Corrigendum to "Ttc21b deficiency attenuates autosomal dominant polycystic kidney disease in a kidney tubular- and maturation-dependent manner." Kidney Int. 2022;102:577-591.

DOI of original article: https://doi.org/10.1016/j.kint.2022.04.034 The authors regret that an incorrect sequence for a quantitative reverse transcription–polymerase chain reaction primer appeared in Supplementary Table S3. The primer and corrected sequence are as follows: mGli1-F: 5′ - CTGACTGTGCCCGAGAGTG – 3. Supplementary Table S3 has been corrected in the Supplementary Material. The authors would like to apologize for any inconvenience caused. Download .pdf (.14 MB) Help with pdf files Supplementary File (PDF) Ttc21b deficiency attenuates autosomal dominant polycystic kidney disease in a kidney tubular- and maturation-dependent mannerKidney InternationalVol. 102Issue 3PreviewPrimary cilia are sensory organelles built and maintained by intraflagellar transport (IFT) multiprotein complexes. Deletion of several IFT-B genes attenuates polycystic kidney disease (PKD) severity in juvenile and adult autosomal dominant polycystic kidney disease (ADPKD) mouse models. However, deletion of an IFT-A adaptor, Tulp3, attenuates PKD severity in adult mice only. These studies indicate that dysfunction of specific cilia components has potential therapeutic value. To broaden our understanding of cilia dysfunction and its therapeutic potential, we investigate the role of global deletion of an IFT-A gene, Ttc21b, in juvenile and adult mouse models of ADPKD. Full-Text PDF