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CEA_SGF:E00008#transgenic_IIb-tk

ABSTRACT: To investigate genes that are involved in hematopoietic cells production in vivo, we used microarray technology combined with a transgenic mouse model IIb-tk previously developed in our laboratory (Tropel et al., 1997). In these mice, the promoter region of the murine CD41 (GPIIb) gene was used to target the expression of the thymidine kinase (tk) toxigene in cells specifically expressing the CD41 gene. The strength of the model resides in the fact that the depletion of the entire myelo-megakaryocytic lineage including stem cells/early progenitors by ganciclovir (GCV) administration could be inverted by discontinuing the treatment. A nearly full recovery of mature myelo-megakaryocytic cells is then observed within 3 days. To determine at the molecular level how BM cells could be regenerated in vivo following the eradication of all myeloid progenitors by the GCV treatment, microarray technology was applied. The strategy involved monitoring early transcriptional changes for the first 3-day of BM regeneration. Keywords: time-course

ORGANISM(S): Mus musculus

PROVIDER: GSE1290 | GEO | 2004/04/09

SECONDARY ACCESSION(S): PRJNA90205

REPOSITORIES: GEO

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CEA_SGF:E00008#transgenic_IIb-tk

Project description:To investigate genes that are involved in hematopoietic cells production in vivo, we used microarray technology combined with a transgenic mouse model IIb-tk previously developed in our laboratory (Tropel et al., 1997). In these mice, the promoter region of the murine CD41 (GPIIb) gene was used to target the expression of the thymidine kinase (tk) toxigene in cells specifically expressing the CD41 gene. The strength of the model resides in the fact that the depletion of the entire myelo-megakaryocytic lineage including stem cells/early progenitors by ganciclovir (GCV) administration could be inverted by discontinuing the treatment. A nearly full recovery of mature myelo-megakaryocytic cells is then observed within 3 days. To determine at the molecular level how BM cells could be regenerated in vivo following the eradication of all myeloid progenitors by the GCV treatment, microarray technology was applied. The strategy involved monitoring early transcriptional changes for the first 3-day of BM regeneration.

2010-06-09 | E-GEOD-1290 | biostudies-arrayexpress

CEA_SGF:E00009#switch_lympho_mega

Project description:we analyzed the gene expression profile of newly produced transgenic bone marrow subpopulations and compared it to the expression patterns obtained from cells isolated from wild type mice at different stages of the hematopoietic differentiation process. These populations were enriched in HSC, CMP, CD41+ c-kit+ and CD41+ c-kit- populations for the myelo-megakaryocytic lineage; and for the B lymphoid lineage, the populations were enriched in CLP, Pro-B and mature B lymphocytes. To produce comparable profiles total bone marrow RNA was used as a common reference. Keywords: repeat sample

2004-12-01 | GSE1289 | GEO

Quantitative proteomic analysis of gastric cancer cells treated by bifidobacterium infantis-mediated herpes simplex virus-TK/ganciclovir.

Project description:MKN-45 cells were treated with PBS, BF-TK, BF/GCV or BF-TK/GCV for 48 h (GCV, 167 µg/ml), respectively. BF-TK (n = 3), BF/GCV (n = 3) or BF-TK/GCV (n = 3) groups were analyzed in triplicate.

