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

Bengi Acar-Perk, Karen Bräutigam, Regina Grunewald, Andreas Schmutzler, Christian Schem, Norbert Arnold, Walter Jonat, Jörg Weimer

4 Zitate (Scopus)

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.

OriginalspracheEnglisch
ZeitschriftComparative Medicine
Jahrgang60
Ausgabenummer2
Seiten (von - bis)118-122
Seitenumfang5
ISSN1532-0820
PublikationsstatusVeröffentlicht - 04.2010

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