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• W2116984961 abstract "SAMHD1 is a host restriction factor that limits retroviral replication at the reverse transcription step, and it is counteracted by HIV-2 Vpx, which targets SAMHD1 for degradation by the proteasome. The mechanism of SAMHD1 virus restriction is controversial; both dNTPase and RNase functions have been proposed as essential for its antiviral activity. However, the exonuclease activity cannot be associated with the SAMHD1 active site. SAMHD1 restriction is deactivated by phosphorylation mediated by cyclin-dependent kinases and is tightly linked to cell-cycle entry and progression. Recent studies have established an association between SAMHD1 restriction, innate sensing of DNA, and protective immune responses. SAMHD1 links virus replication, innate immune responses, and cell-cycle progression, determining disease outcomes of viral infections, autoimmune diseases, and cancer. SAMHD1 is a triphosphohydrolase enzyme that controls the intracellular level of deoxyribonucleoside triphosphates (dNTPs) and plays a role in innate immune sensing and autoimmune disease. SAMHD1 has also been identified as an intrinsic virus restriction factor, inactivated through degradation by HIV-2 Vpx or through a post-transcriptional regulatory mechanism. Phosphorylation of SAMHD1 by cyclin-dependent kinases has been strongly associated with inactivation of the virus restriction mechanism, providing an association between virus replication and cell proliferation. Tight regulation of cell proliferation suggests that viruses, particularly HIV-1 replication, latency, and reactivation, may be similarly controlled by multiple checkpoint mechanisms that, in turn, regulate dNTP levels. In this review, we discuss how SAMHD1 is a viral restriction factor, the mechanism associated with viral restriction, the pathway leading to its inactivation in proliferating cells, and how strategies aimed at controlling virus restriction could lead to a functional cure for HIV. SAMHD1 is a triphosphohydrolase enzyme that controls the intracellular level of deoxyribonucleoside triphosphates (dNTPs) and plays a role in innate immune sensing and autoimmune disease. SAMHD1 has also been identified as an intrinsic virus restriction factor, inactivated through degradation by HIV-2 Vpx or through a post-transcriptional regulatory mechanism. Phosphorylation of SAMHD1 by cyclin-dependent kinases has been strongly associated with inactivation of the virus restriction mechanism, providing an association between virus replication and cell proliferation. Tight regulation of cell proliferation suggests that viruses, particularly HIV-1 replication, latency, and reactivation, may be similarly controlled by multiple checkpoint mechanisms that, in turn, regulate dNTP levels. In this review, we discuss how SAMHD1 is a viral restriction factor, the mechanism associated with viral restriction, the pathway leading to its inactivation in proliferating cells, and how strategies aimed at controlling virus restriction could lead to a functional cure for HIV." @default.
• W2116984961 created "2016-06-24" @default.
• W2116984961 creator A5048104582 @default.
• W2116984961 creator A5071096601 @default.
• W2116984961 date "2015-11-01" @default.
• W2116984961 modified "2023-10-18" @default.
• W2116984961 title "SAMHD1: At the Crossroads of Cell Proliferation, Immune Responses, and Virus Restriction" @default.
• W2116984961 cites W1542158376 @default.
• W2116984961 cites W1570518269 @default.
• W2116984961 cites W1570519707 @default.
• W2116984961 cites W1918328834 @default.
• W2116984961 cites W1964567249 @default.
• W2116984961 cites W1966129768 @default.
• W2116984961 cites W1968782528 @default.
• W2116984961 cites W1973629508 @default.
• W2116984961 cites W1973793109 @default.
• W2116984961 cites W1975031262 @default.
• W2116984961 cites W1978010534 @default.
• W2116984961 cites W1980705501 @default.
• W2116984961 cites W1980923315 @default.
• W2116984961 cites W1981915622 @default.
• W2116984961 cites W1988622942 @default.
• W2116984961 cites W1992007798 @default.
• W2116984961 cites W2000367861 @default.
• W2116984961 cites W2000918346 @default.
• W2116984961 cites W2003789674 @default.
• W2116984961 cites W2007352147 @default.
• W2116984961 cites W2008892095 @default.
• W2116984961 cites W2014616178 @default.
• W2116984961 cites W2017760549 @default.
• W2116984961 cites W2019039109 @default.
• W2116984961 cites W2019388385 @default.
• W2116984961 cites W2020148863 @default.
• W2116984961 cites W2020265617 @default.
• W2116984961 cites W2021736427 @default.
• W2116984961 cites W2025962058 @default.
• W2116984961 cites W2026185351 @default.
• W2116984961 cites W2026218505 @default.
• W2116984961 cites W2027853473 @default.
• W2116984961 cites W2030834210 @default.
• W2116984961 cites W2033387179 @default.
• W2116984961 cites W2035581654 @default.
• W2116984961 cites W2037913221 @default.
• W2116984961 cites W2046024621 @default.
• W2116984961 cites W2051087118 @default.
• W2116984961 cites W2059141256 @default.
• W2116984961 cites W2061155570 @default.
• W2116984961 cites W2062400835 @default.
• W2116984961 cites W2063675796 @default.
• W2116984961 cites W2064416623 @default.
• W2116984961 cites W2066106215 @default.
• W2116984961 cites W2068349374 @default.
• W2116984961 cites W2069554621 @default.
• W2116984961 cites W2070137904 @default.
• W2116984961 cites W2074692601 @default.
• W2116984961 cites W2078786014 @default.
• W2116984961 cites W2086137483 @default.
• W2116984961 cites W2089845951 @default.
• W2116984961 cites W2091140326 @default.
• W2116984961 cites W2098619105 @default.
• W2116984961 cites W2100575013 @default.
• W2116984961 cites W2100904521 @default.
• W2116984961 cites W2112569051 @default.
• W2116984961 cites W2114538357 @default.
• W2116984961 cites W2117891939 @default.
• W2116984961 cites W2127664187 @default.
• W2116984961 cites W2130309413 @default.
• W2116984961 cites W2131403247 @default.
• W2116984961 cites W2132260726 @default.
• W2116984961 cites W2133608634 @default.
• W2116984961 cites W2136400402 @default.
• W2116984961 cites W2140270640 @default.
• W2116984961 cites W2142759365 @default.
• W2116984961 cites W2144375618 @default.
• W2116984961 cites W2149233112 @default.
• W2116984961 cites W2151637767 @default.
• W2116984961 cites W2154750531 @default.
• W2116984961 cites W2154777971 @default.
• W2116984961 cites W2154792934 @default.
• W2116984961 cites W2158931098 @default.
• W2116984961 cites W2164223256 @default.
• W2116984961 cites W2164561631 @default.
• W2116984961 cites W2167099283 @default.
• W2116984961 cites W2240213927 @default.
• W2116984961 cites W2320158336 @default.
• W2116984961 cites W2325080109 @default.
• W2116984961 cites W2333804036 @default.
• W2116984961 cites W2341674440 @default.
• W2116984961 cites W256888946 @default.
• W2116984961 cites W652862567 @default.
• W2116984961 cites W798143013 @default.
• W2116984961 doi "https://doi.org/10.1016/j.tim.2015.08.002" @default.
• W2116984961 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/26439297" @default.
• W2116984961 hasPublicationYear "2015" @default.
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