MafB enhances oncogenic Notch signaling in T-ALL [Microarray]
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ABSTRACT:
PROVIDER: PRJNA414388 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:MafB enhances oncogenic Notch signaling in T-ALL
| PRJNA414384 | ENA
Project description:MafB enhances oncogenic Notch signaling in T-ALL [ChIP-Seq]
| PRJNA414387 | ENA
Project description:Notch dependent gene expression in T6E cell line Transcription profiles of Notch signaling active, inactive and recovered were compared
2017-10-17 | GSE104991 | GEO
Project description:MafB effect on H3K27ac in T6E cell line
2017-10-17 | GSE104992 | GEO
Project description: Not available
| S-EPMC5885022 | biostudies-literature
Project description:This SuperSeries is composed of the SubSeries listed below.
2017-10-17 | GSE104993 | GEO
Project description:MafA and MafB transcription factors have been shown to be key regulators of insulin and glucagon transcription. MafB is essential for alpha and beta cell differentiation, as MafB deficient mice produced fewer insulin+ and glucagon+ cells during development, with MafA expressed in remaining insulin+ cells. In contrast, beta cell development was reported to be normal in a total MafA knock out, although the animals developed beta cell dysfunction and diabetes as adults. However, we have found that MafB expression is elevated during development and retained in adult insulin+ cells after conditional removal of MafA in the pancreas. These studies will evaluate the broader significance of these insulin and glucagon regulators in alpha and beta cell development and function. Our efforts will focus on determining if the concerted actions of MafA and MafB factors are significant to beta cell formation, and we specifically plan to: Determine how alpha and beta cell differentiation is affected in MafA/MafB compound mutant mice during pancreas development. cDNA microarray studies (pancchip 6.0) with wild type, MafAKO, MafB-/-, and MafAKOMafB-/- mutant E18.5 pancreata will be performed to comprehensively identify genes controlled by MafA and MafB in developing alpha and beta cells.
2014-11-04 | E-MTAB-3070 | biostudies-arrayexpress
Project description:MafB is a member of the large Maf family of transcription factors that share similar basic region/leucine zipper DNA binding motifs and N-terminal activation domains.Although it is well known that MafB is specifically expressed in macrophages, characterization of the null mutant phenotype in these tissues has not been previously reported. To investigate suspected MafB functions macrophages, we generated mafB/green fluorescent protein (GFP) knock-in null mutant mice. MafB deficiency was found to dramatically suppress F4/80 expression in nonadherent macrophages. To investigate detail function of MafB in nonadherent macrophages, we performed microarray analysis.
2010-02-23 | GSE20419 | GEO
Project description:MafB is a member of the large Maf family of transcription factors that share similar basic region/leucine zipper DNA binding motifs and N-terminal activation domains.Although it is well known that MafB is specifically expressed in macrophages, characterization of the null mutant phenotype in these tissues has not been previously reported. To investigate suspected MafB functions macrophages, we generated mafB/green fluorescent protein (GFP) knock-in null mutant mice. MafB deficiency was found to dramatically suppress F4/80 expression in nonadherent macrophages. To investigate detail function of MafB in nonadherent macrophages, we performed microarray analysis. Macrophages were derived from day 14.5 fetal livers of mafB- /- and WT mice. Suspensions of single fetal liver cells were prepared by mechanical disruption . A total of 106 cells in suspension were centrifuged at 1,200 rpm for 5 min, and the cell pellet was resuspended in Dulbeccoâs modified Eagleâs medium supplemented with 10% fetal calf serum (heat inactivated), streptomycin and penicillin (100 units/ml), and macrophage colony-stimulating factor (M-CSF) (10 ng/ml) and then seeded either onto a nonadhesive dishes coated with hydrophilic polymers (Hydrocell; Cell Seed, Tokyo). The culture medium was not changed throughout the experiment. M-CSF (final concentration, 10 ng/ml) was added every day from day 4 onwards. One, 2, 4, and 6 days after seeding, the cells were harvested and analyzed by flow cytometry. After 6 day culture, macrophages of Mafb-/- and WT were use microarray analysis .
2010-02-27 | E-GEOD-20419 | biostudies-arrayexpress
Project description:Purpose: To investigate the impact of oncogenic Notch on the 3D genome organization of cancer cells. Methods: We generated cohesin HiChIP and 1D epigenomic data sets in two different Notch-dependent cancer cell types, triple-negative breast cancer (TNBC) and mantle cell lymphoma (MCL), in the Notch-on and -off states. Results: We report here that Notch transcription complexes control their direct target genes through two distinct regulatory modes: either through existing loops or by facilitating new long-range regulatory interactions. This combination of pre-existing and Notch-promoted loops coalesce enhancers and promoters to form highly interacting clusters, termed “3D cliques”. Notch preferentially activates enhancers and promotes looping interactions within highly connected 3D cliques that regulate key oncogenes. Conclusions: These observations suggest a general mechanism that oncogenic transcription factors can exploit to regulate the transcriptional outputs of cancer cells.
2019-02-27 | GSE116869 | GEO