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we have shown that low-level SAMHD1 expression in AML blasts at diagnosis identifies a sizeable patient subset with favorable EFS and OS upon treatment with HDAC-containing consolidation regimens.
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This finding identifies the Endogenous reverse transcription step as an additional step of HIV-1 replication cycle that SAMHD1 restricts in nondividing myeloid target cells.
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cyclin E2 participates in regulating viral replication through the CDK2/SAMHD1 phosphorylation pathway in an HBV infection system.
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the state of type I IFN induction and response to, in SAMHD1 knockout (KO) human monocytic cells, was examined.
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findings suggest that accessory protein-mediated proteosomal degradation of SAMHD1 did not exist among the ancestral non-primate lentiviruses and was uniquely gained by some primate lentiviruses after their transmission to primate species.
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SAMHD1 activation is the predominant mechanism of HIV-1 restriction induced by type I, type II, and type III IFN signaling in macrophages.
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Data show that SAM Domain and HD Domain-Containing Protein 1 (SAMHD1) is specifically targeted by protein phosphatase 2 regulatory subunit Balpha protein (PP2A-B55alpha) holoenzymes during mitotic exit.
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SAMHD1 activity can significantly enhance or decrease the anti-HIV-1 efficacy of nucleotide analogue reverse transcription inhibitors presumably as a result of modulating dNTP pools that compete for recruitment by viral polymerases.
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SAMHD1 is not localized in dot-like structures under DNA double-strand break induction in HeLa cells.
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study considerably extends the picture of pathways involved in molecular pathogenesis of T-PLL and identifies the tumor suppressor gene SAMHD1 with ~20% of T-PLL affected by destructive lesions likely as major player in T-PLL pathogenesis.
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Compared with control cells, infection of SAMHD1-silenced human monocytic cells or primary macrophages with Sendai virus or HIV-1, or treatment with inflammatory stimuli, induces significantly higher levels of NF-kappaB activation and IFN-I induction. SAMHD1 down-regulates innate immune responses to viral infections and inflammatory stimuli.
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SAMHD1 is thus an important player in the replication stress response, which prevents chronic inflammation by limiting the release of single-stranded DNA from stalled replication forks
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Low SAMHD1 expression is associated with HIV-1 infection.
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Multiple domains of SAMHD1(e.g., N-terminus, nuclear localization signal, linker, HD domain, and C-terminus)are essential for Vpx-induced degradation.[review]
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findings indicate a novel role for SAMHD1 in regulating HIV-1 latency, which enhances our understanding of the mechanisms regulating proviral gene expression in CD4(+) T cells.
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results demonstrate that the interaction of CD81 with SAMHD1 controls the metabolic rate of HIV-1 replication by tuning the availability of building blocks for reverse transcription, namely dNTPs
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Immune activation during HIV-1 infection influences SAMHD1 expression and degradation.
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Studies of the phosphomimetic and tetramerization-defective mutants of SAMHD1 reveal poor correlation between tetramerization propensity and dNTPase activity observed in vitro and the ability of the proteins to deplete cellular dNTPs and to restrict retroviral restriction. These results suggest that enzymatic activity of SAMHD1 may be subject to additional cellular regulatory mechanisms that have not yet been elucidated.
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Upregulation of endogenous SAMHD1 expression is attributed to the phosphorylation and nuclear translocation of IRF3.
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Findings define a dNTPase-independent function for SAMHD1 in HR-mediated DSB repair by facilitating CtIP accrual to promote DNA end resection, providing insight into how SAMHD1 promotes genome integrity.
