Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA407419 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR6040850_1.fastq.gz | Fastqsanger.gz | |||
| SRR6040850_2.fastq.gz | Fastqsanger.gz | |||
| SRR6040851_1.fastq.gz | Fastqsanger.gz | |||
| SRR6040851_2.fastq.gz | Fastqsanger.gz | |||
| SRR6040852_1.fastq.gz | Fastqsanger.gz |
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Project description:rRNA-depleted RNA isolated from livers of control male and female mice and from male mice with hepatocyte-specific STAT5ab-KO was analyzed by RNA-seq. This study revealed a substantial, albeit incomplete loss of liver sex bias in hepatocyte-specific STAT5a/STAT5b (collectively, STAT5)-deficient mouse liver. Notably, in male liver, many male-biased genes were down regulated in direct association with the loss of STAT5 binding; many female-biased genes, which show low STAT5 binding, were de-repressed, indicating an indirect mechanism for repression by STAT5.
2020-12-01 | GSE103885 | GEO
Project description:A series of dual-channel gene expression profiles obtained using Agilent Mouse TOE 75k microarrays was used to examine the sex-dependent and STAT5a-dependent differences in gene expression in adult mouse liver. This series is comprised of 3 randomly chosen independent male and female wildtype mouse liver cDNA samples and 3 randomly chosen independent male and female STAT5a-deficient mouse liver cDNA samples, totalling 12 samples. The samples were paired randomly to generate 4 comparisons of M-WT:F-WT, M-WT:M-KO, F-KO:F-WT, F-KO:M-KO. Comparison of the set of sex-dependent genes with the set of genes responsive to the loss of STAT5a in females shows a small group of the sex-specific genes were also regulated by STAT5a in females. These results indicate a role for STAT5a in female gene expression to a lesser degree than that shown for STAT5b in males. Keywords: genetic knockout and sex response
2007-07-30 | GSE7169 | GEO
Project description:A series of dual-channel gene expression profiles obtained using Rosetta/Merck Mouse TOE 75k microarrays was used to examine the sex-dependent and STAT5b-dependent differences in gene expression in adult mouse liver. This series is comprised of 4 pools of 3 randomly chosen independent wildtype male and female mouse liver cDNA samples and 4 pools of 3 randomly chosen independent STAT5b-deficient male and female mouse liver cDNA samples, totaling 16 pools. The pools were paired randomly to generate 4 comparisons of M-WT:F-WT, M-WT:M-KO, F-KO:F-WT, and F-KO:M-KO. Comparison of the set of sex-dependent genes with the set of genes responsive to the loss of STAT5b in males shows that 75% of the sex-specific genes were also regulated by STAT5b in males. Only 20% of the sex-specific genes retained sex-specificity in the absence of STAT5b, indicating a large role for STAT5b in sex-specific liver gene expression. Keywords: genetic knockout and sex response
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Project description:RRBS (reduced representation bisulfite sequencing) analysis of hepatocyte-specific STAT5a/STAT5b Knockout (STAT5ab-KO) mouse liver to identify differentially methylated regions (DMRs)
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Project description:RNA-Seq of immortalized Stat5a-/-, Stat5b-/-, and wildtype BCR/ABLp185+ cell lines was used to identify STAT5A and STAT5B specific target genes.
