.e myeloid from CD34+ hematopoietic stem cells using a transcription factor PU.1 and its mutated form. Gene expression analysis was performed after treating cells with protein factors and different cytokine combinations. Cells were given six different treatments including control-PU.1 only and PU.1 with cytokines combination; Y244D only and Y244D with cytokines combination and only cytokine combination (IL3, GMCSF, Flt2, MCSF, and SCF). After 5 days of incubation, cells were washed and pellet was preserved in RNAlater (Ambion) to be shipped to Genotypic Technologies Pvt. Ltd. (Bangalore) for microarray analysis.
2020-09-30 | GSE108720 | GEO
Project description:Mast cells, activated by antigen via the high affinity receptor for IgE (FcεRI), release an array of pro-inflammatory mediators that contribute to allergic disorders such as asthma and anaphylaxis. The KIT ligand, stem cell factor (SCF), is critical for mast cell expansion, differentiation and survival, and, under acute conditions, enhances mast cell activation. However, extended SCF exposure in vivo conversely protects against fatal antigen-mediated anaphylaxis. In investigating this dichotomy, we identified a novel mode of regulation of the mast cell activation phenotype through SCF-mediated programming. We found that mouse bone marrow-derived mast cells chronically exposed to SCF displayed a marked attenuation of FcεRI-mediated degranulation and cytokine production. The hypo-responsive phenotype was not a consequence of altered signals regulating calcium flux or protein kinase C, but of ineffective cytoskeletal reorganization, with evidence implicating a down-regulation of expression of the Src kinase Hck. Collectively, these findings demonstrate a major role for SCF in the homeostatic control of mast cell activation with potential relevance to mast cell-driven disease and the development of novel approaches for the treatment of allergic disorders. Mouse bone marrow-derived mast cells were treated with IL3, IL3+IL33, or IL3+SCF. Six replicates each.
2012-05-01 | E-GEOD-35332 | biostudies-arrayexpress
Project description:BCOR is a component of a variant Polycomb group repressive complex 1 (PRC1) complex. Recently, we and others reported recurrent somatic BCOR loss-of-function mutations in myelodysplastic syndrome and acute myelogenous leukaemia (AML). However the role of BCOR in normal hematopoiesis is largely unknown. Here, we explored the function of BCOR in myeloid cells using myeloid murine cell models with Bcor conditional loss-of-function or overexpression alleles. Bcor mutant bone marrow cells showed significantly higher proliferation and differentiation rates with reduced protein levels of RING1B, a ubiquitin ligase subunit of PRC1 family complexes. Global RNA expression profiling in murine cells and AML patient samples with BCOR loss-of-function mutation suggested that loss of BCOR expression is associated with proliferation and myeloid differentiation and decreased stem cell quiescence. Further, we used a MLL-AF9 murine model of AML and found that loss of Bcor increased serial replating efficiency, enhanced MLL-AF9 in blocking cell differentiation, and increased expression of Evi1 which is associated with leukemic transformation. Our results strongly suggest that BCOR plays an indispensable role in maintaining hematopoietic stem cell (HSC) quiescence by inhibiting myeloid stem cell proliferation and differentiation and offer a mechanistic explanation for how BCOR regulates gene expression such as Hox genes. We took advantage of a mouse conditional Bcor allele which has exons 9 and 10 been flanked by LoxP sites to allow their removal via expression of Cre recombinase. Excision of these exons results in a frame shift and a premature stop codon causing nonsense mediated decay and/or carboxy-terminal deletion of the BCOR protein. CD34+ cells were sorted from control or Bcor mutant cells cultured under myeloid stem/progenitor conditions (IL3, 6 and SCF). We used microarrays to detail the global programme of gene expression in Control and Bcor mutant CD34+ cells.
2015-12-31 | E-GEOD-69620 | biostudies-arrayexpress
Project description:Expansion for hematopoietic cells from umbilical cord blood is a strategy for use this cell source in clinic transplants, however, it is important to know about the genomic changes that can occur in expanded cells. In order to detect global expression profiles changes in hematopoietic stem and progenitors cells generated in vitro, we analyzed hematopoietics populations obtained by FACS in fresh from umbilical cord blood. HSC (fHSC) was defined as CD34+ CD38- CD71- CD45RA- Lin- and were cocultured with stromal cell line OP-9 plus FL, SCF, IL3, IL6, TPO, GMCSF and G-CSF by 7 days, after time we repurified HSC population by FACS using same immunophenotype (ivHSC). In other hand, fresh erythroid progenitors cells (fEPC) were identified as CD34+CD38+CD71+CD45RA- Lin- and fresh myeloid progenitors cells (fMPC) were identified as CD34+CD38+CD71-CD45RA+Lin-. In vitro progenitors cells (ivEPC and ivMPC) were obtained by culturing fHSC in Stemspan serum-free media plus SCF, TPO, IL6, FL and IL3 by 10 days, after time cells were repurified by FACS using same immunophenotype for fresh progenitors. In vitro generated cells were compared with their corresponding fresh population cells.
