PTEN organizes multicellular architecture by non-catalytic scaffolding of spatially localized β-Arrestin1/ARHGAP21/Cdc42 protein complexes to control mitotic spindle orientation, multicellular configuration and lumen formation.
Systematic CRISPR-based editing of tRNA genes revealed that different human cells that span a range of growth rates and different modes of proliferation states require diverse tRNA sets.
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.
Arabidopsis deploys the core signalling module that perceives distinct stress signals, such as DNA damage and heat stresses, and represses G2/M-specific genes, thereby causing cell cycle arrest.
Phosphoproteomics identifies β-arrestin 2 phosphorylation at Thr383 by MEK as a key step of GPCR-induced Erk½ activation, thus providing new insight into the molecular mechanism underlying β-arrestin-dependent GPCR-operated signaling.
β-arrestins recruit Nedd4 ubiquitin E3 ligase to mGlu7 receptor and facilitate ubiquitination, endocytosis, ERK signaling, and stability of mGlu7 at presynaptic terminals.
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.
Time-resolved and site-directed in vivo photo-crosslinking analysis of VemP allows identification of both cis- and trans-elements required for its regulated arrest-cancelation.
