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the cell-cycle-dependent post-translation modification of TREX1 regulates its interaction with OST (zeige DDOST ELISA Kits).
The effect of topical TREX1 knockdown and local interferon (zeige IFNA ELISA Kits) production on HIV transmission in human cervicovaginal explants and humanized mice, is reported.
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 (zeige 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 (zeige EXO1 ELISA Kits) expression levels are associated with poor prognosis
showed that patients with SSc (zeige CYP11A1 ELISA Kits) or SLE have AAb against EphB2 (zeige EPHB2 ELISA Kits), a protein involved in angiogenesis, and THEX1 (zeige 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.
the cell-cycle-dependent post-translation modification of TREX1 regulates its interaction with OST.
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 (zeige NT5C2 ELISA Kits)-AMP (zeige TMPRSS5 ELISA Kits) synthase (cGAS) is essential for all aspects of the autoimmune disease in 3' repair exonuclease (zeige 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 (zeige TLR3 ELISA Kits), -4, -7, and -9 ligands also augments Trex1 expression through autocrine IFN-beta (zeige IFNB1 ELISA Kits) production and triggering of the IFN signaling pathway
knocking out the DNA sensor cyclic GMP (zeige NT5C2 ELISA Kits)-AMP (zeige TMPRSS5 ELISA Kits) synthase completely abrogates spontaneous induction of IFN-stimulated genes in TREX1-deficient cells.
Spontaneous type I INF (zeige GIF ELISA Kits) dependent cutaneous pathology in TREX1 deficiency illustrates common pathogenetic pathway in chilblain lupus.
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