Nup358 restricts ER-mitochondria connectivity by modulating mTORC2/Akt/GSK3β signalling.

ER-mitochondria contact sites (ERMCSs) regulate processes, including calcium homoeostasis, energy metabolism and autophagy. Previously, it was shown that during growth factor signalling, mTORC2/Akt gets recruited to and stabilizes ERMCSs. Independent studies showed that GSK3β, a well-known Akt substrate, reduces ER-mitochondria connectivity by disrupting the VAPB-PTPIP51 tethering complex.

SUMOylation modulates the function of DDX19 in mRNA export.

Nuclear export of mRNAs is a critical regulatory step in eukaryotic gene expression. The mRNA transcript undergoes extensive processing, and is loaded with a set of RNA-binding proteins (RBPs) to form export-competent messenger ribonucleoprotein particles (mRNPs) in the nucleus. During the transit of mRNPs through the nuclear pore complex (NPC), the DEAD-box ATPase - DDX19 (herein referring to DDX19A and DDX19B) - remodels mRNPs at the cytoplasmic side of the NPC, by removing a subset of RNA-binding proteins to terminate mRNP export.