COL2CREERT2, A MOUSE MODEL FOR A CHONDROCYTE-SPECIFIC AND INDUCIBLE GENE DELETION

被引：16

作者：

Chen, M. ^{[1
]}

Li, S. ^{[2
]}

Xie, W. ^{[2
,3
]}

Wang, B. ^{[4
,5
]}

Chen, D. ^{[2
]}

机构：

[1] Columbia Univ, Ctr Craniofacial Regenerat, New York, NY 10032 USA

[2] Rush Univ, Med Ctr, Dept Biochem, Chicago, IL 60612 USA

[3] Liaoning Univ Tradit Chinese Med, Shenyang 110032, Liaoning, Peoples R China

[4] Tianjin Med Univ, Metab Dis Hosp, Key Lab Hormones & Dev, Minist Hlth, Tianjin 300070, Peoples R China

[5] Tianjin Med Univ, Inst Endocrinol, Tianjin 300070, Peoples R China

来源：

EUROPEAN CELLS & MATERIALS | 2014年 / 28卷

关键词：

Animals; cartilage development; cartilage physiology; chondrocytes; gene expression; OSTEOARTHRITIS-LIKE PHENOTYPE; ARTICULAR CHONDROCYTES; CONDITIONAL ACTIVATION; RECOMBINASE ACTIVITY; BINDING-PROTEIN; CRE RECOMBINASE; BONE-FORMATION; SMAD3; GENE; EXPRESSION; TAMOXIFEN;

D O I：

10.22203/eCM.v028a16

中图分类号：

Q813 [细胞工程];

学科分类号：

摘要：

In 2007 and 2008, we published two articles reporting a tamoxifen (TM)-inducible, chondrocyte-specific gene-targeting mouse model in which the expression of CreERT2 is driven by the type II collagen promoter (Col2CreERT2). The fusion protein is specifically expressed and translocated into the nucleus upon TM administration, which in turn triggers gene recombination. Since then, this animal model has become a powerful tool to study the molecular mechanism of skeletal development and degenerative cartilage diseases, including knee joint osteoarthritis (OA), temporomandibular joint (TMJ) OA, and intervertebral disc (IVD) degeneration. In this review article, we summarise the application of Col2CreERT2 mice and discuss the potential usage of this animal model in a broad spectrum of cartilage development and molecular pathology studies.

引用

页码：236 / 245

页数：10

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