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data do not support the concept of retroelement-derived cDNA as key triggers of systemic autoimmunity in Trex1-deficient humans and mice
Aicardi-Goutieres syndrome protein TREX1 suppresses L1 and maintains genome integrity through exonuclease (show EXO1 ELISA Kits)-independent ORF1p depletion.
Analysis of mRNA expression profiles in breast tumors demonstrates that those with lower Trex1 and higher BLM and EXO1 (show EXO1 ELISA Kits) expression levels are associated with poor prognosis
showed that patients with SSc (show CYP11A1 ELISA Kits) or SLE have AAb against EphB2 (show EPHB2 ELISA Kits), a protein involved in angiogenesis, and THEX1 (show ERI1 ELISA Kits), a 3'-5' exoribonuclease involved in histone mRNA degradation.
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 606609).
Trex1 expression in dendritic cells is essential to prevent breakdown of self-tolerance ensuing from aberrant detection of endogenous DNA.
Data show that oligosaccharyltransferase (OST) activity is dysregulated in three prime exonuclease 1 knockout (Trex1-/-) cells.
Data show that cyclic GMP (show NT5C2 ELISA Kits)-AMP (show TMPRSS5 ELISA Kits) synthase (cGAS) is essential for all aspects of the autoimmune disease in 3' repair exonuclease (show EXO1 ELISA Kits) 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 ELISA Kits), -4, -7, and -9 ligands also augments Trex1 expression through autocrine IFN-beta (show IFNB1 ELISA Kits) production and triggering of the IFN signaling pathway
knocking out the DNA sensor cyclic GMP (show NT5C2 ELISA Kits)-AMP (show TMPRSS5 ELISA Kits) synthase completely abrogates spontaneous induction of IFN-stimulated genes in TREX1-deficient cells.
Spontaneous type I INF (show GIF ELISA Kits) dependent cutaneous pathology in TREX1 deficiency illustrates common pathogenetic pathway in chilblain lupus.
Upon proinflammatory stimulation, Trex1(-/-) macrophages increase CD86 (show CD86 ELISA Kits), TNF-alpha (show TNF ELISA Kits) & IFN-alpha (show IFNA ELISA Kits) production, & Ag presentation to CD4 (show CD4 ELISA Kits)(+) 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
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