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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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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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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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