RNA-seq analysis of 12 cases with BCL11B rearrangement
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ABSTRACT:
PROVIDER: PRJNA681241 | ENA |
REPOSITORIES: ENA
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Project description:This study identified a cytogenetic-molecular entity, we named BCL11B-R, that showed a typical constellation of genomic features, namely BCL11B activation via chromosome translocations at 14q32, a distinct transcriptome profile, and FLT3 mutations.
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Project description:This study identified a cytogenetic-molecular entity, we named BCL11B-R, that showed a typical constellation of genomic features, namely BCL11B activation via chromosome translocations at 14q32, a distinct transcriptome profile, and FLT3 mutations.
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Project description:Affymetrix SNP array data for acute leukemias with a 14q32/BCL11B rearrangement
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Project description:B-cell leukemia/lymphoma 11B (Bcl11b) is a transcription factor showing predominant expression in the striatum. To date, there are no known gene targets of Bcl11b in the nervous system. Here, we define targets for Bcl11b in striatal cells by performing genome-wide expression profiling. Transcriptome-wide analysis revealed that 694 genes were significantly altered in striatal cells over-expressing Bcl11b, including genes showing striatal-enriched expression similar to Bcl11b. Functional analysis on the gene target list identified significant association of Bcl11b to brain-derived neurotrophic factor/neurotrophin signaling. These data implicate Bcl11b as a novel regulator of the BDNF signaling pathway, which is disrupted in many neurological disorders. n=4 wt STHdh striatal cells and n=4 Bcl11b-transfected STHdh striatal cells
2011-08-01 | E-GEOD-31096 | biostudies-arrayexpress
Project description:Epigenetic landscapes can provide insight into regulation of gene expression and cellular diversity. Here, we examined the transcriptional and epigenetic profiles of seven human blood NK cell populations, including adaptive NK cells. The BCL11B gene, encoding a transcription factor (TF) essential for T cell development and function, was the most extensively regulated, with expression increasing throughout NK cell differentiation. Several Bcl11b-regulated genes associated with T cell-signaling were specifically expressed in adaptive NK cell subsets. Regulatory networks revealed reciprocal regulation at distinct stages of NK cell differentiation, with Bcl11b repressing RUNX2 and ZBTB16 in canonical and adaptive NK cells, respectively. A critical role for Bcl11b in driving NK cell differentiation was corroborated in BCL11B mutated patients and by ectopic Bcl11b expression. Moreover, Bcl11b was required for adaptive NK cell responses in a murine CMV model, supporting expansion of these cells. Together, we define the TF regulatory circuitry of human NK cells and uncover a critical role for Bcl11b in promoting NK cell differentiation and function.
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Project description:The differentiation of preadipocytes into adipocytes is controlled by several transcription factors, including peroxisome proliferator-activated receptor γ (PPARγ) and CCAAT/enhancer-binding protein α (C/EBPα), which are known as master regulators of adipogenesis. BCL11B is a zinc finger-type transcription factor that regulates the development of the skin and central nervous and immune systems. Here, we found that BCL11B was expressed in the white adipose tissue (WAT), particularly the subcutaneous WAT and that BCL11Bâ/â mice had a reduced amount of subcutaneous WAT. During adipogenesis, BCL11B expression transiently increased in 3T3-L1 preadipocytes and mouse embryonic fibroblasts (MEFs). The ability for adipogenesis was reduced in BCL11B knockdown 3T3-L1 cells and BCL11Bâ/â MEFs, whereas the ability for osteoblastogenesis was unaffected in BCL11Bâ/â MEFs. Luciferase reporter gene assays revealed that BCL11B stimulated C/EBPβ activity. Furthermore, the expression of downstream genes of the Wnt/β-catenin signaling pathway was not suppressed in BCL11Bâ/â MEFs during adipogenesis. Thus, this study identifies BCL11B as a novel regulator of adipogenesis, which works, at least in part, by stimulating C/EBPβ activity and suppressing the Wnt/β-catenin signaling pathway. MEFs were derived from embryonic day 12.5 BCL11B+/+ and BCL11Bâ/â C57BL6 mice embryos. After 2 times passage, MEFs were differentiated using the adipocyte differentiation medium and 10 μM pioglitazone. After 12 h of adipocyte differentiation, gene expression profiles were analyzed by DNA microarray.
2016-09-05 | E-GEOD-83980 | biostudies-arrayexpress
Project description:Transcriptional profiling of mouse iNKT cells comparing wild type and Bcl11b deficient cell. The mice were treated with 4 μg of α-galactosylceramide. Goal was to determine the effects of transcription factor Bcl11b removal in iNKT cells. Intraperitoneal treatment with 4 μg of α-Galactosylceramide. Two pair of wild type (BCL11b F/F Vα14 transgenic) and Knock out (BCL11b F/F PLZF-Cre Vα14 transgenic)) mice were treated. Lymphocytes from spleen and liver were enriched and stain with PBS-57 Loaded CD1d tetramer. Pure iNKT cells were collected through cell sorter.
2016-08-10 | E-GEOD-73679 | biostudies-arrayexpress
Project description:Review on the role of Bcl11b in thymus and periphery and impact on diseases RNA was extracted from DP thymocytes of bcl11bf/fCd4cre/tcra-/- and tcra-/- mice. Tcra-/- mice only have preselected DP thymocytes. Such mice were used to determine the role of Bcl11b before selection, considering the defective positive selection in bcl11bf/fcd4cre mice. RNA was isolated and submitted for library generation and microarray analysis to determine expression profile of bcl11b-/- preselected DP thymocytes.
2014-04-12 | E-GEOD-56714 | biostudies-arrayexpress