Parallel studies in primary human airway cells and stem cell-derived enteroids show that Enterovirus D-68 differentially infects and induces innate immune signaling in the respiratory and intestinal epithelium.

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

Single-cell and bulk expression analyses reveal that HCMV latent infection drives cells towards a weaker immune-responsive state, which is important for its expression and reactivation.

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

MiRNA-mediated suppression of MAVS expression in embryonic stem cells is necessary to inactivate the type I interferon response.

Hepatitis C virus evades IRF1-dependent intrinsic antiviral immunity by exploiting cyclophilin A and its regulation of PKR.

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.

Mg²⁺-dependent JAK1-mediated phosphorylation sensitizes TRPV2 activity and thermo-threshold, which is counterbalanced by PTPN1-mediated dephosphorylation, highlighting a role of phosphorylation homeostasis in setting the basal activity of TRPV2.

Organoids developed from matched human placental tissue define differences in antiviral signaling between cell types comprising the maternal-fetal interface.