Fig. 8.

Scheme of the proposed cellular mechanisms involved in the induction and accumulation of CLEC10A ligands. a Under normal conditions, glycan structures of newly synthesized mucin-like proteins are elongated in the Golgi compartment and transported to the plasma membrane (PM). For degradation, proteins are internalized and delivered via early endosomes (E.E.) to the lysosome or are recycled. b Estrogen depletion, 4-hydroxy-tamoxifen or cell stress inducing substances lead to the accumulation of CLEC10A ligands at the plasma membrane through several mechanisms: 1) increase in levels of acceptor protein such as MUC1, 2) increased expression of GalNT2 and GalNT6 and translocation of GalNTs to the trans Golgi compartment and 3) impaired degradation due to dysfunctional endosomes and lysosomes