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ADGRG2, an orphan GPCR, when coupled to CFTR via a regional Gq signaling on the apical membrane, acts to regulate efferent duct fluid reabsorption making it essential for male fertility.

Cell cycle arrest in response to a double-stranded break is initially maintained by the DNA damage checkpoint and later by the spindle assembly checkpoint.

Metabolic cues enlist ubiquitin ligase adaptors for the selective control of cellular nutrient acquisition strategies.

NF-κB oscillations synchronize to external perturbations as a damped oscillator, producing different transcription dynamics.

A novel regulatory step in the endocytic pathway, which occurs post-internalization, takes place at the trans-Golgi network and involves the arrestin-related protein Rod1 and the ubiquitin ligase Rsp5.

Spontaneous growth arrest of transformed melanocytes (resulting in benign “moles”) does not result from cell-autonomous oncogene-induced senescence, but can be explained by collective mechanisms used in normal tissue size control.

Systematic screen of HIV-1 Vif mutants identifies synthetic and naturally occurring amino acid polymorphisms separating PPP2R5 and APOBEC3 family protein depletion and uncovers the mechanism of Vif-dependent cell cycle arrest.

The far C-terminal domain of CpxII interferes with SNARE assembly and thereby arrests tonic exocytosis.

Development, validation, and use of an effector membrane translocation biosensor platform reveals G protein coupling selectivity signatures for 100 GPCRs that range from remarkable selectivity to full promiscuity toward the different G protein subtypes.

Wnts can act synergistically to affect G2 arrest via transcriptional upregulation of a Checkpoint Kinase in the absence of any detectable DNA damage.