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data identifies miR (zeige MLXIP Proteine)-103 regulation of TREX1 as a potent modulator of the tumour microenvironment.
Thus, the intracellular level of TREX1 pivotally modulates innate immune induction by HIV-1. Partial HIV-1 genomes are the TREX1 target and are sensed by cGAS.
TREX1-deficient neurons also exhibited increased apoptosis and formed three-dimensional cortical organoids of reduced size.
Homozygote R114C mutation in TREX1 gene was shown in two siblings, one with chilblains and another with chilblains accompanied with cerebral vasculitis.
TREX1 frame-shift mutations induce autoantibodies against mostly non-nuclear antigens, patients carrying these mutations are likely be ANA (zeige BTG3 Proteine) negative
The activation of interferon (zeige IFNA Proteine)-induced genes is controlled by the JAK (zeige JAK3 Proteine)-STAT (zeige STAT1 Proteine) system; therefore, JAK (zeige JAK3 Proteine) inhibitors were successfully used in several cases to treat type 1 interferonopathies. Experience with this treatment modality is continuously growing.
the cell-cycle-dependent post-translation modification of TREX1 regulates its interaction with OST (zeige DDOST Proteine).
The effect of topical TREX1 knockdown and local interferon (zeige IFNA Proteine) 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 Proteine)-independent ORF1p depletion.
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 Proteine)-AMP (zeige TMPRSS5 Proteine) synthase (cGAS) is essential for all aspects of the autoimmune disease in 3' repair exonuclease (zeige EXO1 Proteine) 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 Proteine), -4, -7, and -9 ligands also augments Trex1 expression through autocrine IFN-beta (zeige IFNB1 Proteine) production and triggering of the IFN signaling pathway
knocking out the DNA sensor cyclic GMP (zeige NT5C2 Proteine)-AMP (zeige TMPRSS5 Proteine) synthase completely abrogates spontaneous induction of IFN-stimulated genes in TREX1-deficient cells.
Spontaneous type I INF (zeige GIF Proteine) 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