mProX™ Human STAT1 Stable Cell Line

Chu, Zhenzhen. et al. "A DNA/RNA heteroduplex oligonucleotide coupling asparagine depletion restricts FGFR2 fusion-driven intrahepatic cholangiocarcinoma." Molecular therapy. Nucleic acids, 2023.
The article discusses the development of a cholesterol-conjugated DNA/RNA heteroduplex oligonucleotide targeting the chimeric site in the FGFR2 fusion message, in order to improve the targeting of FGFR2 fusions, which is an unmet clinical need for the pan-FGFR inhibitor, pemigatinib. This inhibitor has been approved to treat intrahepatic cholangiocarcinoma (ICC) with FGFR2 fusion mutations. The study highlights the potential of this novel approach to enhance the efficacy of pemigatinib and overcome its pan selectivity and resistance.
Chu, Zhenzhen. et al. "A DNA/RNA heteroduplex oligonucleotide coupling asparagine depletion restricts FGFR2 fusion-driven intrahepatic cholangiocarcinoma." Molecular therapy. Nucleic acids, 2023.
Pubmed: 37869260   DOI: 10.1016/j.omtn.2023.102047

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.
The hyperexpression of human leukocyte antigen class I (HLA-I) molecules on pancreatic beta-cells is a well-established characteristic of the pathogenesis of type 1 diabetes. This phenomenon has important clinical implications as it increases the susceptibility of beta-cells to attack by autoreactive CD8+ T-cells, causing accelerated disease progression. This review delves into the key factors that contribute to HLA-I hyperexpression on beta-cells and assesses their clinical significance. Current evidence suggests that interferons released from beta-cells, particularly type I or III interferons triggered by viral infections or incited by autoreactive immune cells, are likely drivers of this process. Activation of Janus Kinase/Signal Transducer and Activator of Transcription (JAK/STAT) pathways is responsible for the subsequent induction of interferon stimulated genes. Various models have demonstrated that exposure to interferons leads to increased HLA-I expression in beta-cells and that STAT1, STAT2, and interferon regulatory factor 9 (IRF9) play pivotal roles in mediating this response depending on the type of interferon involved. Notably, elevated levels of STAT1 have been observed in the beta-cells of individuals newly diagnosed with type 1 diabetes, with a direct correlation found between STAT1 expression and HLA-I hyperexpression at the level of individual islets. These findings can be reproduced in different models and suggest that STAT1 may serve as an important biomarker for the assessment of HLA-I hyperexpression in beta-cells during the early stages of type 1 diabetes.
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