Preparing your results

Our searching services are busy right now. Your search will reload in five seconds.

X
Forgot Password

If you have forgotten your password you can enter your email here and get a temporary password sent to your email.

A defect in a novel ADAMTS family member is the cause of the belted white-spotting mutation.

http://www.ncbi.nlm.nih.gov/pubmed/12925592

Several features of the pigment defect in belted (bt) mutant mice suggest that it occurs as a result of a defect in melanocyte development that is unique from those described for other classical white-spotting mutations. We report here that bt mice carry mutations in Adamts20, a novel member of the ADAMTS family of secreted metalloproteases. Adamts20 shows a highly dynamic pattern of expression in the developing embryo that generally precedes the appearance of melanoblasts in the same region, and is not expressed in the migrating cells themselves. Adamts20 shows remarkable homology with GON-1, an ADAMTS family protease required for distal tip cell migration in C. elegans. Our results suggest that the role of ADAMTS proteases in the regulation of cell migration has been conserved in mammalian development.

Pubmed ID: 12925592 RIS Download

Mesh terms: ADAM Proteins | Animals | Cell Movement | Disintegrins | Embryo, Mammalian | Gene Expression Regulation, Developmental | Humans | In Situ Hybridization | Melanocytes | Metalloendopeptidases | Mice | Mice, Inbred C57BL | Mutation | Phylogeny | Pigmentation | Skin

Research resources used in this publication

None found

Research tools detected in this publication

None found

Data used in this publication

None found

Associated grants

  • Agency: NIAMS NIH HHS, Id: AR049930
  • Agency: NICHD NIH HHS, Id: HD29028
  • Agency: NHGRI NIH HHS, Id: HG02155

Publication data is provided by the National Library of Medicine ® and PubMed ®. Data is retrieved from PubMed ® on a weekly schedule. For terms and conditions see the National Library of Medicine Terms and Conditions.