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Microarray analysis in acute myeloid leukemia (AML)-derived THP-1 cells expressing or not SAMHD1

ABSTRACT: Gene expression analysis in THP-1 cells with SAMHD1 knockout (KO) compared to THP-1 control cells expressing endogenous SAMHD1 reveals that the expression of more than 1000 genes is significantly affected by SAMHD1.

ORGANISM(S): Homo sapiens

PROVIDER: GSE113610 | GEO | 2018/06/18

REPOSITORIES: GEO

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Microarray analysis in acute myeloid leukemia (AML)-derived THP-1 cells expressing or not SAMHD1

Project description:Microarray analysis in acute myeloid leukemia (AML)-derived THP-1 cells expressing or not SAMHD1

| PRJNA453392 | ENA

SAMHD1 is recurrently mutated in T-cell prolymphocytic leukemia

Project description:We identified novel recurrent genetic lesions in T-PLL affecting genes involved in JAK/STAT signaling (PTPRC), epigenetic regulation (PRDM2), or DNA damage repair (SAMHD1, PARP10, HERC1, HERC2). Mutations of the tumor suppressor gene SAMHD1 causing amino-acid exchanges or protein truncations as well as copy number variations in SAMHD1 were seen in 20% of cases.

2018-07-23 | GSE100844 | GEO

SAMHD1 is recurrently mutated in T-cell prolymphocytic leukemia [RNA-seq]

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Gene expression analysis of murine peritoneal macrophages deficient for SAMHD1 and IFNAR

Project description:To investigate the contribution of type-1 IFN signalling to the upregulation of IFN- stimulated genes in SAMHD1-deficient cells, we performed global gene expression analysis of SAMHD1-deficient IFNAR-/- macrophages. Peritoneal macrophages from ten SAMHD1-deficient IFNAR-/- and six SAMHD1-deficient controls were FACS sorted. RNA was subjected to next generation mRNA sequencing.

2013-07-01 | E-GEOD-45358 | biostudies-arrayexpress

SAMHD1 modulates in vitro proliferation of acute myeloid leukemia-derived THP-1 cells through the PI3K-Akt-p27 axis.

Project description:Sterile alpha motif and HD domain-containing protein 1 (SAMHD1) is a mammalian dNTP hydrolase that acts as a negative regulator in the efficacy of cytarabine treatment against acute myeloid leukemia (AML). However, the role of SAMHD1 in AML development and progression remains unknown. We have reported that SAMHD1 knockout (KO) in the AML-derived THP-1 cells results in enhanced proliferation and reduced apoptosis, but the underlying mechanisms are unclear. Here we show that SAMHD1 KO in THP-1 cells increased PI3K activity and reduced expression of the tumor suppressor PTEN. Pharmacological inhibition of PI3K activity reduced cell proliferation specifically in SAMHD1 KO cells, suggesting that SAMHD1 KO-induced cell proliferation is mediated via enhanced PI3K signaling. However, PI3K inhibition did not significantly affect SAMHD1 KO-reduced apoptosis, implicating the involvement of additional mechanisms. SAMHD1 KO also led to enhanced phosphorylation of p27 at residue T157 and its mis-localization to the cytoplasm. Inhibition of PI3K activity reversed these effects, indicating that SAMHD1 KO-induced changes in p27 phosphorylation and localization is mediated via PI3K-Akt signaling. While SAMHD1 KO significantly enhanced THP-1 cell migration in vitro, SAMHD1 KO attenuated the ability of THP-1 cells to form subcutaneous tumors in xenografted immunodeficient mice. This effect correlated with significantly increased expression of tumor necrosis factor ? (TNF-?) in tumors, which may suggest that TNF-?-mediated inflammation could account for the decreased tumorigenicity in vivo. Our findings implicate that SAMHD1 can regulate AML cell proliferation via modulation of the PI3K-Akt-p27 signaling axis, and that SAMHD1 may affect tumorigenicity by downregulating inflammation.

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The ribonuclease activity of SAMHD1 is required for HIV-1 restriction

Project description:SAMHD1 restricts HIV-1 replication in dendritic and other myeloid cells. SAMHD1 has been shown to possess a dGTP-dependent dNTP triphosphatase (dNTPase) activity and is proposed to inhibit HIV-1 replication by depleting the intracellular dNTP pool. Arguing against a role for SAMHD1 dNTPase in HIV-1 restriction, the phosphorylation of SAMHD1 regulates the restriction activity toward HIV-1 without affecting its ability to decrease cellular dNTP levels. Here, we show that SAMHD1 is a phospho-regulated RNase and that the RNase function is required for HIV-1 restriction. Mutation of the SAMHD1 D137 residue in the allosteric site (SAMHD1D137N) abolishes dNTPase activity but has no effect on RNase activity. This dNTPase-defective SAMHD1D137N mutant is able to restrict HIV-1 infection to nearly the same extent as wild-type SAMHD1. SAMHD1 associates with and degrades the HIV-1 genomic RNA during the early phases of infection. SAMHD1 silencing in macrophages and CD4+ T cells from healthy donors increases HIV-1 RNA stability, thus rendering the cells permissive for HIV-1 infection. Furthermore, the phosphorylation of SAMHD1 at position T592 abolishes the RNase activity toward HIV-1 RNA, and consequently the ability of SAMHD1 to restrict HIV-1 infection, uncovering the phosphorylation of SAMHD1 T592 as a negative regulatory mechanism of RNase activity. Together, our results demonstrate that SAMHD1 is an essential RNase that prevents HIV-1 infection by directly degrading HIV-1 genomic RNA in a phosphorylation-regulated manner. The unique property of SAMHD1 that cleaves HIV-1 genomic RNA with no sequence preferences could be exploited to develop a new class of intervention for error-prone retroviruses.

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2012-12-01 | E-GEOD-37236 | biostudies-arrayexpress

Microarray Expression Profiling of Punicalagin, Myricetin and Quercetin Treated Leukemia Cell Line (THP-1)

Project description:THP-1 monocyte were differentiated to macrophage using PMA for 24 hrs, then (THP-1) macrophage were treated with DMSO, Punicalagin, Myricetin or Quercetin for 24 hrs. Transcriptional expression profiling was performed with Affymetrix GeneChips. Target preparation, hybridization, washing and staining, and probe array scanning were done to process array.

2021-06-30 | GSE160430 | GEO

Gene expression analysis of murine SAMHD1 deficient peritoneal macrophages (S1056 to S1075)

Project description:To elucidate responses of myeloid cells to SAMHD1 deficiency in the absence of exogenous viral infection, we performed global gene expression analysis of SAMHD1 deficient macrophages. Peritoneal macrophages from 10 mutants and 10 controls were FACS sorted. Isolated RNA was subjected to next generation mRNA sequencing.

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