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RNA-seq analysis after the treatment with DMSO or dTAG-13 in TAL1-FKBP12 Jurkat cells

ABSTRACT: RNA-seq analysis was performed in a TAL1-FKBP12 Jurkat cell line to analyze gene expression changes after dTAG-13 treatmentat at various time points (1h, 2h, 4h, 6h, 8h, 16h, 24h, 48h and 72h).

ORGANISM(S): Homo sapiens

PROVIDER: GSE225939 | GEO | 2023/11/20

REPOSITORIES: GEO

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4C-seq analysis in TAL1-FKBP12 Jurkat cells

Project description:4C analysis was performed in TAL1-FKBP12 Jurkat cells to analyze chromatin-chromatin interactions after DMSO or dTAG-13 treatment.

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H3K27ac Hi-ChIP analysis in TAL1-FKBP12 Jurkat cells

Project description:H3K27ac Hi-ChIP analysis was performed in TAL1-FKBP12 Jurkat cells to analyze active chromatin-chromatin interactions after DMSO or dTAG-13 treatment.

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ChIP-seq analysis for TAL1-FKBP12 Jurkat cells

Project description:ChIP-seq analysis was performed in a Jurkat cell line to analyze DNA bindings of TAL1-FKBP12 protein using an anti-HA antibody after DMSO or dTAG-13 treatment.

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Cut&Run analysis for transcription factors in TAL1-FKBP12 Jurkat cells

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TAL1 knock down in Jurkat cells

Project description:We used microarray profiling in Jurkat cells to uncover TAL1 dependent genes in a leukemic context. Clonal Jurkat lines expressing a Doxycycline (Dox) -inducible shRNA against TAL1 coding sequence were generated. A clone in which Dox treatment led to 80% decrease of TAL1 mRNA was chosen.

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TAL1 knock down in Jurkat cells

Project description:We used microarray profiling in Jurkat cells to uncover TAL1 dependent genes in a leukemic context.

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Mechanisms Underlying Dilated Cardiomyopathy Associated with FKBP12 Deficiency

Project description:To define the role of the immunophilin FKBP12 in cardiac function, two conditional models of FKBP12 deficiency were created using Fkbp1a floxed (FL) mice expressing Cre+ recombinase under the control of different promoters (α-myosin heavy chain, αMHC, and muscle creatine kinase, MCK) that differ in both developmental stage of expression (E9 versus E 13) and Cre+ expression levels. In adult mice FKBP12 was reduced by 96% and 86% in αMHC-Cre+- and MCK-Cre+-FKBP12 deficient mice, respectively, compared to FL mice. FL mice and mice hemizygous for the αMHC Cre+ recombinase only (to assess potential cytotoxic effects of the Cre+ recombinase) were used as controls. Of these four strains of mice, only the αMHC-Cre+-FKBP12 deficient mice developed an early-onset dilated cardiomyopathy (DCM) and displayed both increased cardiomyocyte sarcoplasmic reticulum Ca2+ leak and large elevations (assessed with RNAseq and western blots) in Ankyrin repeat domain 1 protein (ANKRD1), a negative regulator of cardiac gene expression in response to stress. These data suggest that an FKBP12 deficiency that begins during cardiac development and reduces FKBP12 below a critical level causes RyR2 mediated Ca2+ leak and ANKRD1 elevation, leading to cardiac structural remodeling and the development of DCM. This Ca2+ leak/ANKRD1 pathway may represent a common and targetable mechanism for DCM.

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H3K27 methylation changes in Jurkat cells in response to TAL1-KD

Project description:T-cell Acute Lymphoblastic Leukemia (T-ALL) is a heterogeneous group of hematological tumors composed of distinct subtypes that vary in their genetic abnormalities, gene expression signatures and prognoses. However, it remains unclear whether T-ALL subtypes differ at the functional level, and as such T-ALL treatments are uniformly applied across subtypes leading to variable responses between patients. Here we reveal the existence of a subtype-specific epigenetic vulnerability in T-ALL whereby a particular subgroup of T-ALL characterized by expression of the oncogenic transcription factor TAL1 is uniquely sensitive to variations in dosage and activity of the histone 3 lysine 27 (H3K27) demethylase UTX. Specifically, we identify UTX as a co-activator of TAL1. Furthermore, we demonstrate that UTX, previously described as a tumor suppressor in T-ALL, is in fact a potent oncogene essential for maintaining the leukemic phenotype of TAL1-positive (but not TAL1-negative) T-ALL. Exploiting this subtype-specific epigenetic vulnerability, we designed a novel therapeutic approach based on UTX inhibition through in vivo administration of an H3K27 demethylase inhibitor that is highly effective against TAL1-positive primary human leukemia. These findings provide the first opportunity to develop personalized epigenetic therapy for T-ALL patients.

2016-02-01 | GSE72298 | GEO

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