RNA sequencing of preB-ALL NALM-6 cells with or without XIAP-knockdown, using prime-seq
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PROVIDER: PRJNA762711 | ENA |
REPOSITORIES: ENA
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Project description:In this study we performed molecular manipulation of XIAP in vivo using microRNA-30 flanked shRNA expression in cell lines models of r/r ALL. Interestingly, upon strong XIAP knockdown, r/r ALL cells were outcompeted in vivo, while intermediate knockdown sensitized cells to chemotherapy. Using prime-seq we wanted to characterized NALM-6 cells expressing different XIAP levels.
2021-09-15 | GSE184011 | GEO
Project description:Nalm 6 WT; Nalm6 BKO; Nalm 6 A hets
| PRJNA623327 | ENA
Project description:BLNK (BASH/SLP-65) encodes an adaptor protein within the B-cell receptor signaling. Loss-of-function mutations of BLNK are observed in human preB-ALL, and a subset of Blnk knock-out mice develop preB-ALL. To understand the molecular mechanism of preB-ALL development associated with the Blnk mutation, retroviral tagging was applied on Blnk KO mice using Moloney murine leukemia virus (MoMLV). The Blnk mutation significantly accelerated the disease onset of MoMLV-induced leukemia and increased the incidence of preB-ALL. Cebpb was identified as the most frequent common retroviral integration site, suggesting that Cebpb upregulation cooperates with Blnk mutation. Transgenic expression of the LAP (liver-enriched activator protein) isoform of C/EBP-beta significantly accelerated preB-ALL development of Blnk ko mice. We used microarrays to detail the global program of gene expression in mouse preB-ALL
2021-10-27 | GSE110737 | GEO
Project description:BLNK (BASH/SLP-65) encodes an adaptor protein within the B-cell receptor signaling. Loss-of-function mutations of BLNK are observed in human preB-ALL, and a subset of Blnk knock-out mice develop preB-ALL. To understand the molecular mechanism of preB-ALL development associated with the Blnk mutation, retroviral tagging was applied on Blnk KO mice using Moloney murine leukemia virus (MoMLV). The Blnk mutation significantly accelerated the disease onset of MoMLV-induced leukemia and increased the incidence of preB-ALL. Cebpb was identified as the most frequent common retroviral integration site, suggesting that Cebpb upregulation cooperates with Blnk mutation. Transgenic expression of the LAP (liver-enriched activator protein) isoform of C/EBP-beta significantly accelerated preB-ALL development of Blnk ko mice. We used microarrays to detail the global program of gene expression in mouse preB-ALL
2021-10-27 | GSE110738 | GEO
Project description:X-linked inhibitor of apoptosis (XIAP) is the most potent endogenous caspase inhibitor preventing cell death via caspase-9, -7 and -3 (initiator and executioner caspase pathways). Using short hairpin RNA (shRNA) against XIAP, stably expressed in a parent HCT116 human colon cancer cell line, a series of clones have been developed. XIAP mRNA levels were established by RT-PCR, the four X (XIAP knockdown) clonal cell lines show 82-93% reduction in XIAP mRNA when compared to the four L (luciferase control) cell lines. Immunoblot analysis showed a 67-89% reduction in XIAP protein in X cell lines compared to L. RNA was analysed by microarray and XIAP knockdown was confirmed in 7 probe sets, there was no significant compensation of other IAP family members. XIAP knockdown induced a 2-fold increase in the basal level of apoptosis without modification of caspase 3/7 activity. Finally, XIAP knockdown sensitises cells to radiotherapy by 20%, to recombinant TRAIL by a 3-fold factor, and to paclitaxel and docetaxel by >2 fold factor. Future work should focus on targeted agents such as rhTRAIL in combination with strategies to down regulate XIAP. XIAP antisense is now in clinical development in oncology.
