mProX™ Human STING1 Stable Cell Line

Product Information

Target Family

Other Targets

Target Protein Species

Human

Host Cell Type

HEK293;CHO-K1;PANC-1

Target Classification

Other Targets Drug Discovery Assays and Products

Target Research Area

Cardiovascular Research

Related Diseases

Sting-Associated Vasculopathy, Infantile-Onset; Sting-Associated Vasculopathy With Onset In Infancy

Gene ID

Human:340061

UniProt ID

Human:Q86WV6

Product Properties

Biosafety Level

Level 1

Activity

Yes

Quantity

10⁶ cells per vial

Applications

STING1, also known as Stimulator of Interferon Genes, is a crucial protein in the human body that plays a pivotal role in the innate immune response to cytosolic DNA. When DNA is detected in the cytoplasm, STING1 becomes activated, leading to the production of type I interferons and other pro-inflammatory cytokines. This mechanism is essential for the body's defense against viral infections and certain bacterial infections. Moreover, STING1 has been identified as a potential therapeutic target for autoimmune diseases, where the immune system mistakenly attacks the body's own cells. This is because aberrant activation of STING1 can lead to excessive inflammation, contributing to the pathogenesis of these diseases. Additionally, the STING1 pathway has been implicated in cancer, particularly in the context of the tumor microenvironment. Activation of STING1 in tumor cells can lead to an immune response against the tumor, making it a promising target for cancer immunotherapy. Recent research has also highlighted the role of STING1 in cardiovascular diseases, neurodegenerative diseases, and metabolic disorders, underscoring its importance in various physiological and pathological processes.

Protocols

Please visit our protocols page.

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FAQ

chat Casey Johnson (Verified Customer)

What role does STING1 play in ferroptosis and pancreatic cancer? Jan 20 2023

chat Patrick Liam (Creative Biolabs Scientific Support)

STING1 promotes ferroptosis, a form of cell death, through MFN1/2-dependent mitochondrial fusion, impacting the sensitivity of pancreatic cancer cells to this process. Jan 20 2023

chat Peyton Brown (Verified Customer)

How is STING1 involved in the formation of the rafeesome and its secretion? Oct 08 2023

chat Patrick Liam (Creative Biolabs Scientific Support)

Activated STING1 is secreted through its packaging into the rafeesome, a novel organelle formed by the fusion of non-canonical autophagosome with an early endosome. Oct 08 2023

Published Data

Fig.1 Knockdown of STING1 in PANC1 cells

The analysis of STING1 expression in PANC1 cells was performed using Western blotting, with a focus on the comparison between control cells and STINGKD cells.

Ref: Li, Changfeng, et al. "STING1 promotes ferroptosis through MFN1/2-dependent mitochondrial fusion." Frontiers in cell and developmental biology 9 (2021): 698679.

Pubmed: 34195205

DOI: 10.3389/fcell.2021.698679

Research Highlights

Rhzioual Berrada, Kenza. et al. "Lung Transplantation under a Janus Kinase Inhibitor in Three Patients with SAVI Syndrome." Journal of clinical immunology, 2023.
The rare autoinflammatory disease known as Stimulator of Interferon Genes (STING)-associated Vasculopathy with Onset in Infancy (SAVI) is caused by a mutation in the STING1 gene. It is characterized by recurrent fever episodes and skin and respiratory issues, including interstitial lung disease and alveolar hemorrhage. In most cases, SAVI involves respiratory complications, which can progress to severe lung fibrosis and may require lung transplantation (LT). While three patients with SAVI have received LT, two of them have died due to multiple organ failure or sepsis within months or years after the procedure. The diagnosis of SAVI was made post-LT, preventing the implementation of targeted treatment like the Janus kinase 1 and 2 inhibitor ruxolitinib, which could potentially improve the respiratory condition of these patients. This article aims to present the experiences of three SAVI patients who received ruxolitinib prior to undergoing LT at three major lung transplantation centers in France. The study also discusses any post-transplant complications that arose and the overall outcomes of the patients.
Rhzioual Berrada, Kenza. et al. "Lung Transplantation under a Janus Kinase Inhibitor in Three Patients with SAVI Syndrome." Journal of clinical immunology, 2023.
Pubmed: 37814086 DOI: 10.1007/s10875-023-01595-4

Wang, Yulin. et al. "STING activation promotes autologous type I interferon-dependent development of type 1 regulatory T cells during malaria." The Journal of clinical investigation, 2023.
The development of effective malaria vaccines and improved drug treatment protocols is crucial for the eradication of malaria. However, the rapid formation of immune regulatory networks in response to malaria parasites poses a challenge. In this study, the authors identified STING, a molecule involved in interferon production, as a key mediator for the development of IL-10 and IFN-Œ≥-producing CD4+ T cells during Plasmodium falciparum infection. The importance of type I IFN signaling for the development of these cells was validated in a preclinical malaria model. Additionally, STING expression and activation were found to increase in CD4+ T cells following infection in healthy individuals, specifically in IL-10 and IFN-Œ≥-producing cells. These findings highlight the critical role of STING in promoting type I IFN production and the activation of IL-10 and IFN-Œ≥-producing CD4+ T cells during malaria.
Wang, Yulin. et al. "STING activation promotes autologous type I interferon-dependent development of type 1 regulatory T cells during malaria." The Journal of clinical investigation, 2023.
Pubmed: 37781920 DOI: 10.1172/JCI169417