Cell Signaling Technology

Product Pathways - Innate Immunity

Phospho-SAMHD1 (Thr592) Antibody #15038

No. Size Price
15038S 100 µl ( 10 western blots ) ¥3,900.00 现货查询 购买询价
15038 carrier free & custom formulation / quantityemail request
Applications Dilution Species-Reactivity Sensitivity MW (kDa) Isotype
W 1:1000 Human,Mouse, Endogenous 69, 72 Rabbit
IP 1:50

Species cross-reactivity is determined by western blot.

Applications Key: W=Western Blotting, IP=Immunoprecipitation,

Specificity / Sensitivity

Phospho-SAMHD1 (Thr592) Antibody recognizes endogenous levels of SAMHD1 protein only when phosphorylated at Thr592.

Source / Purification

Polyclonal antibodies are produced by immunizing animals with a synthetic phosphopeptide corresponding to residues surrounding Thr592 of human SAMHD1 protein. Antibodies are purified by protein A and peptide affinity chromatography.

Western Blotting

Western Blotting

Western blot analysis of extracts from THP-1 cells, untreated (-) or treated with TPA #4174 (80 nM, 16 hr; +), using Phospho-SAMHD1 (Thr592) Antibody (upper) and SAMHD1 Antibody #12361 (lower).

Western Blotting

Western Blotting

Western blot analysis of extracts from THP-1 cells, untreated (-) or treated with calf intestinal phosphatase (CIP) and λ phosphatase (+), using Phospho-SAMHD1 (Thr592) Antibody (upper) and SAMHD1 Antibody #12361 (lower).

IP

IP

Immunoprecipitation of phospho-SAMHD1 (Thr592) from THP-1 cell extracts using Normal Rabbit IgG #2729 (lane 2) or Phospho-SAMHD1 (Thr592) Antibody (lane 3). Lane 1 is 10% input. Western blot analysis was performed using Phospho-SAMHD1 (Thr592) Antibody.

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).

  1. Rice, G.I. et al. (2009) Nat Genet 41, 829-32.
  2. Laguette, N. et al. (2011) Nature 474, 654-7.
  3. Hrecka, K. et al. (2011) Nature 474, 658-61.
  4. Powell, R.D. et al. (2011) J Biol Chem 286, 43596-600.
  5. Goldstone, D.C. et al. (2011) Nature 480, 379-82.
  6. Lahouassa, H. et al. (2012) Nat Immunol 13, 223-8.
  7. Cribier, A. et al. (2013) Cell Rep 3, 1036-43.
  8. White, T.E. et al. (2013) Cell Host Microbe 13, 441-51.

Application References

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For Research Use Only. Not For Use In Diagnostic Procedures.

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