RNAseq in human TALL cells expressing shRNA control or against SIRT1
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE193023 | GEO | 2024/01/01
REPOSITORIES: GEO
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Project description:RNAseq in human TALL cells expressing shRNA control or against SIRT1
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Project description:SIRT1 is a nuclear NAD+-dependent protein deacetylase. Expression microarray analysis was used to study the effect of SIRT1 knockdown on gene expression in MCF-7 breast cancer cells. Experiment Overall Design: SIRT1 stable knockdown was achieved using two retroviral shRNA constructs. An shRNA directed against Luciferase was used to generate the Luc control cells. Three independent biological replicates with matching Luc controls were analyzed using Affymetrix U133A 2.0 microarrays. Experiment Overall Design: These 6 samples were part of a 15-sample microarray analysis (GSE12971) examining expression regulation by SIRT1, PARP-1, PARG and macroH2A. All 15 samples were included for the following data normalization steps: data sets obtained using the GCOS software were grouped based on date of experiment and adjusted for batch effect using the parametric empirical Bayes method (Combat R); all values < 0.01 were adjusted to 0.01; the data were log2 transformed, median centered for each array, and median centered for each gene.
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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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Project description:Sirtuin-1 (Sirt1), a class III histone/protein deacetylase is central to cellular metabolism, stress responses and aging, but its contributions to various host immune functions have been little investigated. To study the role of Sirt1 in T-cell functions, we undertook targeted deletions by mating mice with a floxed Sirt1 gene to mice expressing CD4-cre or Foxp3-cre recombinase, respectively. We found that Sirt1 deletion left conventional T-effector cell activation, proliferation and cytokine production largely unaltered. However, Sirt1 targeting promoted the expression and acetylation of Foxp3, a key transcription factor in T-regulatory (Treg) cells, and increased Treg suppressive functions in vitro and in vivo. Consistent with these data, mice with targeted deletions of Sirt1 in either CD4+ T-cells or Foxp3+ Treg cells exhibited prolonged survival of MHC-mismatched cardiac allografts. Allografts in Sirt1 targeted recipients showed long-term preservation of myocardial histology and infiltration by Foxp3+ Treg cells. Comparable results were seen in wild-type allograft recipients treated with Sirt1 inhibitors, such as EX-527 and splitomicin. Hence, Sirt1 may inhibit Treg functions and its targeting may have therapeutic value in autoimmunity and transplantation.
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Project description:Sirtuin-1 (Sirt1), a class III histone/protein deacetylase is central to cellular metabolism, stress responses and aging, but its contributions to various host immune functions have been little investigated. To study the role of Sirt1 in T-cell functions, we undertook targeted deletions by mating mice with a floxed Sirt1 gene to mice expressing CD4-cre or Foxp3-cre recombinase, respectively. We found that Sirt1 deletion left conventional T-effector cell activation, proliferation and cytokine production largely unaltered. However, Sirt1 targeting promoted the expression and acetylation of Foxp3, a key transcription factor in T-regulatory (Treg) cells, and increased Treg suppressive functions in vitro and in vivo. Consistent with these data, mice with targeted deletions of Sirt1 in either CD4+ T-cells or Foxp3+ Treg cells exhibited prolonged survival of MHC-mismatched cardiac allografts. Allografts in Sirt1 targeted recipients showed long-term preservation of myocardial histology and infiltration by Foxp3+ Treg cells. Comparable results were seen in wild-type allograft recipients treated with Sirt1 inhibitors, such as EX-527 and splitomicin. Hence, Sirt1 may inhibit Treg functions and its targeting may have therapeutic value in autoimmunity and transplantation. RNA from three independent samples from magnetically separated CD4+CD25+ Treg of Sirt1 knock out, compared to wild type (C57BL6) control
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