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MafB enhances oncogenic Notch signaling in T-ALL [ChIP-Seq]

ABSTRACT: MafB effect on H3K27ac in T6E cell line

ORGANISM(S): Mus musculus

PROVIDER: GSE104992 | GEO | 2017/10/17

SECONDARY ACCESSION(S): PRJNA414387

REPOSITORIES: GEO

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MafB enhances oncogenic Notch signaling in T-ALL

Project description:MafB enhances oncogenic Notch signaling in T-ALL

| PRJNA414384 | ENA

MafB enhances oncogenic Notch signaling in T-ALL [ChIP-Seq]

Project description:MafB enhances oncogenic Notch signaling in T-ALL [ChIP-Seq]

| PRJNA414387 | ENA

MafB enhances oncogenic Notch signaling in T-ALL [Microarray]

Project description:MafB enhances oncogenic Notch signaling in T-ALL [Microarray]

| PRJNA414388 | ENA

MafB enhances oncogenic Notch signaling in T-ALL [Microarray]

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

MAFB enhances oncogenic Notch signaling in T cell acute lymphoblastic leukemia.

Project description: Not available

| S-EPMC5885022 | biostudies-literature

MafB enhances oncogenic Notch signaling in T-ALL

Project description:This SuperSeries is composed of the SubSeries listed below.

2017-10-17 | GSE104993 | GEO

MAFB ChIPseq in Human EndoCBH2 cells

Project description:The intent of this experiment was to determine MAFB binding sites in human pancreatic beta cells. This is particularly relevant as MAFB is not expressed in mature rodent beta cells; thus, it may perform unique functions in human. Sequencing was performed following IP with an anti-MAFB antibody using chromatin isolated from the human pancreatic beta cell line, EndoCBH2 cells. Cells were proliferating and untreated when collected.

2020-03-17 | E-MTAB-8612 | biostudies-arrayexpress

Gene expression profiling of MafA, MafB, and MafA/MafB Mutants in E18.5 pancreas

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

Non adherent macrophage of mafb null and WT

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

Transcriptome profile of MafB-cKO of podocyte

Project description:The transcription factor MafB is essential for differentiation and foot process formation of podocytes. In order to identify the downstream targets of MafB, we analyzed the Mafb-deficient podocyte by RNA-seq. We found slit diaphragm-related protein (Nphs1, Magi2), Rho GTPase-activating protein (Arhgap24, Iqgap2) and podocyte-specific transcription factor (Tcf21) were significantly reduced in MafB cKO glomeruli. This indicates that one of these factors might be directly regulated by MafB to maintain its function in podocyte maintenance.

2021-08-03 | GSE96044 | GEO

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