2008-12-01 | GSE11618 | GEO
Project description:PreB cells were analyzed for differences in gene expression before and after the overexpression of miR-221. In order to dissect possible targets for the miR-221, gene expression profiles of preB cells un-induced or induced for the miR-221 expression after 8, 16 and 24 hours were compared. All induction time-points, e.g. after 8, 16 and 24 hours were compared to un-induced preB cells and to each other group. Gene expression profiles of un-induced preB cells, preB cells induced for miR-221 expression after 8, 16, and 24 hours were analyzed using Affymetrix MG 430 2.0 whole genome arrays. Each time-point was performed in triplicates for un-induced preB cells and preB cells induced for miR-221 expression after 8, 16, and 24 hours (12 arrays in total). To obtain genes significantly downregulated upon induction of miR-221, the expression profiles of un-induced preB cells were compared to preB cells activated for 8, 16, or 24 h and were also compared to each other. After total RNA extraction, reverse transcription, cDNA extraction, the biotinylated cRNA was transcribed, fragmented, and 15 M-BM-5g cRNA hybridized in triplicates for each of the four groups to the 12 GeneChip arrays: Group1, un-induced preB cells, Group2, preB cells induced for miR-221 expression after 8h, Group3, preB cells induced for miR-221 expression after 16h, Group4, preB cells induced for miR-221 expression after 24h.
2013-06-05 | E-GEOD-47643 | biostudies-arrayexpress
Project description:PreB cells were analyzed for differences in gene expression before and after the overexpression of miR-221. In order to dissect possible targets for the miR-221, gene expression profiles of preB cells un-induced or induced for the miR-221 expression after 8, 16 and 24 hours were compared. All induction time-points, e.g. after 8, 16 and 24 hours were compared to un-induced preB cells and to each other group.
2013-06-05 | GSE47643 | GEO
Project description:CFU-PreB colonies are reduced in number and size in Hspa9+/- mice compared to wildtype littermates. We compared the expression profiles of these colonies to gain insight into the mechanism driving this difference. HSPA9 is located on chromosome 5q31.2 in humans, a region that is commonly deleted in patients with myeloid malignancies [del(5q)], including myelodysplastic syndromes (MDS). HSPA9 expression is reduced by 50% in patients with del(5q)-associated MDS, consistent with haploinsufficient levels. Zebrafish mutants and knockdown studies in human and mouse cells have implicated a role for HSPA9 in hematopoiesis. To comprehensively evaluate the effects of Hspa9 haploinsufficiency on hematopoiesis, we generated an Hspa9 knockout mouse model. While homozygous knockout of Hspa9 is embryonic lethal, mice with heterozygous deletion of Hspa9 (Hspa9+/-) are viable and have a 50% reduction in Hspa9 expression. Hspa9+/- mice have normal basal hematopoiesis and do not develop MDS. However, Hspa9+/- mice have a cell-intrinsic reduction in bone marrow CFU-PreB colony formation without alterations in the number of B-cell progenitors in vivo, consistent with a functional defect in Hspa9+/- B-cell progenitors. We further reduced Hspa9 expression (<50%) using RNAi and observe reduced B-cell progenitors in vivo, indicating that appropriate levels (≥50%) of Hspa9 are required for normal B-lymphopoiesis in vivo. Knockdown of Hspa9 in an IL-7 dependent mouse B-cell line reduced Stat5 phosphorylation following IL-7 receptor stimulation, supporting a role for Hspa9 in Stat5 signaling in B-cells. Collectively, these data implicate a role for Hspa9 in B-lymphopoiesis and Stat5 activation downstream of IL-7 signaling. Bone marrow cells from 5 Hspa9+/+ and 5 Hspa9+/- mice were independently cultured in CFU-PreB methylcellulose medium for 7 days. PreB colonies were isolated and B220+ cells were flow sorted for RNA isolation.
2015-02-04 | E-GEOD-65588 | biostudies-arrayexpress
Project description:Expression profile of miRNAs in NALM-6 cells were analyzed after TSA treatment for 6h, compared with non-treated cells.
2009-11-06 | E-MEXP-2047 | biostudies-arrayexpress
Project description:Kasumi-7, Kasumi-9, NAGL-1, and NALM-1 cell lines were subjected to ChIP-seq analysis using anti-H3K27Ac antibody. Input signal reads are also provided.
2020-06-30 | E-MTAB-8463 | biostudies-arrayexpress