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用于骨骼疾病研究的小鼠 Cre 模型。

Mouse Cre Models for the Study of Bone Diseases.

机构信息

Department of Oral and Craniofacial Sciences, School of Dentistry, University of Missouri, 650 E. 25th Street, Kansas, MO, 64108, USA.

出版信息

Curr Osteoporos Rep. 2018 Aug;16(4):466-477. doi: 10.1007/s11914-018-0455-7.

DOI:10.1007/s11914-018-0455-7
PMID:29934753
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6397767/
Abstract

PURPOSE

Transgenic Cre lines are a valuable tool for conditionally inactivating or activating genes to understand their function. Here, we provide an overview of Cre transgenic models used for studying gene function in bone cells and discuss their advantages and limitations, with particular emphasis on Cre lines used for studying osteocyte and osteoclast function.

RECENT FINDINGS

Recent studies have shown that many bone cell-targeted Cre models are not as specific as originally thought. To ensure accurate data interpretation, it is important for investigators to test for unexpected recombination events due to transient expression of Cre recombinase during development or in precursor cells and to be aware of the potential for germ line recombination of targeted genes as well as the potential for unexpected phenotypes due to the Cre transgene. Although many of the bone-targeted Cre-deleter strains are imperfect and each model has its own limitations, their careful use will continue to provide key advances in our understanding of bone cell function in health and disease.

摘要

目的

转基因 Cre 系是一种非常有价值的工具,可用于条件性地使基因失活或激活,以了解其功能。本文概述了用于研究骨细胞中基因功能的 Cre 转基因模型,并讨论了它们的优缺点,特别强调了用于研究骨细胞和破骨细胞功能的 Cre 系。

最近的发现

最近的研究表明,许多针对骨细胞的 Cre 模型并不像最初想象的那样具有特异性。为了确保准确解释数据,研究人员非常有必要针对由于 Cre 重组酶在发育过程中或前体细胞中的瞬时表达而导致的意外重组事件进行测试,并了解靶向基因的生殖系重组以及由于 Cre 转基因而导致的意外表型的可能性。尽管许多针对骨的 Cre 缺失菌株并不完美,并且每种模型都有其自身的局限性,但只要谨慎使用,它们将继续为我们深入了解健康和疾病状态下骨细胞的功能提供关键进展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dcf9/6397767/2658b7954e44/nihms-1013985-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dcf9/6397767/4a5b8fe5db7f/nihms-1013985-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dcf9/6397767/2658b7954e44/nihms-1013985-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dcf9/6397767/4a5b8fe5db7f/nihms-1013985-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dcf9/6397767/2658b7954e44/nihms-1013985-f0002.jpg

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NOTCH2 Hajdu-Cheney Mutations Escape SCF-Dependent Proteolysis to Promote Osteoporosis.NOTCH2 Hajdu-Cheney突变逃避SCF依赖的蛋白水解作用以促进骨质疏松症。
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骨特异性赖氨酰羟化酶2基因敲除小鼠的产生及其表型。
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