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Follicular B (FoB) cells purified from miR-17-92 transgenic mice

ABSTRACT: We have generated a miR-17-92 transgenic allele (termed miR-17-92 Tg) whose expression can be turned on conditionally by Cre recombinase (Xiao et al, Nature Immunology, 9:405-14, 2008). The mice were crossed to CD19-Cre mice to turn on the transgene expression specifically in B cells.

ORGANISM(S): Mus musculus

PROVIDER: GSE30877 | GEO | 2011/07/22

SECONDARY ACCESSION(S): PRJNA144263

REPOSITORIES: GEO

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Follicular B (FoB) cells purified from miR-17-92 transgenic mice, stimulated with LPS/IL-4 for 13.5 or 25.5 hours

2014-04-01 | GSE56377 | GEO

Follicular B (FoB) cells purified from miR-17-92 transgenic mice

Project description:We have generated a miR-17-92 transgenic allele (termed miR-17-92 Tg) whose expression can be turned on conditionally by Cre recombinase (Xiao et al, Nature Immunology, 9:405-14, 2008). The mice were crossed to CD19-Cre mice to turn on the transgene expression specifically in B cells. Follicular B(FoB) cells were purified from CD19-Cre;miR-17~92 Tg/Tg mice (FoBtg1, FoBtg2, FoBtg3) and miR-17~92 Tg/Tg mice (FoBwt1, FoBwt2, FoBwt3) by MACS depletion of cells positive for CD5, CD43, and CD93 (also known as AA4.1). The purity of follicular B cells was examined by flow cytometry and was greater than 95% for all samples. Total RNA was extracted using RNeasy kit (QIAGEN).

2011-07-21 | E-GEOD-30877 | biostudies-arrayexpress

Follicular B (FoB) cells purified from miR-17-92 transgenic mice, stimulated with LPS/IL-4 for 13.5 or 25.5 hours

Project description:We have generated a miR-17-92 transgenic allele (termed miR-17-92 Tg) whose expression can be turned on conditionally by Cre recombinase (Xiao et al, Nature Immunology, 9:405-14, 2008). The mice were crossed to CD19-Cre mice to turn on the transgene expression specifically in B cells. Follicular B(FoB) cells were purified from CD19-Cre;miR-17~92 Tg/Tg mice (TG1, TG2, TG3) and miR-17~92 Tg/Tg mice (WT1, WT2, WT3) by MACS depletion of cells positive for CD5, CD43, and CD93 (also known as AA4.1). The purified B cells were stimulated with LPS/IL-4 for 13.5hr or 25.5hr. The purity of follicular B cells was examined by flow cytometry and was greater than 95% for all samples. Total RNA was extracted using RNeasy kit (QIAGEN).

2014-04-01 | E-GEOD-56377 | biostudies-arrayexpress

Follicular B (FoB) cells purified from miR-17-92 tKO mice

2014-04-01 | GSE56376 | GEO

Ribosome Profiling analysis of Follicular B (FoB) cells purified from WT, miR-17~92 transgenic and miR-17-92 tKO mice

Project description:We have generated a miR-17~92 transgene and fl/fl allele whose expression can be turned on and off conditionally by Cre recombinase. The mice were crossed to CD19-Cre mice to turn on and off the expression of miR-17~92 specifically in B cells and stimulated LPS/IL-4 for 25.5hr. tKO mice were generated in the miR-106a-363-/-;miR-106b-25-/- background, so that all three homologous cluster of miR-17~92 family miRNAs are deleted in B cells.

2017-03-08 | GSE83684 | GEO

Follicular B (FoB) cells purified from miR-17-92 tKO mice, stimulated with LPS/IL-4, 13.5hr

2014-04-01 | GSE56378 | GEO

Follicular B (FoB) cells purified from miR-17-92 tKO mice

Project description:We have generated a miR-17~92 fl/fl allele whose expression can be turned off conditionally by Cre recombinase in the miR-106a-363-/-;miR-106b-25-/- background. The mice were crossed to CD19-Cre mice to turn off the expression of miR-17~92 specifically in B cells. Follicular B(FoB) cells were purified from CD19-Cre;miR-17~92 fl/fl;miR-106a-363;miR-106b~25 mice (tKO1, tKO2, tKO3) and CD19-cre (Control1, Control2, Control3) by MACS depletion of cells positive for CD9, CD43, and CD93 (also known as AA4.1). The purity of follicular B cells was examined by flow cytometry and was greater than 95% for all samples. Total RNA was extracted using RNeasy kit (QIAGEN).

