SCUBA

TRIM69 — Tripartite motif containing 69

TRIM69 belongs to a gene co-expression module in 4 of 28 SCUBA cell types. Each module groups genes that rise and fall together in that cell type; the genes it shares a module with are its closest co-expression partners there.

TRIM69's module in each cell type

Cell typeModuleShares the module with
CD4⁺ T cellsCCR5 effector migration
migration & adhesion
ARHGEF12, BLM, CCR5, EMC6, ERGIC2, IGF2R, KAT2B, PSMD12 +10 moreView in SCUBA
Gamma-delta T cellsEOMES Effector Program
T cell maturation
AGK, ANKZF1, ATG16L2, C6orf120, CARD8, CBX1, CDK5RAP3, CENPT +25 more
MonocytesIRF1 Innate Activation
Innate immunity
BAZ1A, CFLAR, FNIP2, IRF1, MARCKS, NABP1, THAP2, ZFYVE16View in SCUBA
Mucosal-associated invariant T cellType I Interferon
Inflammation
ABCF2, ACAA2, ANXA2R, BST2, CHST12, IRF9, LY6E, LYSMD2 +6 more

About the gene

SynonymsRNF36, Trif, TRIMLESS
Chromosome15: 44728988-44767829
Predicted locationIntracellular
Essential geneNo
Protein classEnzymes, Predicted intracellular proteins
Molecular functionTransferase
Biological processApoptosis, Ubl conjugation pathway

Function

E3 ubiquitin ligase that plays an important role in antiviral immunity by restricting different viral infections including dengue virus or vesicular stomatitis indiana virus. Ubiquitinates viral proteins such as dengue virus NS3 thereby limiting infection. In addition, acts as a key mediator of type I interferon induced microtubule stabilization by directly associating to microtubules independently of its E3 ligase activity. Also plays a role in cataract formation together with TP53. Mechanistically, inhibits UVB-induced cell apoptosis and reactive oxygen species (ROS) production by inducing TP53 ubiquitination. Regulates centrosome dynamics and mitotic progression by ubiquitinating STK3/MST2; leading to its redistribution to the perinuclear cytoskeleton and subsequent phosphorylation by PLK1.

Human Protein Atlas · Open Targets · UniProt

Gene annotation from the Human Protein Atlas and UniProt; see sources & licences.