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trim22 is a broad and multifunctional host anti-viral factor induced by interferons.
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TRIM22 may act as epigenetic inhibitor of HIV-1 transcription by preventing the binding of the host cell transcription factor Sp1 to the viral promoter.
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Upregulation of TRIM22 triggers the expression and oligomerization of Bak and subsequently leads to cytochrome c release in a caspase-9- and caspase-3-dependent manner. Both the RING domain and the SPRY domain of the TRIM22 molecule are associated with its pro-apoptotic function.
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miR-215 facilitated HCV replication via inactivation of the NF-kappaB pathway by inhibiting TRIM22, providing a novel potential target for HCV infection.
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Suppression of interferon-mediated anti-HBV response by single CpG methylation in the 5'-UTR of TRIM22.
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Wthis study identified a genetic variation (rs7935564 G allele) in TRIM22 gene, which encodes TRIM22 protein acting like a HIV restriction factor, as being associated with good response to dendritic cell-based immunotherapy
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TRIM5 and TRIM22 single nucleotide polymorphisms are associated to increased odds of significant liver fibrosis and sustained virological response after pegIFNalpha/RBV therapy in human immunodeficiency virus/hepatitis C virus coinfected patients.
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Infant with severe IBD characterized by granulomatous colitis and severe perianal disease, we identified a homozygous variant of TRIM22 that affects the ability of its product to regulate NOD2.
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Interferon-alpha-induced TRIM22 interrupts hepatitis c virus replication by ubiquitinating NS5A.
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regulation of FoxO4 protein expression and cell survival by TRIM22 controls TLR3-mediated IFN type I gene induction, preventing excessive antiviral response through dsRNA-induced apoptosis.
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TRIM22 could interact with IkappaB kinase (IKK)alpha but not IKKbeta and could increase the level and phosphorylation of IKKalpha through its really interesting new gene (RING) and spla-ryanodine receptor (SPRY) domains.
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Demonstrated that TRIM22 acts as a negative regulator of HIV-1 replication via inhibition of basal Sp1-driven proviral transcription.
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propose that TRIM22 is a direct target gene of PR and that it can mediate progesterone actions in uterine cells
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Data show that capsid protein p24-DsRed-Monomer was co-localized with tripartite motif containing 22 (TRIM22)-EGFP in HEK293T cells.
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A number of putative structural and functional residues, including several sites that undergo post-translational modification, were also identified in TRIM22.
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our data characterize the extensive genetic variation in TRIM22 and identify rs1063303:G>C as a highly prevalent SNP that influences its function.
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Upregulation of TRIM22 may be associated with responsiveness to Peg-IFNalpha-2a/RBV combination therapy in hepatitis C.
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TRIM5alpha and TRIM22 have differential transcriptional regulation and distinct anti-HIV roles according to infection phase.
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Data report that markers in two TRIMs, TRIM5 and TRIM22 and a marker in BST2, associated statistically with the risk of getting MS.
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TRIM22 genetic diversity affects HIV-1 replication in vitro and it is a potentially novel determinant of HIV-1 disease severity
