Transporter that mediates resorption of neutral amino acids across the apical membrane of renal and intestinal epithelial cells (PubMed:15286787, PubMed:15286788, PubMed:18424768, PubMed:18484095, PubMed:19185582, PubMed:26240152). This uptake is sodium-dependent and chloride-independent (PubMed:15286787, PubMed:19185582, PubMed:15286788). Requires CLTRN in kidney or ACE2 in intestine for cell surface expression and amino acid transporter activity (PubMed:19185582, PubMed:18424768). L-alanine(in) + Na(+)(in) = L-alanine(out) + Na(+)(out) L-cysteine(in) + Na(+)(in) = L-cysteine(out) + Na(+)(out) L-glutamine(in) + Na(+)(in) = L-glutamine(out) + Na(+)(out) glycine(in) + Na(+)(in) = glycine(out) + Na(+)(out) L-isoleucine(in) + Na(+)(in) = L-isoleucine(out) + Na(+)(out) L-leucine(in) + Na(+)(in) = L-leucine(out) + Na(+)(out) L-methionine(in) + Na(+)(in) = L-methionine(out) + Na(+)(out) L-phenylalanine(in) + Na(+)(in) = L-phenylalanine(out) + Na(+)(out) L-serine(in) + Na(+)(in) = L-serine(out) + Na(+)(out) L-tryptophan(in) + Na(+)(in) = L-tryptophan(out) + Na(+)(out) L-tyrosine(in) + Na(+)(in) = L-tyrosine(out) + Na(+)(out) L-valine(in) + Na(+)(in) = L-valine(out) + Na(+)(out) Interacts in a tissue-specific manner with ACE2 in small intestine and with CLTRN in the kidney (By similarity). Interacts with CLTRN; this interaction is required for trafficking of SLC6A19 to the plasma membrane and for its catalytic activation in kidneys (By similarity). Interacts with ACE2; this interaction is required for trafficking of SLC6A19 to the plasma membrane and for its catalytic activation in intestine (PubMed:32132184). Interacts with ANPEP; the interaction positively regulates its amino acid transporter activity (By similarity). Colocalizes with ACE2 on the apical membrane of cells lining villi of the jejunum, ileum and on kidney proximal tubules. Robust expression in kidney and small intestine, with minimal expression in pancreas (PubMed:18424768, PubMed:15286787). Also expressed in stomach, liver, duodenum, ileocecum, colon and prostate. Not detected in testis, whole brain, cerebellum, fetal liver, spleen, skeletal muscle, uterus, heart or lung. The disease is caused by variants affecting the gene represented in this entry. The disease may be caused by variants affecting the gene represented in this entry. SLC6A19 deficiency combined with haploinsufficiency of SLC6A20 or partially inactivating mutations in SLC36A2, can be responsible for hyperglycinuria. The disease may be caused by variants affecting the gene represented in this entry. SLC6A19 deficiency combined with haploinsufficiency of SLC6A20 or partially inactivating mutations in SLC36A2, can be responsible for iminoglycinuria. Additional polymorphisms and mutations in SLC6A18 can contribute to the IG phenotype in some families. Belongs to the sodium:neurotransmitter symporter (SNF) (TC 2.A.22) family. SLC6A19 subfamily.