SCUBA

TIFA — TRAF interacting protein with forkhead associated domain

TIFA belongs to a gene co-expression module in 3 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.

TIFA's module in each cell type

Cell typeModuleShares the module with
EndothelialNF-κB Activation
Inflammation
C2CD4B, HSPA6, ICAM5, IER3, MAP3K8, NFKBIA, NFKBID, PMAIP1 +5 moreView in SCUBA
Innate lymphoid cellsInnate Stress Signaling
Inflammation
C19orf25, DNAJC15, IFI16, KIF5B, KRCC1, MAP2K6, PCMTD1, PLIN2 +7 moreView in SCUBA
Lymphatic endothelialDNA Damage Autophagy
Stress
CKS2, COQ10B, GADD45A, HBP1, MAP1LC3B, MSX1, NR1D1, PHLDA2 +2 moreView in SCUBA

About the gene

SynonymsMGC20791, T2BP, T6BP, TIFAA
Chromosome4: 112272968-112285955
Predicted locationIntracellular
Essential geneNo
Protein classPredicted intracellular proteins
Biological processImmunity, Innate immunity

Function

Adapter molecule that plays a key role in the activation of pro-inflammatory NF-kappa-B signaling following detection of bacterial pathogen-associated molecular pattern metabolites (PAMPs). Promotes activation of an innate immune response by inducing the oligomerization and polyubiquitination of TRAF6, which leads to the activation of TAK1 and IKK through a proteasome-independent mechanism. TIFA-dependent innate immune response is triggered by ADP-D-glycero- beta-D-manno-heptose (ADP-Heptose), a potent PAMP present in all Gram- negative and some Gram-positive bacteria: ADP-Heptose is recognized by ALPK1, which phosphorylates TIFA at Thr-9, leading to TIFA homooligomerization and subsequent activation of pro-inflammatory NF- kappa-B signaling.

Human Protein Atlas · Open Targets · UniProt

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