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The expression of TREX1 was closely related to the cytobiology characteristics of osteosarcoma stem cell.
Heterozygous mutations in TREX1 were reported in SLE patients.
This study reviewed that Neurologic Phenotypes Associated with Mutations in TREX1 in patients with Aicardi-Goutieres Syndrome.
Aicardie-Goutieres syndrome is described in a patient with a homozygous p.Arg114His mutation in the TREX1 gene.
CDK11 was found associated with the TREX/THOC, which recruited this kinase to DNA. Once at the viral genome, CDK11 phosphorylated serines at position 2 in the CTD of RNAPII, which increased levels of cleavage and polyadenylation factors at the HIV 3' end. In its absence, cleavage of viral transcripts was greatly attenuated.
Aicardi-Goutieres syndrome 1 is caused by mutations in the three prime repair exonuclease 1 gene (TREX1, MIM (show MTSS1 Proteins) 606609).
Functional analysis of retinal vasculopathy with cerebral leukodystrophy-associated TREX1 T270 frameshift-mutated fibroblasts showed a prevalent localization of the protein in the cytosol, rather than in the perinuclear region
Here we briefly describe the human diseases so-far associated with mutations in TREX1, which include Aicardi-Goutieres syndrome, familial chilblain lupus, systemic lupus erythematosus and retinal vasculopathy with cerebral leukodystrophy
Studies indicate that the biosensing strategy is based on the protection of DNA duplex from exonuclease (show EXO1 Proteins) III (Exo III)-mediated digestion by specific binding of estrogen receptor (ER (show ESR1 Proteins)) to its DNA response element.
The authors observed that the minor allele of SNP rs3135941 in Trex1 is associated with faster HIV-1 disease progression.
Data show that oligosaccharyltransferase (OST) activity is dysregulated in three prime exonuclease 1 knockout (Trex1-/-) cells.
Data show that cyclic GMP (show NT5C2 Proteins)-AMP (show TMPRSS5 Proteins) synthase (cGAS) is essential for all aspects of the autoimmune disease in 3' repair exonuclease (show EXO1 Proteins) Trex1 knockout mice.
Dysfunctional dsDNA degradation by TREX1 D18N induces disease in mice that recapitulates many characteristics of human lupus.
DC activation induced by TLR3 (show TLR3 Proteins), -4, -7, and -9 ligands also augments Trex1 expression through autocrine IFN-beta (show IFNB1 Proteins) production and triggering of the IFN signaling pathway
knocking out the DNA sensor cyclic GMP (show NT5C2 Proteins)-AMP (show TMPRSS5 Proteins) synthase completely abrogates spontaneous induction of IFN-stimulated genes in TREX1-deficient cells.
Spontaneous type I INF (show GIF Proteins) dependent cutaneous pathology in TREX1 deficiency illustrates common pathogenetic pathway in chilblain lupus.
Upon proinflammatory stimulation, Trex1(-/-) macrophages increase CD86 (show CD86 Proteins), TNF-alpha (show TNF Proteins) & IFN-alpha (show IFNA Proteins) production, & Ag presentation to CD4 (show CD4 Proteins)(+) T cells, but decrease apoptotic T cell clearance. Trex1 is a negative regulator of macrophage inflammatory activation.
Oxidized DNA Is less susceptible to TREX1 degradation; the oxidized base 8-hydroxyguanosine, a marker of oxidative damage in DNA, potentiated cytosolic immune recognition by decreasing its susceptibility to 3' repair exonuclease 1 -mediated degradation
regulates lysosomal biogenesis and interferon (show IFNA Proteins)-independent activation of antiviral genes
The structures of the mutant TREX1 proteins provide insight into the dysfunction relating to human disease.
This gene encodes a nuclear protein with 3' exonuclease activity. The encoded protein may play a role in DNA repair and serve as a proofreading function for DNA polymerase. Mutations in this gene result in Aicardi-Goutieres syndrome, chilblain lupus, Cree encephalitis, and other diseases of the immune system. Alternative splicing results in multiple transcript variants.
three prime repair exonuclease 1
, 3' repair exonuclease 1
, 3'-5' exonuclease TREX1
, DNase III
, deoxyribonuclease III
, three prime exonuclease 1
, trophoblast expressed 1