FOXC1mediated TRIM22 regulates the excessive proliferation and inflammation of fibroblastlike synoviocytes in rheumatoid arthritis via NFkappaB signaling pathway.
Results suggest that TRIM22-augmented autophagy prevents intracellular Mtb to evade autophagic clearance thereby inhibiting the persistence of Mtb infections.
miR-215 facilitated HCV replication via inactivation of the NF-kappaB pathway by inhibiting TRIM22 providing a novel potential target for HCV infection.
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.
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.
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
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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