Render Target: STATIC
Render Timestamp: 2024-11-22T11:13:16.950Z
Commit: 5c4accf06eb7154018ba3f54329c7590f97f534a
XML generation date: 2024-09-30 01:56:55.946
Product last modified at: 2024-10-22T10:30:33.229Z
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PDP - Template Name: Monoclonal Antibody
PDP - Template ID: *******c5e4b77
R Recombinant
Recombinant: Superior lot-to-lot consistency, continuous supply, and animal-free manufacturing.

Phospho-SAMHD1 (Thr592) (D7O2M) Rabbit mAb #89930

Filter:
  • WB
  • IP
  • F

    Supporting Data

    REACTIVITY H M R
    SENSITIVITY Endogenous
    MW (kDa) 72
    Source/Isotype Rabbit IgG
    Application Key:
    • WB-Western Blotting 
    • IP-Immunoprecipitation 
    • F-Flow Cytometry 
    Species Cross-Reactivity Key:
    • H-Human 
    • M-Mouse 
    • R-Rat 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000
    Immunoprecipitation 1:200
    Flow Cytometry (Fixed/Permeabilized) 1:800

    Storage

    Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA, 50% glycerol and less than 0.02% sodium azide. Store at –20°C. Do not aliquot the antibody.

    For a carrier free (BSA and azide free) version of this product see product #27254.

    Protocol

    Specificity / Sensitivity

    Phospho-SAMHD1 (Thr592) (D7O2M) Rabbit mAb recognizes endogenous levels of SAMDH1 protein only when phosphorylated at Thr592.

    Species Reactivity:

    Human, Mouse, Rat

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Thr592 of human SAMHD1 protein.

    Background

    SAM domain and HD domain-containing protein 1 (SAMHD1) is a negative regulator of the cell-intrinsic innate immune response (1). Research studies have identified mutations in SAMHD1 as a cause of Aicardi-Goutieres syndrome, an autoimmune disease characterized by elevated production of interferon-α and symptoms resembling congenital viral infection (1). SAMHD1 was identified as the restriction factor that renders most myeloid cells refractory to human immunodeficiency virus (HIV) infection (2-4). Expression of the viral protein Vpx in refractory cells targets SAMHD1 for ubiquitin-mediated degradation and relieves HIV restriction. SAMHD1 prevents autoimmunity and HIV infection by hydrolyzing intracellular deoxynucleoside triphosphates (dNTPs), thereby limiting inappropriate immune activation by self nucleic acid and inhibiting reverse transcription of the HIV genome (4-6).
    Phosphorylation of Thr592 by cyclin A2/CDK1 was identified as a regulatory mechanism that controls SAMHD1 activity (7,8). SAMHD1 is phosphorylated in proliferating cells, which inhibits its ability to block HIV infection. In resting cells or in cells treated with PMA (TPA) or IFN-α, SAMHD1 phosphorylation is decreased and cells are refractory to HIV infection (7,8).
    For Research Use Only. Not For Use In Diagnostic Procedures.
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