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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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MiRNA expression in the spleen of C57BL mice, p53-knockout C57BL mice, and NO2-knockout C57BL mice.

ABSTRACT: The goal of the study is to assess whether inflammation-induced oxidative and nitrosative stress modulates miRNA expression in mouse model deficient in either p53 or NOS2 RNA was extracted from the spleen of C57BL mice (WT, NOS2 knockout, and p53 knockout) that were C. Parvum treated or saline control treated. 4 or 5 mice were utilized for each grouping.

ORGANISM(S): Mus musculus

SUBMITTER: Ewy Mathe

PROVIDER: E-GEOD-30218 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Inflammation regulates microRNA expression in cooperation with p53 and nitric oxide.

Mathé Ewy E Nguyen Giang H GH Funamizu Naotake N He Peijun P Moake Matthew M Croce Carlo M CM Hussain S Perwez SP

International journal of cancer 20111101 3

microRNA (miRNA) are small non-coding RNA targeting mRNAs leading to their instability and diminished translation. Altered expression of miRNA is associated with cancer. Inflammation and nitric oxide modulates the development of lymphomas in p53 knockout mice and there exists a negative feedback loop between p53 and NOS2. Using a genetic strategy, we tested the hypothesis that inflammation-induced oxidative and nitrosative stress modulates miRNA expression in mouse model deficient in either p53 ...[more]

PMID: 22042537

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miRNA expression in the spleen of C57BL mice, p53-knockout C57BL mice, and NO2-knockout C57BL mice.

Project description:The goal of the study is to assess whether inflammation-induced oxidative and nitrosative stress modulates miRNA expression in mouse model deficient in either p53 or NOS2

2012-06-18 | GSE30218 | GEO

PD-1 Knockout Engineered T Cells for Advanced Colorectal Cancer with MSI high expression

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Expression profiles of TIS21/BTG2/PC3 gene knockout in liver of C57BL/6J mice in response to starvation

Project description:TIS21/BTG2/PC3 has been known as one of the primary response genes regulated by p53-dependent and p53-independent manners. In our study, TIS21 reveals various functions as a tumor suppressor in human and mouse tumors. Recently, it has been reported that expression of TIS21 can be induced during starvation in liver, muscle and white adipose tissues. However, there was no report on the role of TIS21 in response to starvation. To investigate any role of TIS21 gene in the metabolic stimulation, we fasted C57BL/6J mice for overnight (20 hour), and then transcriptional profiles of the TIS21-knockout and TIS21-wild type mice were compared. Along with this trial, we also analyzed transcriptional profiles of fetal livers of the 13.5 day-old embryos derived from the TIS21-wild type and knockout mice.

2017-10-24 | GSE105772 | GEO

CCR5 knockout suppresses experimental autoimmune encephalomyelitis in C57BL/6 mice.

Project description: Not available

| S-EPMC4941248 | biostudies-literature

ChIPseq of enterocytes of the jejunum from transgene C57BL/6 mice harboring a CKIαΔgut knock-out

Project description:ChIPseq of enterocytes of the jejunum from transgene C57BL/6 mice to assess the effects of a CKIαΔgut knock-out in the jejunum and a CKIαΔgut/p53 double knock-out. In addition, enterocytes expressing a mutant p53 (R172H) in combination with CKIαΔgut knockout were analyzed.

2020-02-25 | E-MTAB-7858 | biostudies-arrayexpress

Expression profiling analysis of mouse P4 cerebellum in CitK mutant mice proficient or knockout for P53

Project description:Purpose: Citron kinase (CitK) knockout mice show a severe form of primary microcephaly, associated with ataxia and lethal epilepsy. This phenotype is caused by massive apoptosis occuring during embryonic and post-natal brain development, associated with cytokinesis failure. Cerebellum is the tissue showing highest sensitivity to CitK loss. The clinical phenotype of CitK knockout mice is significantly resued by P53 inactivation. In addition, CitK/P53 double knockout brains have almost normal levels of apoptosis, but display high percentage of binucleated and multinucleated cells. The aim of this study was to analyze the gene expression changes produced in developing neural tissue by CitK loss and to determine which alterations are P53-dependent. expression changes Methods: We analyzed by RNA sequencing total RNA extracted from P4 cerebellum of mice characterized by the following genotypes: 1. CitK +/-, P53 +/- (CTRL); 2. CitK -/-, P53 +/- (CitK-KO); 3. CitK +/-, P53 -/- (P53-KO); 4. CitK -/-, P53 -/- (D-KO). Biological triplicates were analyzed per every genotype. Conclusions: The loss of CitK leads to a strong reduction of the expression of pro-neural genes and induces a P53-related pro-apoptotic gene sets. The analysis of D-KO mice reveals that most of these changes are P53-dependent, but many genes implicated in growth arrest are induced through P53-independent mechanisms.

2017-02-09 | GSE83465 | GEO

RNA-seq of bone marrow neutrophils from wild-type mice (C57BL/6) and CD40LG knockout mice.

Project description:We aimed to investigate the effect of CD40L on neutrophil development by comparing the transcription profile of wild-type and knockout mice. Thus, we performed RNA-sequencing of bone marrow neutrophils from wild-type mice (C57BL/6) and CD40LG knockout mice.

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Gene expression data from transgenic and knockout mice

2015-01-08 | GSE64756 | GEO

Differentially expressed genes in Gdown1 knockout and Gdown1/p53 double-knockout mouse liver [RNA-seq]

Project description:To investigate the biological role of Gdown1, differentially expressed genes in Gdown1 knockout and p53/Gdown1 double-knockout mouse liver were analyzed by RNA-seq.

2021-01-06 | GSE144210 | GEO

Gene expression data from transgenic and knockout mice

Project description:Activation of oncogenic ras pathway accounts for up to 90% low-grade superficial urothelial carcinomas of bladder, and p53 deficiency is very common in high-grade muscle invasive carcinomas. These two pathways in bladder urothelial tumorigenesis used to be considered divergent and their potential collaboration has not been illustrated. We did laser capture micro-dissection (LCM) to separate the tumor cells from the whole bladder tissues from H-ras transgenic and p53 knockout mice, as well as normal urothelial cells as control. Microarray was then performed to identify distinct classes of up-regulated genes during tumorigenesis and progression. In order to get the gene expression profiles of carcinoma in situ (CIS), muscle invasive tumors and normal cells, we used LCM to purify the cells from mixture of different types of cells, and then extracted RNA for microarray. There are three groups applied in microarray, which are normal cells as control, CIS (tumor genesis) and invasive tumors (tumor progression).

2015-01-08 | E-GEOD-64756 | biostudies-arrayexpress

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