Literature DB >> 20412686

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

Bengi Acar-Perk1, Karen Bräutigam, Regina Grunewald, Andreas Schmutzler, Christian Schem, Norbert K Arnold, Walter Jonat, Jörg Weimer.   

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.

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Year:  2010        PMID: 20412686      PMCID: PMC2855038     

Source DB:  PubMed          Journal:  Comp Med        ISSN: 1532-0820            Impact factor:   0.982


  16 in total

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Authors:  María Llamazares; Alvaro J Obaya; Angela Moncada-Pazos; Ritva Heljasvaara; Jesús Espada; Carlos López-Otín; Santiago Cal
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  2 in total

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Journal:  Oncotarget       Date:  2018-03-23

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Journal:  Front Immunol       Date:  2018-04-19       Impact factor: 7.561

  2 in total

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