Senescent cells contribute to age-related fat dysfunction and can directly impair healthy fat progenitor function, in part, via the secretion of activin A.

Treatment with a JAK inhibitor normalizes multiple biomarkers of autoinflammation and provides therapeutic benefit for diverse immune skin conditions in individuals with Down syndrome.

During neurogenesis, Neurogenin 1 activates the microRNA miR-9, which directly targets the Jak-Stat pathway to inhibit astrogliogenesis.

Distinct hematopoietic waves interact via transcriptional cascades specific to embryonic hemocytes to ensure the proper immune response in Drosophila.​.

The transcription factor STAT5 mediates the increased breast cancer risk associated with a late age pregnancy, but intermittent anti-STAT5 treatment can lower this risk and thus prevent breast cancer.

An intracellular cytokine receptor 'switch' motif is critical for the dimerization of JAK2 and activation of the JAK2 kinase.

Complex I of the mitochondrial respiratory chain is necessary for interferon gamma-mediated responses in antigen-presenting cells and is required for CD4+ T cell activation.

Systemic treatment with di-methyl-amino-parthenolide facilitates CNS axon regeneration and functional recovery by reducing the induction of microtubule detyrosination by established regenerative therapies.

Hyperactive interferon signaling is a hallmark of trisomy 21 and may contribute to many of the comorbidities associated with Down syndrome.

Functional and mechanistic analyses of cancer cells containing homozygous deletion of TP53 and FXR2 reveal that inhibition of FXR1 blocks cell proliferation in a collateral lethality manner, opening an avenue to develop therapies targeting such cancers.