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RNAseq to profile transcriptomes in bone marrow-derived macrophages from TKO (mir-106a~363-/- mir-106b~25-/- mir-17~92flox/flox Lyz2-Cre) and WT(Lyz2-Cre) mice stimulated with LPS for 3 hours.

ABSTRACT: RNAseq to profile transcriptomes in bone marrow-derived macrophages from TKO (mir-106a~363-/- mir-106b~25-/- mir-17~92flox/flox Lyz2-Cre) and WT(Lyz2-Cre) mice stimulated with LPS for 3 hours.

PROVIDER: PRJNA552797 | ENA |

REPOSITORIES: ENA

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RNAseq to profile transcriptomes in bone marrow-derived macrophages from TKO(mir-106a~363-/- mir-106b~25-/- mir-17~92flox/flox Lyz2-Cre) and WT(Lyz2-Cre) mice

Project description:RNAseq to profile transcriptomes in bone marrow-derived macrophages from TKO(mir-106a~363-/- mir-106b~25-/- mir-17~92flox/flox Lyz2-Cre) and WT(Lyz2-Cre) mice

| PRJNA531934 | ENA

RNAseq to profile transcriptomes in adipose tissue macrophages (ATMs) from TKO(mir-106a~363-/- mir-106b~25-/- mir-17~92flox/flox Lyz2-Cre) and WT(Lyz2-Cre) mice fed with regular chow diet or high fat diet.

Project description:RNAseq to profile transcriptomes in adipose tissue macrophages (ATMs) from TKO(mir-106a~363-/- mir-106b~25-/- mir-17~92flox/flox Lyz2-Cre) and WT(Lyz2-Cre) mice fed with regular chow diet or high fat diet.

| PRJNA666002 | ENA

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

Gene expression profiling of mT/mG;Lyz2.Cre vs IKKbetaf/f;Lyz2.Cre mouse bone marrow derived macrophages

Project description:Gene expresion comparison between tomato Lyz2 Cre and IKKbeta flox/flox Lyz2 Cre bone marrow derived macrophages

2019-06-28 | GSE94880 | GEO

MicroRNAs in the miR-106b family regulate p21/CDKN1A and promote cell cycle progression.

Project description:microRNAs in the miR-106b family are overexpressed in multiple tumor types and are correlated with the expression of genes that regulate the cell cycle. Consistent with these observations, miR-106b family gain of function promotes cell cycle progression, whereas loss of function reverses this phenotype. Microarray profiling uncovers multiple targets of the family, including the cyclin-dependent kinase inhibitor p21/CDKN1A. We show that p21 is a direct target of miR-106b and that its silencing plays a key role in miR-106b-induced cell cycle phenotypes. We also show that miR-106b overrides a doxorubicin-induced DNA damage checkpoint. Thus, miR-106b family members contribute to tumor cell proliferation in part by regulating cell cycle progression and by modulating checkpoint functions. HCT116 Dicerex5 cells were transfected with microRNAs in six-well plates, and RNA was isolated 10 h after transfection. Transcripts containing the miR-106b family hexamers in their 3' UTRs were identified. By microarray analysis, 103 transcripts that contained miR-106b family complementary hexamers in their 3' UTRs were down-regulated by miR-106b, miR-106a, miR-20b, and miR-17-5p within 10 h of transfection.

2010-06-23 | E-GEOD-14831 | biostudies-arrayexpress

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

2014-04-01 | GSE56376 | GEO

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

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

2014-04-01 | GSE56378 | GEO

Bulk RNA-seq of alveolar macrophages from WT (Lepr+/+, Lyz2-Cre) and Lepr KO (Leprfl/fl, Lyz2-Cre) mice

Project description:To study the regulation of Lepr on transcriptome in WT and Lepr KO AMs under resting state and after LPS stimulation, Lepr-sufficient (Lepr+/+, Lyz2-Cre) and Lepr-deficient (Leprfl/fl, Lyz2-Cre) alveolar macrophages (AMs) were isolated by collecting BALF. Lipopolysaccharide (LPS) was added in vitro for 1h or cells were left untreated. Total RNA was extracted for deep sequencing. Gene expression in WT and Lepr KO cells were analyzed.

2022-07-20 | GSE185218 | GEO

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