mProX™ Human STAT2 Stable Cell Line

Product Information

Target Family

Immune Checkpoint

Target Protein Species

Human

Host Cell Type

HEK293;CHO-K1;A375

Target Classification

Immune Checkpoint Cell Lines

Target Research Area

Immunology Research

Related Diseases

Pseudo-Torch Syndrome 3; Immunodeficiency 44

Gene ID

Human:6773

UniProt ID

Human:P52630

Product Properties

Biosafety Level

Level 1

Activity

Yes

Quantity

10⁶ cells per vial

Applications

STAT2, a component of the JAK-STAT signaling pathway, has various applications in different fields. In the context of type 1 diabetes, STAT2 is involved in driving the hyperexpression of human leukocyte antigen class I (HLA-I) molecules on pancreatic beta-cells, which is a hallmark feature of the disease. Understanding the factors that drive HLA-I hyperexpression and the role of STAT2 in this process can provide insights into disease progression and potential therapeutic targets. Additionally, STAT2 is implicated in the inflammatory response in the gastrointestinal tract, particularly in inflammatory bowel disease (IBD). By studying the colon transcriptome of mouse strains, researchers identified modules enriched for IBD-dysregulated genes that are responsive to STAT2. This highlights the role of STAT2 in the gene-by-environment interactions underlying inflammation and IBD. In the field of virology, STAT2 is targeted by viral proteins to antagonize the type I interferon response, which is a crucial defense mechanism against viral infections. For example, Seneca Valley virus (SVV) inhibits the IFN signaling pathway by degrading STAT1, STAT2, and interferon regulatory factor 9 (IRF9) through its proteinase activity. This allows SVV to evade the host immune response and promote viral replication. Overall, STAT2 plays a significant role in autoimmune diseases, inflammatory disorders, and viral infections, making it a valuable target for research and potential therapeutic interventions.

Protocols

Please visit our protocols page.

Customer Reviews

There are currently no Customer reviews or questions for mProX™ Human STAT2 Stable Cell Line (S01YF-1023-PY216). Click the button above to contact us or submit your feedback about this product.

FAQ

chat Casey Smith (Verified Customer)

What is the role of STAT2 in macrophage inflammatory response? Jan 09 2020

chat Patrick Liam (Creative Biolabs Scientific Support)

FABP4 activates the JAK2/STAT2 pathway in macrophages, contributing to the inflammatory response in atherosclerosis. This indicates the involvement of STAT2 in macrophage-mediated inflammation in cardiovascular diseases. Jan 09 2020

chat Morgan Jones (Verified Customer)

Can STAT2 signaling be manipulated for therapeutic purposes? Jun 22 2020

chat Patrick Liam (Creative Biolabs Scientific Support)

STAT2 signaling plays a crucial role in antiviral immune responses. Manipulating STAT2 signaling pathways, such as through the use of specific inhibitors, could be a potential therapeutic strategy in viral infections like COVID-19. Jun 22 2020

Published Data

Fig.1 After ve***en*b treatment, IRF9- or STAT2-knockdown A375 cells had smaller tumors, but IRF9- or STAT2-overexpressing cells had larger tumors.

The level of IRF9/STAT2 expression was linked to the therapeutic impact of VEM treatment in vivo. IRF9 or STAT2 KD enhanced tumor responsiveness to VEM treatment in a subcutaneous mouse tumor model, resulting in decreased tumor volume, tumor weight, and clinical tumor size. IRF9 or STAT2 OE decreased tumor responsiveness to VEM therapy, resulting in increased tumor volume, weight, and clinical tumor size.

Ref: Wang, Dan, et al. "Increased IRF9-STAT2 Signaling Leads to Adaptive Resistance toward Targeted Therapy in Melanoma by Restraining GSDME-Dependent Pyroptosis." Journal of Investigative Dermatology 142.9 (2022): 2476-2487.

Pubmed: 35148998

DOI: 10.1016/j.jid.2022.01.024

Research Highlights

A Russell, Mark. et al. "The role of the interferon/JAK-STAT axis in driving islet HLA-I hyperexpression in type 1 diabetes." Frontiers in endocrinology, 2023.
Human leukocyte antigen class I (HLA-I) hyperexpression on pancreatic beta-cells is a defining characteristic of type 1 diabetes pathogenesis. Its clinical significance lies in its potential to attract autoreactive CD8+ T-cells, hastening disease progression. This literature review delves into the factors driving HLA-I hyperexpression and their impact in clinical contexts. Research has revealed the crucial role of residual beta-cells in mediating HLA-I hyperexpression at all stages of the disease. Possible drivers include interferons from beta-cells (type I or III) and those from autoreactive immune cells (type II). Activation of Janus Kinase/Signal Transducer and Activator of Transcription (JAK/STAT) pathways leads to the induction of interferon stimulated genes. Studies have shown that interferons upregulate HLA-I expression in beta-cells through the involvement of STAT1, STAT2, and interferon regulatory factor 9 (IRF9), depending on the type of interferon. Notably, STAT1 levels are significantly elevated in recent-onset type 1 diabetes, correlating with increased HLA-I hyperexpression on individual beta-cells. This phenomenon can be replicated in various models.
A Russell, Mark. et al. "The role of the interferon/JAK-STAT axis in driving islet HLA-I hyperexpression in type 1 diabetes." Frontiers in endocrinology, 2023.
Pubmed: 37867531 DOI: 10.3389/fendo.2023.1270325

Li, Xiaoxu. et al. "Genetic and dietary modulators of the inflammatory response in the gastrointestinal tract of the BXD mouse genetic reference population." eLife, 2023.
A study was conducted to investigate the impact of dietary, environmental, and genetic factors on inflammatory gut disorders, particularly inflammatory bowel disease (IBD). The study analyzed the colon transcriptome of 52 BXD mouse strains, which were fed a chow or high-fat diet (HFD). Results showed that a subset of BXD strains exhibited an IBD-like transcriptome signature on HFD, suggesting that a combination of genetics and diet plays a significant role in intestinal inflammation. Gene co-expression analyses further revealed that IBD-related modules share network hubs that are both influenced by diet and genetically regulated.
Li, Xiaoxu. et al. "Genetic and dietary modulators of the inflammatory response in the gastrointestinal tract of the BXD mouse genetic reference population." eLife, 2023.
Pubmed: 37855835 DOI: 10.7554/eLife.87569