anti-SAM Domain and HD Domain 1 (SAMHD1) Antibodies

Human SAM Domain and HD Domain 1 (SAMHD1) interaction partners

1. 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.

2. SAMHD1 is not localized in dot-like structures under DNA double-strand break induction in HeLa cells.

3. 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.

4. Compared with control cel (show NFKB1 Antibodies)ls, infection of SAMHD1-silenced human mon (show NFKB1 Antibodies)ocytic cells or primary macrophages with Sendai (show NFKB1 Antibodies)virus or HIV-1, or treatment wit (show NFKBIA Antibodies)h inflammatory stimuli, induces significantly higher levels of NF-kappaB act (show IKBKE Antibodies)ivation and IFN-I induction. SAMHD1 (show IRF7 Antibodies) down-regulates innate immune responses to viral infections and inflammatory stimul (show IKBKE Antibodies)i.

5. 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

6. Low SAMHD1 expression is associated with HIV-1 infection.

7. Multiple domains of SAMHD1(e.g., N-terminus, nuclear localization signal, linker, HD domain, and C-terminus)are essential for Vpx-induced degradation.[review]

8. 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 Antibodies)(+) T cells.

9. results demonstrate that the interaction of CD81 (show CD81 Antibodies) with SAMHD1 controls the metabolic rate of HIV-1 replication by tuning the availability of building blocks for reverse transcription, namely dNTPs

10. Immune activation during HIV-1 infection influences SAMHD1 expression and degradation.

Zebrafish SAM Domain and HD Domain 1 (SAMHD1) interaction partners

1. Data suggest that zebrafish may represent a system for studying the relationship between type I interferon (IFN) signaling and a loss of deoxynucleoside triphosphate triphosphohydrolase SAMHD1 activity.

Mouse (Murine) SAM Domain and HD Domain 1 (SAMHD1) interaction partners

1. SAMHD1 inhibits NF-kappaB (show NFKB1 Antibodies) activation by interacting with NF-kappaB1 (show NFKB1 Antibodies)/2 and reducing phosphorylation of the NF-kappaB (show NFKB1 Antibodies) inhibitory protein IkappaBalpha (show NFKBIA Antibodies). SAMHD1 also interacts with the inhibitor-kappaB kinase epsilon (IKKepsilon (show IKBKE Antibodies)) and IFN regulatory factor 7 (IRF7 (show IRF7 Antibodies)), leading to the suppression of the IFN-I induction pathway by reducing IKKepsilon (show IKBKE Antibodies)-mediated IRF7 (show IRF7 Antibodies) phosphorylation. SAMHD1 down-regulates innate immune responses to ...

2. 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.

3. SAMHD1 crystal structure delineates the SAMHD1 allosteric activation process that governs SAMHD1 enzymatic activities.

4. 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

5. 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.

6. These observations suggest that heterozygous cancer-associated SAMHD1 mutations increase mutation rates in cancer cells.

7. SAMHD1 in the mouse blocks retroviral infection at the level of reverse transcription and is regulated through cell cycle-dependent phosphorylation.

8. phosphorylation of mSAMHD1 at T634 by CDK1 (show CDK1 Antibodies)/2 negatively regulates its HIV-1 restriction in differentiated cells, but does not affect its murine leukemia virus restriction in dividing cells.

9. SAMHD1 restricts HIV-1 replication and regulates interferon production in mouse myeloid cells.

10. Allosteric regulation by dATP and dTTP works similarly in human and mouse SAMHD1.