• Western blot analysis of lysates from HCT116 cells, primary antibody was diluted at 1:1000, 4°C over night

Anti-Phospho-STING1-Ser366 antibody (STJ194750)

SKU:
STJ194750

Current Stock:
Host: Rabbit
Applications: WB
Reactivity: Human/Rat/Mouse
Note: STRICTLY FOR FURTHER SCIENTIFIC RESEARCH USE ONLY (RUO). MUST NOT TO BE USED IN DIAGNOSTIC OR THERAPEUTIC APPLICATIONS.
Short Description: Rabbit polyclonal antibody anti-Phospho-Stimulator of interferon genes protein-Ser366 is suitable for use in Western Blot research applications.
Clonality: Polyclonal
Conjugation: Unconjugated
Isotype: IgG
Formulation: Liquid in PBS containing 50% Glycerol, 0.5% BSA and 0.02% Sodium Azide.
Purification: The antibody was affinity-purified from rabbit serum by affinity-chromatography using specific immunogen.
Concentration: 1 mg/mL
Dilution Range: WB 1:1000-2000
Storage Instruction: Store at-20°C for up to 1 year from the date of receipt, and avoid repeat freeze-thaw cycles.
Gene Symbol: STING1
Gene ID: 340061
Uniprot ID: STING_HUMAN
Specificity: This antibody detects endogenous levels of Human/Rat STING (phospho-Ser366) or mouse STING (phospho-Ser365)
Immunogen: Synthesized phosho peptide around human STING (Ser366)
Post Translational Modifications Phosphorylation by TBK1 leads to activation and production of IFN-beta. Following cyclic nucleotide (c-di-GMP or cGAMP)-binding, activation and translocation from the endoplasmic reticulum, STING1 is phosphorylated by TBK1 at Ser-366 in the pLxIS motif. The phosphorylated pLxIS motif constitutes an IRF3-binding motif, leading to recruitment of the transcription factor IRF3 to induce type-I interferons and other cytokines. The phosphorylated pLxIS motif facilitates SENP2 recruitment during late phase of viral infection. Phosphorylated on tyrosine residues upon MHC-II aggregation. Dephosphorylation by PPP6C leads to inactivation and decreased production of IFN-beta. Phosphorylation at Ser-358 is also required to activate IRF3. Ubiquitinated. Ubiquitinated via 'Lys-63'-linked ubiquitin chains in response to double-stranded DNA treatment, leading to relocalization to autophagosomes and subsequent degradation.this process is dependent on SQSTM1. 'Lys-63'-linked ubiquitination mediated by TRIM56 at Lys-150 promotes homodimerization and recruitment of the antiviral kinase TBK1 and subsequent production of IFN-beta. 'Lys-48'-linked polyubiquitination at Lys-150 occurring after viral infection is mediated by RNF5 and leads to proteasomal degradation. 'Lys-11'-linked polyubiquitination at Lys-150 by RNF26 leads to stabilize STING1: it protects STING1 from RNF5-mediated 'Lys-48'-linked polyubiquitination. 'Lys-33'-linked and 'Lys-48'-linked deubiquitinated by USP20.leading to its stabilization and promotion of innate antiviral response. 'Lys-48'-linked deubiquitinated by USP44.leading to its stabilization and promotion of innate antiviral response. Deubiquitinated by USP13.leading to inhibition of innate antiviral response. (Microbial infection) Deubiquitinated by Epstein-Barr virus BPLF1 on both 'Lys-48' and 'Lys-63'-linked ubiquitin chains.leading to inhibition of cGAS-STING signaling. Sumoylated at Lys-338 by TRIM38 during the early phase of viral infection, promoting its stability by preventing its relocalization to autophagosomes and subsequent degradation. Desumoylated by SENP2 during the late phase of viral infection. Palmitoylation takes place in the Golgi apparatus and creates a platform for the recruitment of TBK1.
Function Facilitator of innate immune signaling that acts as a sensor of cytosolic DNA from bacteria and viruses and promotes the production of type I interferon (IFN-alpha and IFN-beta). Innate immune response is triggered in response to non-CpG double-stranded DNA from viruses and bacteria delivered to the cytoplasm. Acts by binding cyclic dinucleotides: recognizes and binds cyclic di-GMP (c-di-GMP), a second messenger produced by bacteria, and cyclic GMP-AMP (cGAMP), a messenger produced by CGAS in response to DNA virus in the cytosol. Upon binding of c-di-GMP or cGAMP, STING1 oligomerizes, translocates from the endoplasmic reticulum and is phosphorylated by TBK1 on the pLxIS motif, leading to recruitment and subsequent activation of the transcription factor IRF3 to induce expression of type I interferon and exert a potent anti-viral state. In addition to promote the production of type I interferons, plays a direct role in autophagy. Following cGAMP-binding, STING1 buds from the endoplasmic reticulum into COPII vesicles, which then form the endoplasmic reticulum-Golgi intermediate compartment (ERGIC). The ERGIC serves as the membrane source for WIPI2 recruitment and LC3 lipidation, leading to formation of autophagosomes that target cytosolic DNA or DNA viruses for degradation by the lysosome. The autophagy- and interferon-inducing activities can be uncoupled and autophagy induction is independent of TBK1 phosphorylation. Autophagy is also triggered upon infection by bacteria: following c-di-GMP-binding, which is produced by live Gram-positive bacteria, promotes reticulophagy. Exhibits 2',3' phosphodiester linkage-specific ligand recognition: can bind both 2'-3' linked cGAMP (2'-3'-cGAMP) and 3'-3' linked cGAMP but is preferentially activated by 2'-3' linked cGAMP. The preference for 2'-3'-cGAMP, compared to other linkage isomers is probably due to the ligand itself, whichs adopts an organized free-ligand conformation that resembles the STING1-bound conformation and pays low energy costs in changing into the active conformation. 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). (Microbial infection) Antiviral activity is antagonized by oncoproteins, such as papillomavirus (HPV) protein E7 and adenovirus early E1A protein. Such oncoproteins prevent the ability to sense cytosolic DNA.
Protein Name Stimulator Of Interferon Genes Protein
Hsting
Endoplasmic Reticulum Interferon Stimulator
Eris
Mediator Of Irf3 Activation
Hmita
Transmembrane Protein 173
Database Links Reactome: R-HSA-1834941
Reactome: R-HSA-3134975
Reactome: R-HSA-3249367
Reactome: R-HSA-3270619
Reactome: R-HSA-6798695
Reactome: R-HSA-9692916
Reactome: R-HSA-9705671
Cellular Localisation Endoplasmic Reticulum Membrane
Multi-Pass Membrane Protein
Cytoplasm
Perinuclear Region
Endoplasmic Reticulum-Golgi Intermediate Compartment Membrane
Golgi Apparatus Membrane
Cytoplasmic Vesicle
Autophagosome Membrane
Mitochondrion Outer Membrane
Cell Membrane
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
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
Alternative Antibody Names Anti-Stimulator Of Interferon Genes Protein antibody
Anti-Hsting antibody
Anti-Endoplasmic Reticulum Interferon Stimulator antibody
Anti-Eris antibody
Anti-Mediator Of Irf3 Activation antibody
Anti-Hmita antibody
Anti-Transmembrane Protein 173 antibody
Anti-STING1 antibody
Anti-ERIS antibody
Anti-MITA antibody
Anti-STING antibody
Anti-TMEM173 antibody

Information sourced from Uniprot.org

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