Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA245222 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Analysis of liver RNA from SRSF3 hepatocyte knockout mice versus wild-type littermates
| PRJNA152413 | ENA
Project description:SRSF3 (SRp20) is an essential RNA splicing factor. By conditional knockout (KO) of Srsf3, we discovered Srsf3 at its physiological level plays a tumor-suppressive role in mouse liver carcinogenesis. Srsf3 KO in hepatocytes led to disrupt sex disparity in the development of DEN-induced liver cancer and resulted in high incidence of liver cancer in both male and female mice. In contrast, Srsf3 is oncogenic in the mouse mammary glands and Srsf3 KO significantly delayed the development of Erbb2 breast cancer. Srsf3 KO significantly increased the expression of transcription factors Sox4, E2f1, and Myc, calcium channel factor Trpv4, and zinc-binding Trim6 in liver cancer, but did not in Erbb2 breast cancer. Srsf3 KO enhanced the expression of glucose transmembrane transporter Mfsd4a and translation initiator Eif4a2 in DEN-induced liver cancer but reduced Mfsd4a and Eif4a2 expression in breast cancer. More importantly, Srsf3 KO led to reduced expression of hepatocyte ERα and transcription factor Foxa family genes essential for sexual dimorphism in liver cancer and their downstream targets leukemia inhibitory factor receptor Lifr and epidermal growth factor receptor Egfr, but increased expression of Myc. We further evidenced that SRSF3 binds to FOXA1 promoter and is responsible for FOXA1 promoter activity and FOXA1 expression in liver cancer cells. Together, our data highlights a new functional paradigm of SRSF3 at its physiological level in tissue context-dependent gene regulation and in facilitating hepatocyte ERα and FOXA1 expression for sex disparity in liver cancer development.
2026-05-19 | GSE331053 | GEO
Project description:Liver fibrosis model of hepatocyte-specific FOXA2 knockout mice
| PRJNA381475 | ENA
Project description:Histones were isolated from brown adipose tissue and liver from mice housed at 28, 22, or 8 C. Quantitative top- or middle-down approaches were used to quantitate histone H4 and H3.2 proteoforms. See published article for complimentary RNA-seq and RRBS datasets.
2023-06-05 | MSV000092105 | MassIVE
Project description:Analysis of RNA from primary hepatocytes from hepatocyte-specific SRSF1 knockout mice vs. WT
| PRJNA245221 | ENA
Project description:Genome-wide analysis of gene expression patterns in the liver tumors of mir-122 knockout mice
| PRJNA145827 | ENA
Project description:The aim of this study was to assess whether chronic treatment with RPV can modulate the progression of chronic liver disease, especially of non-alcoholic fatty liver disease (NAFLD), through a nutritional model in wild-type mice Mice were daily treated with RPV (p.o.) and fed with normal or high fat diet during 3 months to induce fatty liver disease
2019-12-31 | GSE120484 | GEO
Project description:Acetaminophen is a widely used antipyretic and analgesic drug, and its overdose is the leading cause of drug-induced acute liver failure. This study aimed to investigate the effect and mechanism of Lacticaseibacillus casei Shirota (LcS), an extensively used and highly studied probiotic, on acetaminophen-induced acute liver injury. C57BL/6 mice were gavaged with LcS suspension or saline once daily for 7 days before the acute liver injury was induced via intraperitoneal injection of 300 mg/kg acetaminophen. The results showed that LcS significantly decreased acetaminophen-induced liver and ileum injury, as demonstrated by reductions in the increases in aspartate aminotransferase, total bile acids, total bilirubin, indirect bilirubin and hepatic cell necrosis. Moreover, LcS alleviated the acetaminophen-induced intestinal mucosal permeability, elevation in serum IL-1α and lipopolysaccharide, and decreased levels of serum eosinophil chemokine (eotaxin) and hepatic glutathione levels. Furthermore, analysis of the gut microbiota and metabolome showed that LcS reduced the acetaminophen-enriched levels of Cyanobacteria, Oxyphotobacteria, long-chain fatty acids, cholesterol and sugars in the gut. Additionally, the transcriptome and proteomics showed that LcS mitigated the downregulation of metabolism and immune pathways as well as glutathione formation during acetaminophen-induced acute liver injury. This is the first study showing that pretreatment with LcS alleviates acetaminophen-enriched acute liver injury, and it provides a reference for the application of LcS.
2023-07-26 | PXD044099 |
Project description: Not available
| S-EPMC8784167 | biostudies-literature
Project description:Gene expression analysis of mice liver tumors isolated from β2SP+/- SMAD3+/- mice
| PRJNA286668 | ENA