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Human Polyclonal TMEM173 Primary Antibody for ICC, IF - ABIN4356573
Furr, Chauhan, Moerdyk-Schauwecker, Marriott: A role for DNA-dependent activator of interferon regulatory factor in the recognition of herpes simplex virus type 1 by glial cells. in Journal of neuroinflammation 2011
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Human Polyclonal TMEM173 Primary Antibody for ICC, IF - ABIN4356571
Heiber, Barber: Evaluation of innate immune signaling pathways in transformed cells. in Methods in molecular biology (Clifton, N.J.) 2011
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Human Monoclonal TMEM173 Primary Antibody for CyTOF, FACS - ABIN4899624
Schoggins, MacDuff, Imanaka, Gainey, Shrestha, Eitson, Mar, Richardson, Ratushny, Litvak, Dabelic, Manicassamy, Aitchison, Aderem, Elliott, García-Sastre, Racaniello, Snijder, Yokoyama, Diamond et al.: Pan-viral specificity of IFN-induced genes reveals new roles for cGAS in innate immunity. ... in Nature 2014
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Human Polyclonal TMEM173 Primary Antibody for WB - ABIN2783202
Gerhard, Wagner, Feingold, Shenmen, Grouse, Schuler, Klein, Old, Rasooly, Good, Guyer, Peck, Derge, Lipman, Collins, Jang, Sherry, Feolo, Misquitta, Lee, Rotmistrovsky, Greenhut, Schaefer, Buetow et al.: The status, quality, and expansion of the NIH full-length cDNA project: the Mammalian Gene Collection (MGC). ... in Genome research 2004
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The cGAS-STING cascade contributes to antibacterial defense against L. pneumophila in mice and men, and provides important insight into how the common HAQ TMEM173/STING variant affects antimicrobial immune responses and susceptibility to infection.
summarize recent findings that have pointed towards the STING pathway as an innate immune sensing mechanism driving type I interferon (show IFNA Antibodies) production in the tumor context
C11 (show AKR1C4 Antibodies) depends on signaling through STING to produce antiviral type I interferon (show IFNA Antibodies), which further supports its potential as a therapeutic drug or research tool.
This study demonstrates that the HCMV tegument protein pp65 (show LCP1 Antibodies) inhibits IFN-beta (show IFNB1 Antibodies) production by binding and inactivating cGAS early during infection. In addition, this inhibitory activity specifically targets cGAS, since it can be bypassed via the addition of exogenous cGAMP, even in the presence of pp65 (show LCP1 Antibodies). Notably, STING proteasome-mediated degradation was observed in both the presence and absence of pp65 (show LCP1 Antibodies).
The DNA binding domain of Ku70 was essential for formation of the Ku70-STING complex. Knocking down STING in primary human macrophages inhibited their ability to produce IFN-lambda1 in response to transfection with DNA or infection with the DNA virus HSV-2 (herpes simplex virus-2); STING mediates the Ku70-mediated IFN-lambda1 innate immune response to exogenous DNA or DNA virus infection.
Data show that human cytomegalovirus (HCMV; human betaherpesvirus 5) glycoprotein US9 inhibits the IFN-beta (show IFNB1 Antibodies) response by targeting the mitochondrial antiviral-signaling protein (MAVS (show MAVS Antibodies)) and stimulator of interferon (show IFNA Antibodies) genes (STING)-mediated signaling pathways.
In the current study, we studied the role of MITA (Mediator of IRF3 Activation), a regulator of innate immunity, in the regulation of autophagy and its implication in cell death of breast cancer cells. Here, we report that MITA inhibits the fusion of autophagosome with lysosome as evident from different autophagy flux assays
these studies demonstrate that transcription factors CREB (show CREB1 Antibodies) and c-Myc (show MYC Antibodies) maintain the transcriptional activity of STING
Human T-lymphotropic virus 1 Tax (show CNTN2 Antibodies) protein impairs K63-linked ubiquitination of STING and disrupted the interactions between STING and TBK1 (show TBK1 Antibodies) to evade host innate immunity.
STING activated an antiviral/type I interferon (show IFNA Antibodies) response with live but not killed S. aureus.
DsbA-L (show GSTK1 Antibodies) prevents obesity-induced inflammation and insulin (show INS Antibodies) resistance by suppressing the mtDNA release-activated cGAS-cGAMP-STING pathway.
Nontypeable Haemophilus influenzae DNA as a Pathogen-Associated Molecular Pattern Molecules triggered I-IFN response, which was STING/TBK1 (show TBK1 Antibodies)/IRF3 (show IRF3 Antibodies) dependent.
Intratumoral administration of the STING agonist cyclic di-GMP (show NT5C2 Antibodies) (CDG) or Flt3 Ligand (Flt3L (show FLT3LG Antibodies)) augmented the therapeutic effect of systemic triple checkpoint modulation and promoted the cure of 75% of mice with bilateral TRAMP (show DPT Antibodies)-C2; however, when all agents were administered locally, only CDG mobilized abscopal immunity
provide genetic evidence that cell-autonomous control of lentivirus infection in myeloid cells by SAMHD1 (show SAMHD1 Antibodies) limits virus-induced production of interferons and the induction of co-stimulatory markers
Data show that stimulator of interferon (show IFNA Antibodies) genes (STING)-associated vasculopathy with onset in infancy (SAVI)-associated STING N153S mutation triggers IRF3 (show IRF3 Antibodies)-independent immune cell dysregulation and lung disease in mice.
These results highlight the crucial role of MFN1 (show MFN1 Antibodies) in maintaining the competency of the STING pathway.
to contain the spread of herpes simplex virus type 1 in vivo, STING-dependent signaling leads to the upregulation of tetherin (show BST2 Antibodies), a viral restriction factor
study identifies the AIM2 (show AIM2 Antibodies) inflammasome and cGAS/IFI16 (show IFI16 Antibodies)-STING-type I IFN pathway as a novel mechanism for host innate immunity to the ALVAC vaccine vector.
Facilitator of innate immune signaling that 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. Able to activate both NF-kappa-B and IRF3 transcription pathways to induce expression of type I interferon 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.
transmembrane protein 173
, N-terminal methionine-proline-tyrosine-serine plasma membrane tetraspanner
, endoplasmic reticulum IFN stimulator
, endoplasmic reticulum interferon stimulator
, mediator of IRF3 activation
, mitochondrial mediator of IRF3 activation
, stimulator of interferon genes protein
, Stimulator of interferon genes protein
, mitochondrial transmembrane protein 173