Catalyzes the transfer of galactose from UDP-alpha-D-galactose to lactosylceramide/beta-D-galactosyl-(1->4)-beta-D-glucosyl-(1<->1)-ceramide(d18:1(4E)) to produce globotriaosylceramide/globoside Gb3Cer (d18:1(4E)) (PubMed:10748143). Also able to transfer galactose to galactosylceramide/beta-D-Gal-(1<->1')-Cer (PubMed:10748143). Globoside Gb3Cer is a glycosphingolipid of the globo serie, one of the major types of neutral root structures of glycosphingolipids, that constitute a significant portion of mammalian cell membranes (Probable). Globotriaosylceramide/globoside Gb3Cer in blood and tissue cell membranes is the antigen Pk of blood histogroup P (PubMed:10747952). (Microbial infection) Globotriaosylceramide is one of the cellular ligands for bacterial verotoxins. a beta-D-Gal-(1->4)-beta-D-Glc-(1<->1)-Cer(d18:1(4E)) + UDP-alpha-D-galactose = globoside Gb3Cer (d18:1(4E)) + H(+) + UDP beta-D-Gal-(1<->1')-Cer + UDP-alpha-D-galactose = alpha-D-Gal-(1->4)-beta-D-Gal-(1<->1')-Cer + H(+) + UDP Glycolipid biosynthesis. Ubiquitous. Highly expressed in kidney, heart, spleen, liver, testis and placenta. The conserved DXD motif is involved in enzyme activity. Genetic variation in A4GALT is responsible for the P1PK system blood group phenotypes [MIM:111400]. Different combinations or absence of the P blood group system antigens define 5 different phenotypes: P1, P2, P1(k), P2(k), and p. Genetic variation in A4GALT determines the p phenotype, which is rare and does not express any antigens. It is also known as null phenotype; p individuals have antibodies against P, P1 and Pk antigens in their sera. These antibodies are clinically important because they can cause severe transfusion reactions and miscarriage (PubMed:10993874, PubMed:11896312). Genetic variation in A4GALT is also responsible for the NOR polyagglutination syndrome [MIM:111400]. Polyagglutination is the occurrence of red cell agglutination by virtually all human sera, but not by autologous serum or sera from newborns, creating a risk of complications during transfusions of NOR erythrocytes. It is caused by the unusual Gal(alpha1-4)GalNAc glycolipid epitope (PubMed:22965229). Belongs to the glycosyltransferase 32 family. Lactosylceramide 4-alpha-galactosyltransferase