2023-10-24 | PXD042044 | Pride

CEA_SGF:E00009#switch_lympho_mega

2010-06-05 | E-GEOD-1289 | biostudies-arrayexpress

NP-18 vs. NP-18AR transcriptional profile upon treatment with TK/GCV

2010-07-16 | GSE17137 | GEO

NP-18 vs. NP-18AR transcriptional profile upon treatment with TK/GCV

Project description:Pancreatic cancer-derived cells NP-18 underwent four rounds of treatment with increasing doses of an adenoviral vector encoding TK enzyme and GCV. Surviving cells were termed NP-18AR and displayed decreased sensitivity to treatment. This experiment analyses the transcriptomic effect of TK/GCV treatment on NP-18AR as compared to that of NP-18 cells. Two-condition experiment, where response to treatment in naïve cells (NP-18) was compared to response to treatment in previously treated resistant cells (NP-18AR). Biological replicates: samples from 3 independently generated and independently treated NP-18AR lines (NP-18AR1, NP-18AR2 and NP-18AR3) were hibridized with 3 independently treated samples of NP-18 cells. A total of 9 hybridizations were performed, 2 for NP-18AR1 (including 1 dye-swap), 4 for NP-18AR2 (including 2 dye swaps) and 3 for NP-18AR3 (including 1 dye-swap).

2010-07-16 | E-GEOD-17137 | biostudies-arrayexpress

Cellular senescence in malignant cells promotes tumorigenesis in mouse and patient glioblastoma [p16]

Project description:The goal of this study is to identify the senescent cells expressing high level of p16Ink4a (p16Ink4a Hi) in GBMs and characterize their action on the tumor microenvironment at an early timepoint. We introduced the p16-3MR transgene in the GBM mouse model to selectively delete p16Ink4a Hi senescent cells upon ganciclovir (GCV) injection. We compared p16-3MR+GCV to WT+GCV control GBMs that were harvested 7 days after the last GCV injection.

2022-12-15 | GSE198439 | GEO

Difference in gene expression signatures for progenies of lenalidomide-treated megakaryocyte/erythrocyte progenitors

Project description:To clarigy the molecular mechanism underlying the IMiD-induced megakaryocytic lineage commitment in human megakaryocyte/erythrocyte progenitors, we performed transcriptome analysis of CD41-CD105+ and CD41+CD105- cells obtained from megakaryocyte/erythrocyte progenitors treated with lenalidomide for 72 hours. Differentially expressed genes were comprehensively evaluated by gene set enrichment analysis. CD105-CD41+ cells showed the enrichment in the expression of genes related to megakaryocytes and platelet, whereas genes related to erythroid lineage were negatively enriched. CD41+CD105- cells expressed higher levels of transcription factors required for megakaryocyte differentiation including FLI1, RUNX1, and MEIS1. Furthermore, we performed a knockdown strategy with small interfering RNA against MEIS1 mRNA, confirming that lenalidomide-induced megakaryocyte commitment should be due to the up-regulation of MEIS1 in megakaryocyte/erythrocyte progenitors.

2021-11-25 | GSE162212 | GEO

Early removal of senescent cells protects retinal ganglion cells loss in experimental ocular hypertension

Project description:Experimental ocular hypertension (IOP) induces senescence of retinal ganglion cells (RGCs) that mimicks events occurring in human glaucoma. An established transgenic p16-3MR mouse model in which the systemic administration of the small molecule ganciclovir (GCV) selectively kills p16INK4a-expressing cells was used to compare transcriptomes of retinas from IOP and control eyes in GCV-treated and non-treated mice, to investigate how experimental removal of senescent p16INK4a-positive cells impacts retinal cells in conditions resembling glaucoma.

2020-12-01 | GSE141725 | GEO

Cellular senescence in malignant cells promotes tumorigenesis in mouse and patient glioblastoma [10X scRNA-seq]

Project description:The goal of this study is to identify the senescent cells expressing high level of p16Ink4a (p16Ink4a Hi) in GBMs, at an early timepoint. We introduced the p16-3MR transgene in the GBM mouse model to selectively delete p16Ink4a Hi senescent cells upon ganciclovir (GCV) injection. We compared two p16-3MR+GCV to two WT+GCV control GBMs that were harvested 7 days after the last GCV injection. p16Ink4a Hi senescent cells were a subset of malignant cells, mostly grouped in the astrocyte cluster and to a lesser extend in the NP-like cluster. We also found that p16Ink4a Hi senescent cells deletion modifies the cell state of malignant cells and modulates the tumor microenvironment. This study allowed us to define a GBM senescence signature.

2022-12-15 | GSE168038 | GEO

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