function:Acts as a facilitator of innate immune signaling. Able to activate both NF-kappa-B and IRF3 transcription pathways to induce expression of type I interferon (IFN-alpha and IFN-beta) and exert a potent anti-viral state following expression. May be involved in translocon function, the translocon possibly being able to influence the induction of type I interferons. May be involved in transduction of apoptotic signals via its association with the major histocompatibility complex class II (MHC-II). Mediates death signaling via activation of the extracellular signal-regulated kinase (ERK) pathway.,PTM:Phosphorylated on tyrosine residues upon MHC-II aggregation.,subunit:Associates with the MHC-II complex (By similarity). Interacts with DDX58/RIG-I, MAVS/VISA and SSR2.,tissue specificity:Ubiquitously expressed.,
Endoplasmic reticulum membrane ; Multi-pass membrane protein . Cytoplasm, perinuclear region . Endoplasmic reticulum-Golgi intermediate compartment membrane ; Multi-pass membrane protein . Golgi apparatus membrane ; Multi-pass membrane protein . Cytoplasmic vesicle, autophagosome membrane ; Multi-pass membrane protein . Mitochondrion outer membrane ; Multi-pass membrane protein . Cell membrane ; Multi-pass membrane protein . In response to double-stranded DNA stimulation, translocates from the endoplasmic reticulum through the endoplasmic reticulum-Golgi intermediate compartment and Golgi to post-Golgi vesicles, where the kinase TBK1 is recruited (PubMed:19433799, PubMed:30842659, PubMed:30842653, PubMed:29694889). Upon cGAMP-binding, translocates to the endoplasmic reticulum-Golgi intermediate compartment (ERGIC) in a process that is dependent on COPII vesicles; STING1-containing ERGIC serves as a membrane source for LC3 lipidation, which is a key step in autophagosome biogenesis (PubMed:30842662). .
Ubiquitously expressed. Expressed in skin endothelial cells, alveolar type 2 pneumocytes, bronchial epithelium and alveolar macrophages.
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