2019-10-01 | GSE121246 | GEO
Project description:Two highly conserved transcription factors STAT5A and STAT5B play an identical role in the intracellular signaling pathway upon cytokine stimulation, while gene deletion experiments have revealed separable and overlapping functions of STAT5. This questions whether the phenotypic differences in the organ development observed in the individual knockout mice result from isoform-specific functions or quantitative differences in the expression levels of each STAT5 isoform among tissues. To elucidate the redundancy and isoform-specificity of STAT5 for development at molecular levels, mice carrying only a single allele of either Stat5a or Stat5b were generated. Both of these mice overcame the lethal anemia observed in Stat5ab-null mice, indicating that development of erythroid cell lineage was totally dependent on the dosage of STAT5. The blocked progression of B cell lineage at the pre-pro B cell stage in Stat5ab-/- mice was rescued in the presence of a single allele of either Stat5a or Stat5b, while the number of total B220+ cells in bone marrow was smaller in Stat5abnull/Stat5b- mice than Stat5abnull/Stat5a- mice. The paucity of alveolar progenitor cells in the Stat5ab-null mammary epithelium was rescued by a single allele of either Stat5a but not Stat5b, suggesting cell-type dependent isoform-specific function. Genome-wide gene expression analyses revealed that different steps of cell lineage progression require different gene sets which expression requires the different isoform of STAT5 in a dose-dependent manner in the mammary epithelium. Taken together, this study demonstrates that dose-dependent isoform specificity of STAT5A and STAT5B controls progression and differentiation of each cell lineage. Six days after observation of a plug, mammary tissues from three of each Stat5a-/- mice, Stat5ab+/null mice, Stat5abnull/Stat5b- and Stat5abnull/Stat5a- mice were collected, frozen in liquid nitrogen, and stored at -70 °C
2012-04-30 | E-GEOD-29045 | biostudies-arrayexpress
Project description:A series of dual-channel gene expression profiles obtained using Rosetta/Merck Mouse TOE 75k microarrays was used to examine the sex-dependent and STAT5b-dependent differences in gene expression in adult mouse liver. This series is comprised of 4 pools of 3 randomly chosen independent wildtype male and female mouse liver cDNA samples and 4 pools of 3 randomly chosen independent STAT5b-deficient male and female mouse liver cDNA samples, totaling 16 pools. The pools were paired randomly to generate 4 comparisons of M-WT:F-WT, M-WT:M-KO, F-KO:F-WT, and F-KO:M-KO. Comparison of the set of sex-dependent genes with the set of genes responsive to the loss of STAT5b in males shows that 75% of the sex-specific genes were also regulated by STAT5b in males. Only 20% of the sex-specific genes retained sex-specificity in the absence of STAT5b, indicating a large role for STAT5b in sex-specific liver gene expression. A pool of cDNA from 3 mice is Cy3-labeled and compared to another pool of cDNA from 3 mice that is Cy5-labeled. The pools are then dye-swapped and compared again. The two pairs of data are averaged together, the averages are normalized across the fluorescent reverse pairings, and the log2 value is reported for each average as well as the anti-log. This is replicated 3 times with independent pools of cDNA for each pair of conditions being compared. There are a total of 4 pairs of conditions compared for a grand total of 12 samples.
2010-07-01 | E-GEOD-5072 | biostudies-arrayexpress
Project description:Stat5a and Stat5b proteins are highly homologous with greater than 90% amino acid identity and share binding to the palindromic Stat5 consensus sequence, TTCNNNGAA, but individual roles of each transcription factor in breast cancer have not been thoroughly evaluated. To determine the degree of similarity between transcripts modulated by Stat5a and Stat5b proteins in human breast cancer, we utilized genome-wide transcript profiling to identify genes regulated specifically by Stat5a or Stat5b in response to prolactin.
2012-08-29 | GSE37781 | GEO
Project description:Stat5a and Stat5b proteins are highly homologous with greater than 90% amino acid identity and share binding to the palindromic Stat5 consensus sequence, TTCNNNGAA, but individual roles of each transcription factor in breast cancer have not been thoroughly evaluated. To determine the degree of similarity between transcripts modulated by Stat5a and Stat5b proteins in human breast cancer, we utilized genome-wide transcript profiling to identify genes regulated specifically by Stat5a or Stat5b in response to prolactin. Stat5a or Stat5b was transiently overexpressed using adenoviral gene delivery in MCF7 breast cancer cells followed 16 hr serum starvation and a brief 4 hr exposure to 10nM human prolactin to identify immediate-early transcripts modulated by each transcription factor. Basal activation of Stat5a or Stat5b was not present in cells not stimulated with prolactin. mRNA from each condition was harvested and validated using the Agilent bioanalyzer. cDNA was generated and genome-wide transcript profiling was performed in triplicate using the Affymetrix HuGene 1.0 ST array.
2012-08-29 | E-GEOD-37781 | biostudies-arrayexpress
Project description:The impact of STAT5 on liver DNA methylation was assessed by performing RRBS analysis on male and female mouse liver with a hepatocyte-specific loss of STAT5a and STAT5b. Extensive changes in CpG-methylation were seen in STAT5-deficient liver, where sex differences were abolished at 88% of ~1,500 sex-differentially methylated regions, largely due to increased DNA methylation upon STAT5 loss. STAT5-dependent CpG-hypomethylation was rarely found at proximal promoters of STAT5-dependent genes. Rather, STAT5 primarily regulated the methylation of distal enhancers, where STAT5 deficiency induced widespread hypermethylation at genomic regions enriched for accessible chromatin, enhancer histone marks (H3K4me1, H3K27ac), STAT5 binding, and DNA motifs for STAT5 and other transcription factors implicated in liver sex differences. Thus, the sex-dependent binding of STAT5 to liver chromatin is closely linked to the sex-dependent demethylation of distal regulatory elements linked to STAT5-dependent genes important for liver sex bias.
2020-12-01 | GSE103886 | GEO