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SIRT1 Activation Disrupts Maintenance of Myelodysplastic Syndrome Stem and Progenitor Cells by Restoring TET2 Function [hMeDIP-Seq]

ABSTRACT: SIRT1 Activation Disrupts Maintenance of Myelodysplastic Syndrome Stem and Progenitor Cells by Restoring TET2 Function [hMeDIP-Seq]

PROVIDER: PRJNA481884 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7540950.fastq.gz	Fastqsanger.gz
	SRR7540951.fastq.gz	Fastqsanger.gz
	SRR7540952.fastq.gz	Fastqsanger.gz
	SRR7540953.fastq.gz	Fastqsanger.gz
	SRR7540948.fastq.gz	Fastqsanger.gz

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SIRT1 Activation Disrupts Maintenance of Myelodysplastic Syndrome Stem and Progenitor Cells by Restoring TET2 Function [hMeDIP-Seq]

2018-08-13 | GSE117363 | GEO

SIRT1 Activation Disrupts Maintenance of Myelodysplastic Syndrome Stem and Progenitor Cells by Restoring TET2 Function [microarray expression profiling]

Project description:Improved understanding of mechanisms regulating myelodysplastic syndrome (MDS) hematopoietic stem/progenitor cell (HSPC) growth and self-renewal is critical for developing MDS therapy. We revealed a novel regulatory axis that SIRT1-deficiency induced TET2 hyperacetylation promotes MDS HSPC functions, and provide an approach to target MDS HSPCs by activating SIRT1 deacetylase. Four Groups: Group1: MDS-L cells transduced with lentiviral vector targeting non-silence squence (control shRNA for SIRT1); Group2: MDS-L cells transduced with lentiviral vector containing interference squence targeting SIRT1 (SIRT shRNA); Group 3: MDS-L cells transduced with lentiviral vector targeting non-silence squence (control shRNA for TET2); Group 4: MDS-L cells transduced with lentiviral vector containing interference squence targeting TET2 (TET2 shRNA).

2018-08-13 | GSE117272 | GEO

SIRT1 Activation Disrupts Maintenance of Myelodysplastic Syndrome Stem and Progenitor Cells by Restoring TET2 Function

Project description:SIRT1 Activation Disrupts Maintenance of Myelodysplastic Syndrome Stem and Progenitor Cells by Restoring TET2 Function

| PRJNA481954 | ENA

SIRT1 Activation Disrupts Maintenance of Myelodysplastic Syndrome Stem and Progenitor Cells by Restoring TET2 Function [microarray expression profiling]

Project description:SIRT1 Activation Disrupts Maintenance of Myelodysplastic Syndrome Stem and Progenitor Cells by Restoring TET2 Function [microarray expression profiling]

| PRJNA481584 | ENA

SIRT1 Activation Disrupts Maintenance of Myelodysplastic Syndrome Stem and Progenitor Cells by Restoring TET2 Function.

Project description:Myelodysplastic syndrome (MDS), a largely incurable hematological malignancy, is derived from aberrant clonal hematopoietic stem/progenitor cells (HSPCs) that persist after conventional therapies. Defining the mechanisms underlying MDS HSPC maintenance is critical for developing MDS therapy. The deacetylase SIRT1 regulates stem cell proliferation, survival, and self-renewal by deacetylating downstream proteins. Here we show that SIRT1 protein levels were downregulated in MDS HSPCs. Genetic or pharmacological activation of SIRT1 inhibited MDS HSPC functions, whereas SIRT1 deficiency enhanced MDS HSPC self-renewal. Mechanistically, the inhibitory effects of SIRT1 were dependent on TET2, a safeguard against HSPC transformation. SIRT1 deacetylated TET2 at conserved lysine residues in its catalytic domain, enhancing TET2 activity. Our genome-wide analysis identified cancer-related genes regulated by the SIRT1/TET2 axis. SIRT1 activation also inhibited functions of MDS HSPCs from patients with TET2 heterozygous mutations. Altogether, our results indicate that restoring TET2 function through SIRT1 activation represents a promising means to target MDS HSPCs.

| S-EPMC6143172 | biostudies-literature

SIRT1 Activation Disrupts Maintenance of Myelodysplastic Syndrome Stem and Progenitor Cells by Restoring TET2 Function

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

2018-08-13 | GSE117383 | GEO

hMeDIP-Seq of Tet2 overexpressing hippocampal neurons

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hMeDIP-Seq of Tet2 knockout hippocampal neurons

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LARP7 ameliorates cellular senescence and aging-related atherosclerosis by allosterically enhancing SIRT1 deacetylase activity

Project description:Cell senescence is a cell state characterized with permanent cell cycle arrest and elevated proinflammatory secretome and associated with pleiotropic essential physiopathological processes. The persistent DNA damage response (DDR) is the major stress leading to senescence, however the molecular mechanism underling remains elusive. Here, we identified the La Ribonucleoprotein 7 (LARP7), a 7SK RNA binding protein, as a novel SIRT1 deacetylase activator. It directly interacted with SIRT1 allosteric regulatory domain and enhanced its deacetylase activity. DDR-mediated ATM activation trigged the extracellular shuttling and downregulation of LARP7 that dampened the SIRT1 deacetylase activity and enhanced p53 and NFB (p65) transcriptional activity by augmenting their acetylation. As a consequence, activated p53 and NFB arrested cell growth and promoted SASP genes expression, and thereby accelerated the cellular senescence. Inducible deletion of LARP7 in wildtype mouse led to senescent cell accumulation and premature ageing. Furthermore, we identified that ATM-LARP7-SIRT1-p53/NFB senescent axis was active in the aortic senescence and atherogenesis. Genetic depletion of LARP7 aggravated the atherogenesis but conversely, inhibited ATM activation or restoring LARP7 expression with genetic manipulation alleviated the vascular aging and atherogenesis. Together, this study identifies LARP7 as a novel SIRT1 cellular activator and it’s-mediated ATM-LARP7-SIRT1-p53/NFB axis is attributed to DDR-mediated cellular senescence and aging-related pathologies.

2021-10-30 | GSE160279 | GEO

Convergence of SIRT1 and ATR signaling to modulate replication origin dormancy

Project description:SIRT1 chromatin interactome analysis was performed to identify SIRT1 molecular targets involved in replication initiation from cells containing either WT or H363Y SIRT1. Co-IP-MS of pT530 SIRT1 from chromatin extracts was performed. Files are: 1422 WT SIRT1 untreated U2OS; 1423 WT SIRT1 H2O2 treated, U2OS; 1424 H363Y SIRT1 untreated U2OS; 1425 H363Y SIRT1 H2O2 U2OS; 1426 KO SIRT1 untreated U2OS; 1427 KO SIRT1 H2O2 U2OS; 1428 WT SIRT1 untreated HEK; 1429 WT SIRT1 H2O2 HEK; 1430 WT SIRT1 untreated HCT116; 1431 WT SIRT1 H2O2 HCT116; 1432 WT SIRT1 untreated K562; 1433 WT SIRT1 H2O2 K562. Each sample has 9 fractions.

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