GeneBio Systems
STING/TMEM173 rabbit pAb
STING/TMEM173 rabbit pAb
SKU:ES4218
Couldn't load pickup availability
Size: 100μL
Source:Rabbit
Applications:WB;IHC;IF;ELISA
Reactivity:Human;Mouse
Dilution:Western Blot: 1/500 - 1/2000. IHC-p: 1/100-1/300. ELISA: 1/20000. Not yet tested in other applications.
Immunogen:Synthesized peptide derived from Transmembrane protein 173 at AA range: 301-350
Storage_stability:-20°C/1 year
Clonality:Polyclonal
Isotype:IgG
Concentration:1 mg/ml
Observed_band(KD):38kD
Human_gene_id:340061
Human_swiss_prot_no:Q86WV6
Subcellular_location: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 interme
Other_name:TMEM173; ERIS; MITA; STING; Transmembrane protein 173; Endoplasmic reticulum interferon stimulator; ERIS; Mediator of IRF3 activation; hMITA; Stimulator of interferon genes protein; hSTING
Background:This gene encodes a five transmembrane protein that functions as a major regulator of the innate immune response to viral and bacterial infections. The encoded protein is a pattern recognition receptor that detects cytosolic nucleic acids and transmits signals that activate type I interferon responses. The encoded protein has also been shown to play a role in apoptotic signaling by associating with type II major histocompatibility complex. Mutations in this gene are the cause of infantile-onset STING-associated vasculopathy. Alternate splicing results in multiple transcript variants. [provided by RefSeq, Sep 2014],
