Abstract

Kidney agenesis, “broken heart,” abnormal mast cells, somatic overgrowth, lung dysfunction, and chondrodysplasia are some phenotypes of mice where different genes important for heparan sulfate (HS) expression have been knocked out. What can we learn about HS function by studying these mice? In this Perspective we focus on data obtained so far from mouse models where the targets for the genetic modifications are the various enzymes taking part in HS biosynthesis. In addition, we will briefly discuss some mouse models in which genes for HS proteoglycan core proteins have been knocked out.

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call