2014-04-01 | E-GEOD-56376 | biostudies-arrayexpress

Follicular B (FoB) cells purified from miR-17-92 tKO mice, stimulated with LPS/IL-4, 13.5hr

Project description:We have generated a miR-17~92 fl/fl allele whose expression can be turned off conditionally by Cre recombinase in the miR-106a-363-/-;miR-106b-25-/- background. The mice were crossed to CD19-Cre mice to turn off the expression of miR-17~92 specifically in B cells and stimulated LPS/IL-4 for 13.5hr. Follicular B(FoB) cells were purified from CD19-Cre;miR-17~92 fl/fl;miR-106a-363;miR-106b~25 mice (TKO1, TKO2, TKO3) and WT (WT1, WTl2, WT3) by MACS depletion of cells positive for CD9, CD43, and CD93 (also known as AA4.1). The purified B cells were stimulated with LPS/IL-4 for 13.5hr in B cell media. The purity of follicular B cells was examined by flow cytometry and was greater than 95% for all samples. Total RNA was extracted using RNeasy kit (QIAGEN).

2014-04-01 | E-GEOD-56378 | biostudies-arrayexpress

miR-17-92/106b regulate beta cell mitotic checkpoint and insulin secretion

Project description:Adult beta cells in the pancreas are the sole source of insulin in our body. Beta cell loss or increased demand for insulin, impose metabolic challenges because adult beta cells are generally quiescent and infrequently re-enter the cell division cycle. miR-17-92/106b is a family of proto-oncogene microRNAs, that regulate proliferation in normal tissues and in cancer. Here, we employ mouse genetics to demonstrate a critical role for miR-17-92/106b in glucose homeostasis and in controlling insulin secretion. Mass spectrometry analysis was performed on miR-17-92LoxP/LoxP;106-25-/- MEF lysate, without or with CRE-Adenovirus. miR-17-92LoxP/LoxP;106-25+/+ MEFs with GFP-Adenovirus served as controls. We demonstrate that miR-17-92/106b regulate the adult beta cell mitotic checkpoint and that miR-17-92/106b deficiency results in reduction in beta cell mass in-vivo. Furthermore, protein kinase A (PKA) is a new relevant molecular pathway downstream of miR-17-92/106b in control of adult beta cell division and glucose homeostasis. Therefore, contributes to the understanding of proto-oncogene miRNAs in the normal, untransformed endocrine pancreas, and illustrates new genetic means for regulation of beta cell mitosis and function by non-coding RNAs.

2019-06-17 | PXD012610 | Pride

The transcription factor TAL1 and the miR-17-92 cluster establish a regulatory loop

Project description:A network of gene regulatory factors such as transcription factors and microRNAs establish and maintain the gene expression pattern during hematopoiesis. In this network transcription factors regulate each other and are involved in regulatory loops with microRNAs.The microRNA cluster miR-17-92 is located within the MIR17HG gene and encodes for six mature microRNAs. It is important for hematopoietic differentiation and plays a central role in malignant disease. However, the transcription factors downstream of miR-17-92 are largely elusive and the transcriptional regulation of miR-17-92 is not fully understood. Here we show that miR-17-92 forms a regulatory loop with the transcription factor TAL1. The miR-17-92 cluster inhibits expression of TAL1 and indirectly leads to decreased stability of the TAL1 transcriptional complex. We found that TAL1 and its heterodimerization partner E47 regulate miR-17-92 transcriptionally. Furthermore, miR-17-92 negatively influences erythroid differentiation, a process that depends on gene activation by the TAL1 complex. Our data give example of how transcription factor activity is fine-tuned during normal hematopoiesis. We postulate that disturbance of the regulatory loop between TAL1 and the miR-17-92 cluster could be an important step in cancer development and progression.

2021-09-09 | PXD018052 | Pride

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