[11] Further work on dog kidney cells has shown that a signaling cascade involving the phosphorylation of EGFR by Yes leading to the activation of Rab11FIP5 by MAPK1 upregulates transcytosis.
[12] Transcytosis has been shown to be inhibited by the combination of progesterone and estradiol followed by activation mediated by prolactin in the rabbit mammary gland during pregnancy.
The phosphorylation of caveolin 1 induced by hydrogen peroxide has been shown to be critical to the activation of transcytosis in pulmonary vascular tissue.
Due to the function of transcytosis as a process that transports macromolecules across cells, it can be a convenient mechanism by which pathogens can invade a tissue.
Pharmaceutical companies, such as Lundbeck, are currently exploring the use of transcytosis as a mechanism for transporting therapeutic drugs across the human blood–brain barrier (BBB).
[citation needed] Exploiting the body's own transport mechanism can help to overcome the high selectivity of the BBB, which typically blocks the uptake of most therapeutic antibodies into the brain and central nervous system (CNS).
Monoclonal antibody Trojan horses that target the BBB insulin or transferrin receptor have been in drug development for over 10 years at ArmaGen, Inc., a biotechnology company in Los Angeles.
ArmaGen has re-engineered the missing lysosomal enzyme as a Trojan horse-enzyme fusion protein that crosses the BBB.
Researchers at Genentech proposed the creation of a bispecific antibody that could bind the BBB membrane, induce receptor-mediated transcytosis, and release itself on the other side into the brain and CNS.
The other arm had the previously developed high-affinity anti-BACE1 binding site that would inhibit BACE1 function and prevent amyloid plaque formation.