STAT1
- Known as:
- STAT1
- Catalog number:
- 000478A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- STAT1
Related genes to: STAT1
- Gene:
- STAT1 NIH gene
- Name:
- signal transducer and activator of transcription 1
- Previous symbol:
- -
- Synonyms:
- STAT91, ISGF-3
- Chromosome:
- 2q32.2
- Locus Type:
- gene with protein product
- Date approved:
- 1995-11-08
- Date modifiied:
- 2019-04-23
- Gene:
- STAT2 NIH gene
- Name:
- signal transducer and activator of transcription 2
- Previous symbol:
- -
- Synonyms:
- STAT113
- Chromosome:
- 12q13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1995-11-08
- Date modifiied:
- 2019-04-23
Related products to: STAT1
Related articles to: STAT1
- Mutations in platelet-derived growth factor receptor beta (PDGFRb) cause Kosaki overgrowth syndrome (KOGS). Patients exhibit increased linear growth, craniosynostosis, and thin skin with increased elasticity and scarring. Of the KOGS patients identified to date, three unrelated individuals carried a P584R mutation in the juxtamembrane domain of PDGFRb, resulting in constitutive receptor activation. Due to the limited number of patients, extensive phenotyping and exploration of the molecular basis of disease, including modifier genes, has not been completed. We generated conditional knock-in mice to express mouse PDGFRb with a P583R mutation, corresponding to human P584R, under control of the endogenous Pdgfrb gene. Mutant mice were born at the expected ratio and appeared normal at birth. At 3 weeks of age, mutants began to exhibit connective tissue changes: increased body weight and bone length, craniosynostosis, ectopic bone in the tail and tendons, thin lipodystrophic skin, and high incidence of penile and rectal prolapse. To identify signaling changes caused by mutant PDGFRb signaling, we performed western blotting and phosphoproteomics on dermal fibroblasts. This uncovered increased phosphorylation of PDGFRb, PLCg, Akt1, Shp2, STAT1, STAT2, STAT3, and STAT5. Analysis of 6,621 proteins and 5,386 phosphopeptides identified upregulation of interferon signaling genes linked to STAT1. In many cell types, STAT1 has tumor-suppressor functions and acts to inhibit cell cycle. We generated Stat1-/- Pdgfrb+/P583R mice to test the contribution of STAT1 to KOGS phenotypes. Stat1-deletion exacerbated overgrowth and calvaria dysmorphogensis, and caused keloid-like skin fibrosis. No phenotypes present in the original Pdgfrb+/P583R mice were reverted to normal after Stat1 deletion. Therefore, the P583R mouse model mirrored KOGS phenotypes and increased activation of multiple PDGFRb signaling mediators; in this context, STAT1 activity opposes PDGFRb-driven overgrowth and fibrosis. - Source: PubMed
Publication date: 2026/04/12
Kim JangKwon Hae RyongBerry WilliamOlson Lorin E - Pancreatic ductal adenocarcinoma (PDAC) remains one of the most lethal malignancies because of its typically late diagnosis and limited treatment options, with surgical resection being the primary intervention. Emerging studies have consistently reported associations between PDAC and metabolic dysfunctions, including obesity, chronic inflammation, and diabetes. In this study, we investigated the molecular interplay between PDAC-associated genes and metabolic disorder pathways. - Source: PubMed
Nath DipanwitaDitchfield CaitlinPrice JoshuaSivakumar ShivanJones Simon WAcharjee Animesh - The recent emergence of Severe Acute Respiratory Syndrome Coronavirus (SARS-CoV)-2 highlights the need for greater understanding of the immune evasion mechanisms used by Coronavirus (CoVs) to subvert antiviral responses. Previous global outbreaks caused by Middle East respiratory syndrome coronavirus (MERS-CoV) and SARS-CoV-1 were associated with high mortality rates and limited therapeutic options. Interferon (IFN)-α is the body's natural antiviral agent; but its Janus kinase/signal transducer and activators of transcription (JAK/STAT) signalling pathway is often antagonized by viruses, thereby preventing the upregulation of essential, anti-viral IFN Stimulated Genes (ISGs). Notably, therapeutic IFN-α has disappointingly weak clinical responses in MERS-CoV and SARS-CoV-1 infected patients, indicating that these CoVs inhibit the IFN-α JAK/STAT pathway. We previously identified that MERS-CoV-non-structural protein(nsp)2 