STAT Transcription Factors

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  Subject Areas on Research

  • A comparative transcriptomic analysis of astrocytes differentiation from human neural progenitor cells. 
  • Accelerated cell cycles enable organ regeneration under developmental time constraints in the Drosophila hindgut. 
  • Constitutive Interferon Maintains GBP Expression Required for Release of Bacterial Components Upstream of Pyroptosis and Anti-DNA Responses. 
  • Differential loss of prolyl isomerase or chaperone activity of Ran-binding protein 2 (Ranbp2) unveils distinct physiological roles of its cyclophilin domain in proteostasis. 
  • Differential requirement for STAT by gain-of-function and wild-type receptor tyrosine kinase Torso in Drosophila. 
  • Distinct functional programming of human fetal and adult monocytes. 
  • Enterovirus 2Apro Cleavage of the YTHDF m6A Readers Implicates YTHDF3 as a Mediator of Type I Interferon-Driven JAK/STAT Signaling. 
  • High circulatory leptin mediated NOX-2-peroxynitrite-miR21 axis activate mesangial cells and promotes renal inflammatory pathology in nonalcoholic fatty liver disease. 
  • Inositol phosphate kinase 2 is required for imaginal disc development in Drosophila. 
  • Interorgan regulation of Drosophila intestinal stem cell proliferation by a hybrid organ boundary zone. 
  • JAK inhibitor blocks COVID-19 cytokine-induced JAK/STAT/APOL1 signaling in glomerular cells and podocytopathy in human kidney organoids. 
  • JAK-STAT and G-protein-coupled receptor signaling pathways are frequently altered in epitheliotropic intestinal T-cell lymphoma. 
  • Paracrine signaling through the JAK/STAT pathway activates invasive behavior of ovarian epithelial cells in Drosophila. 
  • Requirement for JAK/STAT signaling throughout border cell migration in Drosophila. 
  • SOCS36E, a novel Drosophila SOCS protein, suppresses JAK/STAT and EGF-R signalling in the imaginal wing disc. 
  • Sox2 cooperates with Lkb1 loss in a mouse model of squamous cell lung cancer. 
  • Tyrosine phosphorylation is required for functional activation of disulfide-containing constitutively active STAT mutants.