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SAMHD1 may play a role in regulation of the innate immune response. Additionally we are shipping SAMHD1 Antibodies (131) and SAMHD1 Proteins (4) and many more products for this protein.
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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.
Compared with control cel (show NFKB1 ELISA Kits)ls, infection of SAMHD1-silenced human mon (show NFKB1 ELISA Kits)ocytic cells or primary macrophages with Sendai (show NFKB1 ELISA Kits)virus or HIV-1, or treatment wit (show NFKBIA ELISA Kits)h inflammatory stimuli, induces significantly higher levels of NF-kappaB act (show IKBKE ELISA Kits)ivation and IFN-I induction. SAMHD1 (show IRF7 ELISA Kits) down-regulates innate immune responses to viral infections and inflammatory stimul (show IKBKE ELISA Kits)i.
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
Low SAMHD1 expression is associated with HIV-1 infection.
Multiple domains of SAMHD1(e.g., N-terminus, nuclear localization signal, linker, HD domain, and C-terminus)are essential for Vpx-induced degradation.[review]
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 (show CD4 ELISA Kits)(+) T cells.
results demonstrate that the interaction of CD81 (show CD81 ELISA Kits) with SAMHD1 controls the metabolic rate of HIV-1 replication by tuning the availability of building blocks for reverse transcription, namely dNTPs
Immune activation during HIV-1 infection influences SAMHD1 expression and degradation.
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.
Upregulation of endogenous SAMHD1 expression is attributed to the phosphorylation and nuclear translocation of IRF3 (show IRF3 ELISA Kits).
Data suggest that zebrafish may represent a system for studying the relationship between type I interferon (show IFNA ELISA Kits) (IFN) signaling and a loss of deoxynucleoside triphosphate triphosphohydrolase SAMHD1 activity.
SAMHD1 inhibits NF-kappaB (show NFKB1 ELISA Kits) activation by interacting with NF-kappaB1 (show NFKB1 ELISA Kits)/2 and reducing phosphorylation of the NF-kappaB (show NFKB1 ELISA Kits) inhibitory protein IkappaBalpha (show NFKBIA ELISA Kits). SAMHD1 also interacts with the inhibitor-kappaB kinase epsilon (IKKepsilon (show IKBKE ELISA Kits)) and IFN regulatory factor 7 (IRF7 (show IRF7 ELISA Kits)), leading to the suppression of the IFN-I induction pathway by reducing IKKepsilon (show IKBKE ELISA Kits)-mediated IRF7 (show IRF7 ELISA Kits) phosphorylation. SAMHD1 down-regulates innate immune responses to ...
SAMHD1's restriction of dNTP supply enhances AID's mutagenicity and that the evolution of Ig hypermutation included the repurposing of antiviral mechanisms based on dNTP starvation.
SAMHD1 crystal structure delineates the SAMHD1 allosteric activation process that governs SAMHD1 enzymatic activities.
provide genetic evidence that cell-autonomous control of lentivirus infection in myeloid cells by SAMHD1 limits virus-induced production of interferons and the induction of co-stimulatory markers
These data support a model in which SAMHD1 catalytic activity is regulated through tetramer stabilization by the carboxyl-terminal tail, phosphorylation destabilizing the complexes and inactivating the enzyme. ISF2 may serve to reduce the dNTP pool to very low levels as a means of restricting virus replication.
These observations suggest that heterozygous cancer-associated SAMHD1 mutations increase mutation rates in cancer cells.
SAMHD1 in the mouse blocks retroviral infection at the level of reverse transcription and is regulated through cell cycle-dependent phosphorylation.
phosphorylation of mSAMHD1 at T634 by CDK1 (show CDK1 ELISA Kits)/2 negatively regulates its HIV-1 restriction in differentiated cells, but does not affect its murine leukemia virus restriction in dividing cells.
SAMHD1 restricts HIV-1 replication and regulates interferon (show IFNA ELISA Kits) production in mouse myeloid cells.
Allosteric regulation by dATP and dTTP works similarly in human and mouse SAMHD1.
This gene may play a role in regulation of the innate immune response. The encoded protein is upregulated in response to viral infection and may be involved in mediation of tumor necrosis factor-alpha proinflammatory responses. Mutations in this gene have been associated with Aicardi-Goutieres syndrome.
SAM domain and HD domain-containing protein 1
, dendritic cell-derived IFNG-induced protein
, deoxynucleoside triphosphate triphosphohydrolase SAMHD1
, monocyte protein 5
, SAM domain- and HD domain-containing protein 1
, IFN-gamma induced
, interferon-gamma-inducible protein Mg11