Abstract:
:The ankyrin repeat and sterile α motif (SAM) domain-containing six gene (Anks6) is a candidate for polycystic kidney disease (PKD). Originally identified in the PKD/Mhm(cy/+) rat model of PKD, the disease is caused by a mutation (R823W) in the SAM domain of the encoded protein. Recent studies support the etiological role of the ANKS6 SAM domain in human cystic diseases, but its function in kidney remains unknown. To investigate the role of ANKS6 in cyst formation, we screened an archive of N-ethyl-N-nitrosourea-treated mice and derived a strain carrying a missense mutation (I747N) within the SAM domain of ANKS6. This mutation is only six amino acids away from the PKD-causing mutation (R823W) in cy/+ rats. Evidence of renal cysts in these mice confirmed the crucial role of the SAM domain of ANKS6 in kidney function. Comparative phenotype analysis in cy/+ rats and our Anks6(I747N) mice further showed that the two models display noticeably different PKD phenotypes and that there is a defective interaction between ANKS6 with ANKS3 in the rat and between ANKS6 and BICC1 (bicaudal C homolog 1) in the mouse. Thus, our data demonstrate the importance of ANKS6 for kidney structure integrity and the essential mediating role of its SAM domain in the formation of protein complexes.
journal_name
Kidney Intjournal_title
Kidney internationalauthors
Bakey Z,Bihoreau MT,Piedagnel R,Delestré L,Arnould C,de Villiers Ad,Devuyst O,Hoffmann S,Ronco P,Gauguier D,Lelongt Bdoi
10.1038/ki.2015.122subject
Has Abstractpub_date
2015-08-01 00:00:00pages
299-310issue
2eissn
0085-2538issn
1523-1755pii
S2157-1716(15)32166-3journal_volume
88pub_type
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pub_type: 共识发展会议,杂志文章,评审
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