English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Zendy Plus

Presents the zaia usage as premium feature

ZAIA

Presents the pdf analysis as premium feature

PDF Analysis

Insights

Presents the summarisation as premium feature

Summarisation

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the access of premium content as premium feature

Premium Content

Zendy Tools

Zendy Open

Mutations in  CRB1 , the human homolog of  Drosophila Crumbs , cause autosomal recessive blinding disorders of the retina. Whereas Crumbs is implicated in apical-basal epithelial polarity and photoreceptor morphogenesis, the role of CRB1 in normal or diseased retina remains unclear. We characterized the retinal organization  in vivo  of patients with  CRB1  mutations and found that, unlike other inherited retinal degenerations studied to date, the  CRB1  mutant retinas are remarkably thick in cross-section and lack the distinct layers of normal adult retina. There are coarse outer and inner zones and a thick surface layer around the optic nerve. The abnormal retinal architecture in  CRB1  mutations resembles that of immature normal retina. The results suggest that the  CRB1  disease pathway disturbs the development of normal human retinal organization by interrupting naturally occurring apoptosis.

Crumbs homolog 1 (CRB1) mutations result in a thick human retina with abnormal lamination