Anti-SAMHD1 antibody [OTI1F9],Abcam,AB117908

Target data Protein that acts both as a host restriction factor involved in defense response to virus and as a regulator of DNA end resection at stalled replication forks (PubMed : 19525956, PubMed : 21613998, PubMed : 21720370, PubMed : 22056990, PubMed : 23601106, PubMed : 23602554, PubMed : 24336198, PubMed : 26294762, PubMed : 26431200, PubMed : 28229507, PubMed : 28834754, PubMed : 29670289). Has deoxynucleoside triphosphate (dNTPase) activity, which is required to restrict infection by viruses, such as HIV-1 : dNTPase activity reduces cellular dNTP levels to levels too low for retroviral reverse transcription to occur, blocking early-stage virus replication in dendritic and other myeloid cells (PubMed : 19525956, PubMed : 21613998, PubMed : 21720370, PubMed : 22056990, PubMed : 23364794, PubMed : 23601106, PubMed : 23602554, PubMed : 24336198, PubMed : 25038827, PubMed : 26101257, PubMed : 26294762, PubMed : 26431200, PubMed : 28229507). Likewise, suppresses LINE-1 retrotransposon activity (PubMed : 24035396, PubMed : 24217394, PubMed : 29610582). Not able to restrict infection by HIV-2 virus; because restriction activity is counteracted by HIV-2 viral protein Vpx (PubMed : 21613998, PubMed : 21720370). In addition to virus restriction, dNTPase activity acts as a regulator of DNA precursor pools by regulating dNTP pools (PubMed : 23858451). Phosphorylation at Thr-592 acts as a switch to control dNTPase-dependent and -independent functions : it inhibits dNTPase activity and ability to restrict infection by viruses, while it promotes DNA end resection at stalled replication forks (PubMed : 23601106, PubMed : 23602554, PubMed : 29610582, PubMed : 29670289). Functions during S phase at stalled DNA replication forks to promote the resection of gapped or reversed forks : acts by stimulating the exonuclease activity of MRE11, activating the ATR-CHK1 pathway and allowing the forks to restart replication (PubMed : 29670289). Its ability to promote degradation of nascent DNA at stalled replication forks is required to prevent induction of type I interferons, thereby preventing chronic inflammation (PubMed : 27477283, PubMed : 29670289). Ability to promote DNA end resection at stalled replication forks is independent of dNTPase activity (PubMed : 29670289). Enhances immunoglobulin hypermutation in B-lymphocytes by promoting transversion mutation (By similarity). See full target information SAMHD1