A mitochondrial membrane-bound protein ATAD1 uses conserved structural elements to remove mislocalized membrane proteins from the outer mitochondrial membrane, achieving proper cell organization.

Functionalized protein binders, anchored to specific regions along the cell cortex, provide a novel approach to directly modify protein localization and dispersal in vivo.

Traumatic injury leads to functional defects in nucleocytoplasmic transport and TDP-43 pathology in multiple model systems.

LKB1 instructs the timing and location of synapse layer emergence in the outer retina by coordinating the regulation of pre- and postsynaptic neuron maturation and transport of synapse-associated proteins.

HiLITR is a molecular reporter of protein localization that enables straightforward, large-scale, fluorescence-activated cell sorting-based discovery of genes that regulate complex cellular processes, such as mitochondrial and ER tail-anchored protein trafficking.

Forcing protein associations across the proteome reveals the cell's tolerance for diverse protein interactions and reveals the interactions that affect growth.

Physiological studies of SLC6A17 and its pathogenic mutations revealed that glutamine is transported into synaptic vesicles (SVs) in an SLC6A17-dependent manner and all pathogenic conditions reduced glutamine level in SVs.

Dysfunctions of myelin peroxisomes cause a lysosomal storage-like disorder associated with alterations in glial and axonal membranes, which is the likely cause of nerve impairment in peroxisomal disorders.