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.