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anti-Human TMEM173 Antikörper:
anti-Mouse (Murine) TMEM173 Antikörper:
anti-Rat (Rattus) 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 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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an electrophoretic mobility shift assay showed that signal transducers and activators of transcription 1 (STAT1 (zeige STAT1 Antikörper)) attach to the GAS motif on the human STING promoter region. This indicates that IFN-gamma (zeige IFNG Antikörper)/Janus kinases/STAT1 (zeige STAT1 Antikörper) 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.
summarize recent findings that have pointed towards the STING pathway as an innate immune sensing mechanism driving type I interferon (zeige IFNA Antikörper) production in the tumor context
C11 (zeige AKR1C4 Antikörper) depends on signaling through STING to produce antiviral type I interferon (zeige IFNA Antikörper), which further supports its potential as a therapeutic drug or research tool.
This study demonstrates that the HCMV tegument protein pp65 (zeige LCP1 Antikörper) inhibits IFN-beta (zeige IFNB1 Antikörper) 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 (zeige LCP1 Antikörper). Notably, STING proteasome-mediated degradation was observed in both the presence and absence of pp65 (zeige LCP1 Antikörper).
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 (zeige IFNB1 Antikörper) response by targeting the mitochondrial antiviral-signaling protein (MAVS (zeige MAVS Antikörper)) and stimulator of interferon (zeige IFNA Antikörper) 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 (zeige CREB1 Antikörper) and c-Myc (zeige MYC Antikörper) maintain the transcriptional activity of STING
Data show that mice defective in cyclic GMP (zeige NT5C2 Antikörper)-AMP (zeige TMPRSS5 Antikörper) synthase (cGAS) or STING protein (STING) are highly susceptible to acute herpes simplex encephalitis (HSE (zeige HSD17B6 Antikörper)) .
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.
DsbA-L (zeige GSTK1 Antikörper) prevents obesity-induced inflammation and insulin (zeige INS Antikörper) 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 (zeige TBK1 Antikörper)/IRF3 (zeige IRF3 Antikörper) dependent.
Intratumoral administration of the STING agonist cyclic di-GMP (zeige NT5C2 Antikörper) (CDG) or Flt3 Ligand (Flt3L (zeige FLT3LG Antikörper)) augmented the therapeutic effect of systemic triple checkpoint modulation and promoted the cure of 75% of mice with bilateral TRAMP (zeige DPT Antikörper)-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 (zeige SAMHD1 Antikörper) limits virus-induced production of interferons and the induction of co-stimulatory markers
STING activated an antiviral/type I interferon (zeige IFNA Antikörper) response with live but not killed S. aureus.
Data show that stimulator of interferon (zeige IFNA Antikörper) genes (STING)-associated vasculopathy with onset in infancy (SAVI)-associated STING N153S mutation triggers IRF3 (zeige IRF3 Antikörper)-independent immune cell dysregulation and lung disease in mice.
These results highlight the crucial role of MFN1 (zeige MFN1 Antikörper) in maintaining the competency of the STING pathway.
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