The primary spongiosa, in particular, was reported to be irregular in SRPS cases with DYNC2H1 mutations [4] with loss of degradation of the mineralized hypertrophic zone, supporting the potential role of the dynein-2 complex in orchestrating the development of normal endochondral bone formation.
![[This page as RDF]](http://data.gesis.org/somesci/static/rdf-icon.gif){kind=icon}