and nsp5 and SARS-CoV-1-nsp14 block the IFN-α JAK/STAT signalling pathway in human epithelial A549 cells; however, the mechanisms behind this inhibition remain unknown. In this study, we explored the factors influencing basal STAT1 and STAT2 phosphorylation and discovered that the expression of MERS-CoV-nsp2 and SARS-CoV-1-nsp14, but not MERS-CoV-nsp5, upregulated IFN-λ1/3 in A549 cells. Neutralization of IFN-λ1/3 revealed that this induction was responsible for the observed basal STAT1 and STAT2 phosphorylation, resulting in reduced responsiveness to exogenous IFN-α. Furthermore, both MERS-CoV-nsp2 and SARS-CoV-1-nsp14 induced the expression of USP18, a negative regulator of the IFN-α JAK/STAT pathway, resulting in reduced responsiveness to exogenous IFN-α. Silencing USP18 reinstated IFN-α-mediated STAT1 phosphorylation and ISG induction. Collectively, these findings shed light on the diverse strategies employed by these CoVs to evade type I IFN antiviral responses. While providing evidence for the ineffectiveness of exogenous IFN-α treatment during CoV infection, our discoveries also identify these viral proteins as potential targets for therapeutic intervention. - Source: PubMed
Publication date: 2026/02/19
Zhang YameiStevenson Nigel J - The genus Orthoflavivirus encompasses a group of medically significant arthropod-borne viruses, such as dengue virus (DENV), Japanese encephalitis virus West Nile virus Zika virus (ZIKV), and others, which pose persistent global public health threats. The host interferon (IFN) system constitutes a pivotal first line of defense against these viral infections. However, orthoflaviviruses have evolved a remarkable array of sophisticated strategies to antagonize both the induction and signaling pathways of type I and III IFNs. This review systematically summarizes the mechanisms by which orthoflaviviruses evade the IFN response, primarily by employing viral proteins to target key host factors in pattern recognition receptor signaling pathways (e.g., RIG-I, MDA5, MAVS, TBK1, STING, IRF3) and the JAK-STAT signaling cascade (e.g., STAT1, STAT2, IFNAR1). Furthermore, we highlight the critical and complex roles of IFNs at the placental and blood-brain barriers (BBB), the primary sites for transplacental transmission and neuroinvasion. At these barriers, IFNs play a dual role: they exert essential antiviral effects to restrict viral replication, but may also contribute to immunopathology. The delicate balance of IFN responses determines the outcomes of congenital infection and neurological diseases. Finally, we discuss the therapeutic potential of harnessing the IFN pathway, while also acknowledging the challenges and need for further studies to translate these insights into effective treatments for flavivirus-associated diseases. - Source: PubMed
Publication date: 2026/02/18
Han JiayinYin YueYuan Jing - Glycolysis is a central metabolic pathway that converts glucose into pyruvate. Although pyruvate has been well documented to be a key and terminal metabolite of glycolysis with both energetic and biosynthetic roles, its non-metabolic functions remain unexplored. Here, we report a pyruvate-mediated protein post-translational modification (PTM), protein pyruvylation. We reveal that high glucose-upregulated glycolysis promotes signal transducer and activator of transcription 1 (STAT1) pyruvylation at Lys201 (K201), which blocks STAT1 and signal transducer and activator of transcription 2 (STAT2) interaction, thus suppressing type I interferon (IFN-I) signaling and antiviral immune activity. Consequently, STAT1-K201R knockin mice exhibit enhanced IFN-I antiviral immunity. Importantly, high glucose promotes STAT1 pyruvylation and attenuates immune response to either virus infection or IFN-I treatment in humans. This study identifies the protein pyruvylation modification, reveals a non-metabolic function of the metabolite pyruvate, and provides insights into how high glucose impairs IFN-I antiviral immunity through pyruvate, offering strategies to improve IFN-I immune activity for both preventing and treating viral infections. - Source: PubMed
Publication date: 2026/02/27
Zuo YiboWang QinTian WanyingWang XinheZheng ZhijinHe WeiZhang RenxiaZhao QianMiao YingYuan YukangZhang TingtingCui QunZhang YuerongLiu ChunyanZhou HaiyanZheng Hui