Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA156111 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:This SuperSeries is composed of the following subset Series: GSE32105: Expression data from mouse livers lacking STAT3 and RelA during pneumonia GSE35513: Expression data from mouse livers lacking NF-kappaB RelA (p65) during pneumonia GSE35514: Expression data from mouse livers lacking STAT3 during pneumonia GSE35515: Expression data from mouse livers expressing or lacking Cre recombinase during pneumonia Refer to individual Series
2012-02-16 | E-GEOD-35516 | biostudies-arrayexpress
Project description:Expression data from mouse livers lacking STAT3 during pneumonia
| PRJNA156109 | ENA
Project description:Expression data from mouse livers lacking STAT3 and RelA during pneumonia
| PRJNA155501 | ENA
Project description:Expression data from mouse livers lacking NF-kappaB RelA (p65) during pneumonia
| PRJNA156107 | ENA
Project description:Tomosyn (STXBP5) is a non-canonical SNARE protein enriched in many secretory cells and implicated in regulation of exocytosis. In neurons, loss of tomosyn affects fusion of synaptic vesicles. Here, we examined the impact of the loss of tomosyn (STXBP5) and its close paralog, tomosyn-2 (STXBP5L), on the proteome of primary mouse hippocampal neurons. To do this, we used a mouse model carrying floxed alleles of Stxbp5 and Stxbp5l genes. Primary hippocampal neurons isolated from these mice were transduced with Cre-recombinase, which expression resulted in a nearly complete loss of the two genes expression. As control, we used neurons from the same culture preparation but expressing Cre-recombinase lacking DNA-binding domain (ΔCre). This dataset provides the comparison of proteome of control ('WT') and Stxbp5/5l double knockout ('DKO') neurons.
2022-12-19 | PXD038442 | Pride
Project description:Cre-recombinase expression under control of an albumin promoter in the presence of floxed alleles is a highly effective and specific way to target gene mutations in hepatocytes. However, some concerns have been raised regarding off-target and/or toxic effects of cre itself, possibly confounding the interpretation of studies employing this approach. We have now used this tool to succesfully target gene deletions in hepatocytes during pneumonia, a condition which results in significant remodeling of the hepatic transcriptome. The goal of this study was to determine what effects, if any, cre expression alone has on hepatic gene expression during bacterial pneumonia. Mutant mice expressed CRE-recombinase under control of an albumin promoter. Results from mutants were compared to wild-type mice on the same genetic background (C57BL/6). Microarray analysis was performed on liver RNA collected from both genotypes of mice in the absence and presence of pneumococcal pneumonia.
2012-02-16 | GSE35515 | GEO
Project description:A common response to physiological duress is the hepatic acute phase response, a process during which the expression of many genes is altered in the liver. Amongst these transcripts are those encoding acute phase proteins, defined as circulating proteins with significantly changed concentrations during an acute phase response. The goal of this study was to determine the influence of two transcription factors, STAT3 and NF-kappaB p65 (RelA), on hepatic gene changes including but not limited to acute phase proteins during bacterial pneumonia. Using the Cre-LoxP system, mice were generated with combined functional deletions of both STAT3 and RelA in hepatocytes. In mutant mice, Cre-recombinase was expressed under transcriptional control of an albumin promoter in the presence of homozygous floxed alleles for both STAT3 and RelA. Wild-type control mice lacked the Cre-recombinase transgene. Microarray analysis was performed on liver RNA collected from both genotypes of mice in the absence and presence of pneumococcal pneumonia. RNA from 4 separate groups of mice (3 mice per group) was analyzed: 1) Uninfected wild-type control mice; 2) Uninfected mutant mice lacking liver STAT3 and RelA; 3) Control mice infected intratracheally for 24h with 10^6 CFU of Streptococcus pneumoniae (serotype 3); and 4) Mutant mice infected intratracheally for 24h with 10^6 CFU of Streptococcus pneumoniae (serotype 3).
2012-02-16 | E-GEOD-32105 | biostudies-arrayexpress
Project description:A common response to physiological duress is the hepatic acute phase response, a process during which the expression of many genes is altered in the liver. Amongst these transcripts are those encoding acute phase proteins, defined as circulating proteins with significantly changed concentrations during an acute phase response. The goal of this study was to determine the influence of STAT3 on hepatic gene changes including but not limited to acute phase proteins during bacterial pneumonia. Using the Cre-LoxP system, mice were generated with functional deletion of STAT3 in hepatocytes. In mutant mice, Cre-recombinase was expressed under transcriptional control of an albumin promoter in the presence of homozygous floxed alleles for STAT3. Wild-type control mice lacked the Cre-recombinase transgene. Microarray analysis was performed on liver RNA collected from both genotypes of mice in the absence and presence of pneumococcal pneumonia.
2012-02-16 | GSE35514 | GEO
Project description:Cre-recombinase expression under control of an albumin promoter in the presence of floxed alleles is a highly effective and specific way to target gene mutations in hepatocytes. However, some concerns have been raised regarding off-target and/or toxic effects of cre itself, possibly confounding the interpretation of studies employing this approach. We have now used this tool to succesfully target gene deletions in hepatocytes during pneumonia, a condition which results in significant remodeling of the hepatic transcriptome. The goal of this study was to determine what effects, if any, cre expression alone has on hepatic gene expression during bacterial pneumonia. Mutant mice expressed CRE-recombinase under control of an albumin promoter. Results from mutants were compared to wild-type mice on the same genetic background (C57BL/6). Microarray analysis was performed on liver RNA collected from both genotypes of mice in the absence and presence of pneumococcal pneumonia. RNA from 2 separate groups of mice (3 mice per group) was analyzed: 1) Control mice infected intratracheally for 24h with 10^6 CFU of Streptococcus pneumoniae (serotype 3); and 2) Mutant mice infected intratracheally for 24h with 10^6 CFU of Streptococcus pneumoniae (serotype 3).
2012-02-16 | E-GEOD-35515 | biostudies-arrayexpress