The t(14,15) in mouse strain CBA/CaH-T(14;15)6Ca/J causes a break in the ADAMTS12 gene.

Abstract

The mouse strain CBA/CaH-T(14;15)6Ca/J carries a homozygous balanced reciprocal translocation between mouse chromosomes 14 and 15, but the break points of this translocation have not previously been examined in detail. Using fluorescent in situ hybridization, we assigned the break point in 14qE3 to a 200-kb region devoid of any known gene. We similarly defined the break point in 15qA1 to a 27-kb region containing involving ADAMTS12. The chromosomal break likely is between exons 2 and 3 of ADAMTS12. This gene encodes a disintegrin and metalloproteinase with thrombospondin motifs, and this product plays crucial roles in both vascularization and cancer progression and has been implicated in the development of arthritis. The CBA/CaH-T(14;15)6Ca/J mouse strain likely is a suitable model for further examination of the influences of defective ADAMTS12 in various pathologic processes.

• Authors: Bengi Acar-Perk, Karen Bräutigam, Regina Grunewald, Andreas Schmutzler, Christian Schem, Norbert K Arnold, Walter Jonat, Jörg Weimer
• Journal: Comparative medicine (Comp Med) Vol. 60 Issue 2 Pg. 118-22 (Apr 2010) ISSN: 2769-819X [Electronic] United States
• PMID: 20412686 (Publication Type: Journal Article)

Chemical References

• ADAM Proteins
• ADAMTS Proteins
• Adamts12 protein, mouse

Topics

• ADAM Proteins (genetics, metabolism)
• ADAMTS Proteins
• Animals
• Cells, Cultured
• Chromosome Breakage
• Chromosomes, Mammalian
• Disease Models, Animal
• Exons
• Female
• Fibroblasts (cytology, metabolism)
• Gene Expression
• Humans
• In Situ Hybridization, Fluorescence
• Male
• Mice
• Mice, Inbred CBA
• Mice, Inbred Strains