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

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

Clinic of Gynecology and Obstetrics

University of Kiel

4 Citations (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.

Original language	English
Journal	Comparative Medicine
Volume	60
Issue number	2
Pages (from-to)	118-122
Number of pages	5
ISSN	1532-0820
Publication status	Published - 04.2010

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title = "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.",

author = "Bengi Acar-Perk and Karen Br{\"a}utigam and Regina Grunewald and Andreas Schmutzler and Christian Schem and Norbert Arnold and Walter Jonat and J{\"o}rg Weimer",

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journal = "Comparative Medicine",

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T1 - The t(14,15) in mouse strain CBA/CaH-T(14;15)6Ca/J causes a break in the ADAMTS12 gene

AU - Acar-Perk, Bengi

AU - Bräutigam, Karen

AU - Grunewald, Regina

AU - Schmutzler, Andreas

AU - Schem, Christian

AU - Arnold, Norbert

AU - Jonat, Walter

AU - Weimer, Jörg

PY - 2010/4

Y1 - 2010/4

N2 - 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.

AB - 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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M3 - Journal articles

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AN - SCOPUS:77951870301

SN - 1532-0820

VL - 60

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JO - Comparative Medicine

JF - Comparative Medicine

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ER -

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

Abstract

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