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Expression analyses and interaction with the anaphase promoting complex protein Apc2 suggest a role for inversin in primary cilia and involvement in the cell cycle

Lookup NU author(s): David Morgan, Dr Lorraine Eley, Professor John SayerORCiD, Professor Tom Strachan, Dr Laura YatesORCiD, Scott Craighead, Professor Judith Goodship


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Homozygous inv mice lack a functional inversin protein and exhibit situs inversus plus severe cystic changes in the kidney and pancreas. Although the inversin sequence has provided few clues to its function, we and others have previously identified calmodulin as a binding partner. We now provide evidence that inversin interacts with the anaphase promoting complex protein Apc2. As expected of an Apc2 target, inversin possesses D-boxes and site-directed mutagenesis of the well-conserved D-box residues abrogates inversin Apc2 interaction. An inversin-specific antibody reveals a dynamic expression pattern throughout the cell cycle and strong expression in the primary cilia of renal epithelium. Our data support a role for inversin in primary cilia and involvement in the cell cycle. Mutations of the proteins polaris, cystin and polycystin-2 which are expressed in renal epithelium primary cilia, lead to renal cystic changes. Aberrant cell proliferation is also involve in cyst development. The data reported here suggest that inversin may provide a link between these two mechanisms.

Publication metadata

Author(s): Morgan D, Eley L, Sayer J, Strachan T, Yates LM, Craighead AS, Goodship JA

Publication type: Article

Publication status: Published

Journal: Human Molecular Genetics

Year: 2002

Volume: 11

Issue: 26

Pages: 3345-3350

ISSN (print): 0964-6906

ISSN (electronic): 1460-2083

Publisher: Oxford University Press


DOI: 10.1093/hmg/11.26.3345


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