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LKB1, Salt-Inducible Kinases, and MEF2C are linked dependencies in acute myeloid leukemia

ABSTRACT: LKB1, Salt-Inducible Kinases, and MEF2C are linked dependencies in acute myeloid leukemia

PROVIDER: PRJNA431204 | ENA |

REPOSITORIES: ENA

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LKB1, Salt-Inducible Kinases, and MEF2C are linked dependencies in acute myeloid leukemia (ChIP-Seq)

Project description:LKB1, Salt-Inducible Kinases, and MEF2C are linked dependencies in acute myeloid leukemia (ChIP-Seq)

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LKB1, Salt-Inducible Kinases, and MEF2C are linked dependencies in acute myeloid leukemia (RNA-Seq)

Project description:LKB1, Salt-Inducible Kinases, and MEF2C are linked dependencies in acute myeloid leukemia (RNA-Seq)

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LKB1, Salt-Inducible Kinases, and MEF2C Are Linked Dependencies in Acute Myeloid Leukemia.

Project description: Not available

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LKB1, Salt-Inducible Kinases, and MEF2C are linked dependencies in acute myeloid leukemia

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

2018-03-12 | GSE109493 | GEO

LKB1, Salt-Inducible Kinases, and MEF2C are linked dependencies in acute myeloid leukemia (ChIP-Seq)

Project description:Genome-wide binding/occupancy profiling by high throughput sequencing

2018-03-12 | GSE109492 | GEO

LKB1, Salt-Inducible Kinases, and MEF2C are linked dependencies in acute myeloid leukemia (RNA-Seq)

Project description:Transcriptome analysis by high throughput sequencing

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Gene expression profiles of Lkb1 WT and KO hematopoietic stem cells (HSCs)

Project description:LKB1 encodes a Ser/Thr kinase and acts as an evolutionarily conserved sensor of cellular energy status in eukaryotic cells. LKB1 functions as the major upstream kinase to phosphorylate AMPK and 12 other AMPK-related kinases, which is required for their activation in many cellular contexts. Once activated, AMPK and AMPK-related kinases phosphorylate a diverse array of downstream effectors to switch on ATP-generating catabolic processes and switch off ATP-consuming anabolic processes, thus restoring energy balance during periods of energetic stress. To study the role and mechanisms of Lkb1 in the regulation of hematopoietic stem cell (HSC) biology, we performed transcriptome analysis of sorted LSK (Lin-, Sca-1+, c-Kit+) cells from Lkb1 WT and KO bone marrows at 1 day post-completing tamoxifen injection (DPI). To identify more proximal molecular effects, we chose 1 DPI due to the modest phenotypes in Lkb1 KO mice, yet documentation of efficient Lkb1 deletion in LSK cells at this very early time point. We treated Lkb1 L/L rosa26CreERT2 and Lkb1 L/L mice (C57BL/Ka-CD45.2:Thy-1.1 background) with Tamoxifen for 5 days to somatically delete Lkb1 in adult mice, and generated Lkb1 WT and KO mice. At 1 DPI, we prepared single-cell suspensions from bone marrow (from femoral and tibial bones), and stained and sorted LSK populations using FACSAria (Becton Dickinson, Mountain View, CA). The RNA was extracted from sorted LSK cells, amplified and subjected to gene profiling. The samples include 3 Lkb1 WT (Lkb1 WT 5-7) and 4 Lkb1 KO (Lkb1 KO 4-7) replicates.

2010-12-01 | E-GEOD-24765 | biostudies-arrayexpress

MEF2C phosphorylation is required for chemotherapy resistance in acute myeloid leukemia [mutant MEF2C]

Project description:In acute myeloid leukemia, chemotherapy resistance remains prevalent and poorly understood. Using functional proteomics of patient AML specimens, we identified MEF2C S222 phosphorylation as a specific marker of primary chemoresistance. We found that transgenic Mef2cS222A/S222A mice engineered to block MEF2C phosphorylation exhibited normal hematopoiesis, but were resistant to leukemogenesis induced by MLL-AF9. MEF2C phosphorylation was required for leukemia stem cell maintenance, induced by MARK kinases in cells, and blocked by selective MARK inhibitor MRT199665, which caused apoptosis of MEF2C-activated human AML cell lines and primary patient specimens, but not those lacking MEF2C. These findings identify signaling-dependent dysregulation of transcription factor control as a determinant of therapy response in AML, with immediate potential for improved diagnosis and therapy for this disease.

2018-07-23 | GSE94453 | GEO

Gene expression profiles of Lkb1 WT and KO hematopoietic stem cells (HSCs)

2010-12-01 | GSE24765 | GEO

MEF2C Protein Isoform Transition to a Repressor Variant is Linked to Development of Heart Failure

Project description:The transcription factor MEF2C has been implicated in the pathogenesis of cardiac remodeling and heart failure. The underlying mechanisms of the MEF2C detrimental effects still remain elusive. MEF2C is unique among the MEF2 family in that alternative splice acceptors in the last exon give forms that include or exclude a short domain, which has an inhibitory effect on the MEF2C activity. Objective: To identify if MEF2Cγ+ repressor variant has a role in the cardiac detrimental effects of MEF2C. Conclusions: We conclude that upregulation of MEF2Cγ+ in adult hearts causes cardiac pathogenic features through dysregulation of cell cycle and dedifferentiation of cardiomyocytes.

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