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在晶状体中表达组成型活性视黄酸受体的转基因小鼠表现出眼部缺陷。

Transgenic mice expressing a constitutively active retinoic acid receptor in the lens exhibit ocular defects.

作者信息

Balkan W, Klintworth G K, Bock C B, Linney E

机构信息

Department of Microbiology and Immunology, Duke University, Durham, North Carolina 27710.

出版信息

Dev Biol. 1992 Jun;151(2):622-5. doi: 10.1016/0012-1606(92)90200-z.

DOI:10.1016/0012-1606(92)90200-z
PMID:1318236
Abstract

Retinoic acid receptors (RARs) modulate gene expression following association with retinoic acid (RA). In transient transfection, an RAR alpha-beta-galactosidase fusion protein (RAR-LacZ) was able to transactivate expression in the absence of RA. When expressed in the ocular lens of transgenic mice, this constitutively active RAR-LacZ fusion gene resulted in founder and progeny animals that exhibited cataracts and microphthalmia, both being characteristics of retinoid-induced teratogenesis. The transgenic phenotypes indicate that retinoid teratogenesis can be mimicked by expression of a constitutively active RAR-LacZ fusion protein in retinoid-sensitive tissues.

摘要

维甲酸受体(RARs)与维甲酸(RA)结合后可调节基因表达。在瞬时转染中,RARα-β-半乳糖苷酶融合蛋白(RAR-LacZ)在无RA的情况下能够反式激活表达。当在转基因小鼠的晶状体中表达时,这种组成型活性RAR-LacZ融合基因导致了出现白内障和小眼症的奠基者动物和后代动物,这两者都是类视黄醇诱导的致畸作用的特征。转基因表型表明,在类视黄醇敏感组织中表达组成型活性RAR-LacZ融合蛋白可模拟类视黄醇致畸作用。

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Transgenic mice expressing a constitutively active retinoic acid receptor in the lens exhibit ocular defects.在晶状体中表达组成型活性视黄酸受体的转基因小鼠表现出眼部缺陷。
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Induction of a RAR beta 2-lacZ transgene by retinoic acid reflects the neuromeric organization of the central nervous system.
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