Involved in the retrograde transport from endosome to plasma membrane, a trafficking pathway that promotes the recycling of internalized transmembrane proteins. Following internalization, endocytosed transmembrane proteins are delivered to early endosomes and recycled to the plasma membrane instead of being degraded in lysosomes. SNX27 specifically binds and directs sorting of a subset of transmembrane proteins containing a PDZ-binding motif at the C-terminus: following interaction with target transmembrane proteins, associates with the retromer complex, preventing entry into the lysosomal pathway, and promotes retromer-tubule based plasma membrane recycling. SNX27 also binds with the WASH complex. Interacts with membranes containing phosphatidylinositol-3-phosphate (PtdIns(3P)). May participate in establishment of natural killer cell polarity. Recruits CYTIP to early endosomes. Core component of the SNX27-retromer, a multiprotein complex composed of SNX27, the WASH complex and the retromer complex. Interacts (via the FERM-like regions) with the WASH complex. Interacts with SNX1. Interacts with CYTIP. Interacts with DGKZ. Interacts with MCC (By similarity). Interacts (via PDZ domain) with a number of target transmembrane proteins (via PDZ-binding motif): ABCC4, ADRB2, ARHGEF7, GRIA1, GRIA2, GRIN1, GRIN2A GRIN2C, KCNJ6, KCNJ9 and SLC2A1/GLUT1. Localizes to immunological synapse in T-cells. In T-cells, recruited from the cytosol to sorting endosomes by phosphoinositide-3-kinase products (By similarity). Expressed in cells of hematopoietic origin. The PDZ domain mediates binding to a subset of proteins containing a PDZ-binding motif at the C-terminus: the specificity for PDZ-binding motif is provided by the 2 residues located upstream of the canonical PDZ-binding motif. The PDZ domain also mediates binding to the retromer complex via direct interaction with VPS26 (VPS26A or VPS26B). The PX domain mediates binding to phosphatidylinositol 3-phosphate (PtdIns(3P)) and localization to early endosome membranes. Growth retardation followed by lethality. Some mice die in the uterus during embryonic development. Newborn mice that survive fail to thrive and all die at different times within the first 3 weeks. The body weight of newborn is lower than wild-type mice, and the postnatal growth is severely retarded, with a clear retardation of body weight gain. The growth retardation is not only reflected in the body weight, but also in multiple organs, such as the spleen, kidney, liver, heart and intestine. Mice also show neuronal deficits in the hippocampus and cortex: despite a normal neuroanatomy, defects in synaptic function, learning and memory and a reduction in the amounts of ionotropic glutamate receptors (NMDA and AMPA receptors) are observed. Truncated N-terminus. Truncated C-terminus.