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anti-Human TMEM173 Antikörper:
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Human Polyclonal TMEM173 Primary Antibody für 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 Monoclonal TMEM173 Primary Antibody für 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 Monoclonal TMEM173 Primary Antibody für ICS, IHC (p) - ABIN2689910
Ablasser, Goldeck, Cavlar, Deimling, Witte, Röhl, Hopfner, Ludwig, Hornung: cGAS produces a 2'-5'-linked cyclic dinucleotide second messenger that activates STING. in Nature 2013
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Human Polyclonal TMEM173 Primary Antibody für 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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We present physiological evidence that UBXN3B positively regulates stimulator-of-interferon genes (STING) signaling. Mechanistic studies demonstrate that UBXN3B interacts with both STING and its E3 ligase TRIM56, and facilitates STING ubiquitination, dimerization, trafficking, and consequent recruitment and phosphorylation of TBK1.
STAG2 deficiency induces interferon responses via cGAS-STING pathway and restricts virus infection.
STING-IRF3 pathway promotes hepatocyte injury and dysfunction by inducing inflammation and apoptosis and by disturbing glucose and lipid metabolism.
Data show that both cyclic GMP-AMP synthase (cGAS) and interferon-gamma inducible protein 16 (IFI16) are required for the activation of membrane protein STING (STING) and an innate immune response to exogenous DNA and DNA viruses.
PUMA promotes the cytosolic release of mitochondrial DNA and activation of the DNA sensors DAI/Zbp1 and STING, leading to enhanced RIP3 and MLKL phosphorylation in a positive feedback loop.
identified nitro-fatty acids as endogenously formed inhibitors of STING signaling and propose for these lipids to be considered in the treatment of STING-dependent inflammatory diseases.
Cells of human individuals carrying HAQ TMEM173, which encodes a common hypomorphic variant of STING, were largely or partly defective in inducing type I IFNs and proinflammatory cytokines upon infection.
Our studies indicate that the (extracellular vesicles) EVs released by HSV-1-infected cells carry innate immune components such as STING and other host and viral factors; they can activate innate immune responses in recipient cells and inhibit HSV-1 replication. The implication of these data is that the EVs released by HSV-1-infected cells could control HSV-1 dissemination promoting its persistence in the host.
data demonstrate that numerous RNA viruses evade cGAS/STING-dependent signaling and affirm the importance of this pathway in shaping the host range of ZIKV.
Immune activation of STING requires palmitoylation at the Golgi.
In the Title.
This study demonstrated that HSV-1 tegument protein VP22 counteracts the cGAS/STING-mediated DNA-sensing antiviral innate immunity signaling pathway by inhibiting the enzymatic activity of cGAS.
an electrophoretic mobility shift assay showed that signal transducers and activators of transcription 1 (STAT1) attach to the GAS motif on the human STING promoter region. This indicates that IFN-gamma/Janus kinases/STAT1 signaling is essential for the STING upregulation in human keratinocytes.
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.
pharmacological activation of STING in macrophages and hepatocytes induces host innate responses that can efficiently control hepatitis B virus replication. Hence, despite not playing a significant role in host innate immune response to HBV infection of hepatocytes, STING is potentially a valuable target for immunotherapy of chronic hepatitis B.
summarize recent findings that have pointed towards the STING pathway as an innate immune sensing mechanism driving type I interferon production in the tumor context
this review summarizes important features of the STING activation pathway and recent highlights about the role of STING in bacterial infections by Chlamydia, Listeria, Francisella, Brucella, Shigella, Salmonella, Streptococcus, and Neisseria genera, with a special focus on mycobacteria.
STING serves to detect - and promote immune defense against - DNA viruses and intracellular bacteria, as described in its initial discovery. The role of STING has since been expanded to include tumor surveillance and immune responses to cancer; indeed, defective STING responses are associated with certain cancers.
C11 depends on signaling through STING to produce antiviral type I interferon, which further supports its potential as a therapeutic drug or research tool.
This study demonstrates that the HCMV tegument protein pp65 inhibits IFN-beta 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. Notably, STING proteasome-mediated degradation was observed in both the presence and absence of pp65.
Ubxn3b(-/-), like Sting(-/-) mice, are highly susceptible to lethal herpes simplex virus 1 (HSV-1) and vesicular stomatitis virus (VSV) infection, which is correlated with deficient immune responses when compared to Ubxn3b(+/+) littermates.
this study shows that STING-/- mice presented defective protective mechanisms of intestinal mucosa, including decreased number of goblet cells, diminished mucus production, and lower levels of secretory IgA
In response to the presence of cytosolic DNA, STING translocates from the endoplasmic reticulum (ER) to the Golgi, and activates TANK-binding kinase 1 (TBK1), a cytosolic kinase that is essential for the activation of STING-dependent downstream signaling. TBK1 binds to STING at the Golgi, not at the ER.
Usp13 deconjugates polyubiquitin chains from STING and prevents the recruitment of Tbk1 to the signalling complex, thereby negatively regulating cellular antiviral responses.
STING-mediated innate immune responses and dendritic cell maturation do not require TICAM-1 in myeloid lineage immune cells.
Data show that mice defective in cyclic GMP-AMP synthase (cGAS) or STING protein (STING) are highly susceptible to acute herpes simplex encephalitis (HSE) .
The STING/type I interferon pathway enhances suppressive inflammation in tumors by recruiting myeloid cells in part via the CCR2 pathway. Germ-line knockouts of CCR2 or treatment with an anti-CCR2 antibody results in blockade of radiation-induced MDSC infiltration.
the induction of STING signaling is contingent on a fine-tuning of intracellular calcium levels.
STING was dispensable for restricting S. pneumoniae during acute pneumonia in mice.
STING has dual functions in host defense, regulating protein synthesis to prevent RNA virus infection and regulating IFN expression to restrict DNA viruses
The findings provide biochemical and imaging evidence for STING degradation by the lysosome and pinpoint trafficking-mediated STING degradation as a previously unanticipated therapeutic target for enhancing STING signaling in cancer therapy.
DsbA-L prevents obesity-induced inflammation and insulin 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/IRF3 dependent.
Intratumoral administration of the STING agonist cyclic di-GMP (CDG) or Flt3 Ligand (Flt3L) augmented the therapeutic effect of systemic triple checkpoint modulation and promoted the cure of 75% of mice with bilateral TRAMP-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 limits virus-induced production of interferons and the induction of co-stimulatory markers
the cloning and characterization of porcine STING (poSTING)
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