2018-06-05 | GSE107497 | GEO
Project description:Aeromonas hydrophila strain:244 Genome sequencing
| PRJNA238162 | ENA
Project description:Geotrichum candidum LMA-244 MLST
| PRJNA482419 | ENA
Project description:Saccharum officinarum IM76-244 Resequencing
| PRJNA1228743 | ENA
Project description:Lung cancer remains the leading cause of cancer-related deaths worldwide. β-arrestin-1 (ARRB1), a scaffolding protein involved in the termination or desensitization of signals arising from activated G-protein-coupled receptors (GPCRs) has been shown to play a role in invasion and proliferation of many cancers, including nicotine-induced proliferation of human non–small cell lung cancers (NSCLCs). In this study, we analyzed nicotine induced and β-arrestin-1 dependent genes from the microarray data. Our analysis show that SCF (Stem cell factor) strongly differentiated smokers from non-smokers implying an important role of this gene in NSCLCs. SCF, a major cytokine is the ligand for the c-Kit proto-oncogene. Here we elucidate the molecular mechanisms by which nicotine as well as EGF induces the expression of SCF in lung adenocarcinoma cell lines A549 and H1650. ChIP assays and transient transfection experiments showed that transcription factor E2F1 can positively regulate SCF expression at the transcriptional level; depletion of E2F1 or β-arrestin-1 prevented the nicotine-mediated induction of SCF. Given that the binding of SCF to c-Kit leads to activation of multiple downstream signaling pathways including Src, PI3K, MEK and EGFR pathways, our data suggest that the SCF plays a central role in lung carcinogenesis, and may be a potential therapeutic target for combating NSCLC. Studies presented here also provide evidence that SCF along with nicotine promotes self-renewal and proliferation of lung cancer stem cells (CSCs). Our findings reveal an important role and prognostic significance of SCF that can serve as a novel prognostic and predictive biomarker for NSCLC.
2013-11-10 | GSE44617 | GEO
Project description:Panicum virgatum exome capture - SPR-244
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Project description:Lung cancer remains the leading cause of cancer-related deaths worldwide. M-NM-2-arrestin-1 (ARRB1), a scaffolding protein involved in the termination or desensitization of signals arising from activated G-protein-coupled receptors (GPCRs) has been shown to play a role in invasion and proliferation of many cancers, including nicotine-induced proliferation of human nonM-bM-^@M-^Ssmall cell lung cancers (NSCLCs). In this study, we analyzed nicotine induced and M-NM-2-arrestin-1 dependent genes from the microarray data. Our analysis show that SCF (Stem cell factor) strongly differentiated smokers from non-smokers implying an important role of this gene in NSCLCs. SCF, a major cytokine is the ligand for the c-Kit proto-oncogene. Here we elucidate the molecular mechanisms by which nicotine as well as EGF induces the expression of SCF in lung adenocarcinoma cell lines A549 and H1650. ChIP assays and transient transfection experiments showed that transcription factor E2F1 can positively regulate SCF expression at the transcriptional level; depletion of E2F1 or M-NM-2-arrestin-1 prevented the nicotine-mediated induction of SCF. Given that the binding of SCF to c-Kit leads to activation of multiple downstream signaling pathways including Src, PI3K, MEK and EGFR pathways, our data suggest that the SCF plays a central role in lung carcinogenesis, and may be a potential therapeutic target for combating NSCLC. Studies presented here also provide evidence that SCF along with nicotine promotes self-renewal and proliferation of lung cancer stem cells (CSCs). Our findings reveal an important role and prognostic significance of SCF that can serve as a novel prognostic and predictive biomarker for NSCLC. Transfection of A549 cell line with control siRNA, Beta arrestin siRNA and then stimulation of nicotine
2013-11-10 | E-GEOD-44617 | biostudies-arrayexpress