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RNA-seq data from wildtype, STAT5A-knockout and STAT5B-knockout BCR/ABLp185+ transformed mouse bone marrow cell lines

ABSTRACT: RNA-Seq of immortalized Stat5a-/-, Stat5b-/-, and wildtype BCR/ABLp185+ cell lines was used to identify STAT5A and STAT5B specific target genes.

ORGANISM(S): Mus musculus

PROVIDER: GSE121246 | GEO | 2019/10/01

REPOSITORIES: GEO

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RNA-seq data from wildtype, STAT5A-knockout and STAT5B-knockout BCR/ABLp185+ transformed mouse bone marrow cell lines

Project description:RNA-seq data from wildtype, STAT5A-knockout and STAT5B-knockout BCR/ABLp185+ transformed mouse bone marrow cell lines

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Prolactin-inducible Stat5a-mediated and Stat5b-mediated gene profiles

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

Prolactin-inducible Stat5a-mediated and Stat5b-mediated gene profiles

2012-08-29 | GSE37781 | GEO

Gene expression profiling of mouse liver with hepatocyte-specific knockout of STAT5a/STAT5b genes (STAT5ab-KO)

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

BCR-ABL affects STAT5A and STAT5B differentially.

Project description: Not available

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GM-CSF-activated STAT5A but not STAT5B regulates macrophage functions and inflammation in atherosclerosis

Project description:Inhibition of STAT5 was recently reported to reduce mouse atherosclerosis. However, the regulatory role of STAT5 isoforms STAT5A and STAT5B in human disease and more specifically in macrophages remains unknown. Here, we demonstrate reciprocal expression regulation of STAT5A and B in human atherosclerotic lesions. The former was highly upregulated in ruptured over stable plaque and correlated with macrophage presence, a finding that was corroborated by the high chromosomal accessibility of STAT5A but not B gene in plaque macrophages. Phosphorylated STAT5 correlated with macrophages confirming its activation status. As macrophage STAT5 is activated by GM-CSF, we studied the effects of its silencing in GM-CSF differentiated human macrophages. STAT5A knockdown blunted NF-kB pathway, phagocytosis, cholesterol metabolism, and apoptosis terms. These changes at transcriptional level could be confirmed at functional level, with significant increases in apoptosis and phagocytosis and decreases in lipid uptake and IL-6, IL8, and TNFa cytokine secretion after STAT5A knockdown. Finally, inhibition of general and isoform A specific STAT5 inhibitor significantly reduced the secretion of TNFa, IL-8 and IL-10 in ex vivo tissue slices of advanced human atherosclerotic plaques. In summary, we identify STAT5A as important determinant of macrophage functions and inflammation in the context of atherosclerosis and show its promise as therapeutic target for human atherosclerotic plaque inflammation.

2023-10-02 | GSE217893 | GEO

A STAT5B-CD9 axis determines self-renewal in hematopoietic and leukemic stem cells

Project description:The transcription factors STAT5A and STAT5B are critical in hematopoiesis and leukemia. They are widely believed to have redundant functions but we describe a unique role for STAT5B in driving the self-renewal of hematopoietic and leukemic stem cells (HSCs/LSCs). We find STAT5B to be specifically activated in HSCs and LSCs, where it induces many genes associated with quiescence and self-renewal, including the surface marker CD9. Levels of CD9 represent a prognostic marker for patients with STAT5-driven leukemia and our findings suggest that anti-CD9 antibodies may be useful in their treatment to target and eliminate LSCs. We show that it is vital to consider STAT5A and STAT5B as distinct entities in normal and malignant hematopoiesis.

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RRBS (reduced representation bisulfite sequencing) analysis of hepatocyte-specific STAT5a/STAT5b Knockout (STAT5ab-KO) mouse liver to identify differentially methylated regions (DMRs)

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

Sex-dependent and STAT5a-dependent Liver Gene Expression

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

Twins with different personalities: STAT5B-but not STAT5A-has a key role in BCR/ABL-induced leukemia.

Project description: Not available

| S-EPMC6755975 | biostudies-literature