Genetic STAT5B immunodysregulatory disorder
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ABSTRACT:
PROVIDER: PRJNA416162 | ENA |
REPOSITORIES: ENA
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Project description:Genetic STAT5B immunodysregulatory disorder
| PRJNA416163 | ENA
Project description:This study demonstrated that genetic background is critical to the STAT5B-mediated lymphomagenesis probably through regulation of STAT5B activation, which results in the alteration of many tumorigenic genes. Chemopreventive compounds that can reduce STAT5B phosphorylation and/or the STAT5B signaling pathway can efficiently block lymphomagenesis, demonstrating that the NOD.Stat5bTg mouse is an excellent model for testing novel chemopreventive strategies.
2012-04-10 | GSE31526 | 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
2006-07-26 | GSE5072 | GEO
Project description:This study demonstrated that genetic background is critical to the STAT5B-mediated lymphomagenesis probably through regulation of STAT5B activation, which results in the alteration of many tumorigenic genes. Chemopreventive compounds that can reduce STAT5B phosphorylation and/or the STAT5B signaling pathway can efficiently block lymphomagenesis, demonstrating that the NOD.Stat5bTg mouse is an excellent model for testing novel chemopreventive strategies. To elucidate the molecular mechanism underlying the activation of Stat5b upon lymphoma onset, we profiled gene expression in thymocytes of NOD.Stat5b mice, Gene expression was analyzed with the Illumina's MouseRef-8 v2.0 Expression beadchips
2012-04-09 | E-GEOD-31526 | biostudies-arrayexpress
Project description:Here we report both TET1-WT and catalytically dead mutant TET1 (TET1-MUT) directly interact with STAT5B in PDX2 B-ALL cells. To study the landscape of TET1 and STAT5B binding in whole genomic DNA and test if the STAT5B binding signal is affected by TET1, we conduct the ChIP-seq assay with flag antibody (TET1-WT, TET1-MUT) and STAT5B antibody (sgNS or sgTET1) respectively. The results showed that TET1 bound peaks overlap with STAT5B very well and the tag density of STAT5B on target genes decreases in TET1-impeded cells. We conclude that TET1 recruit STAT5B to the promoters of its target genes and further promote the target genes’ transcriptions.
2023-02-13 | GSE190852 | GEO
Project description:Stat5b gene is located at IDD4 type 1 diabetes susceptibility interval, and is mutated in NOD mice. This mutation has been linked to diabetes with strong association with autoimmune aetiology. We have treated MIN6 pancreatic beta cell line with Stat5b siRNA and analyzed the differential expression profile in control siRNA treated versus Stat5b siRNA treated cells in an effort to understand the role of Stat5b in diabetes.
2022-12-31 | GSE85496 | 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: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:Regulation of epithelial barrier function is dependent upon precise control of cell survival and activation of inflammatory pathways in response to the enteric flora. These experiments tested differential colon gene expression relative to these pathways in wild type and STAT5b deficient mice. Keywords: Single time point in wild type and STAT5b deficient mice. Colon RNA was isolated from adult wild type and STAT5b deficient mice.
2010-05-25 | E-GEOD-8942 | 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