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斑马鱼中连接蛋白43的短鳍突变导致异常的间隙连接细胞间通讯。

Zebrafish short fin mutations in connexin43 lead to aberrant gap junctional intercellular communication.

作者信息

Hoptak-Solga Angela D, Klein Kathryn A, DeRosa Adam M, White Thomas W, Iovine M Kathryn

机构信息

Lehigh University, Department of Biological Sciences, Iacocca B-217, Bethlehem, PA 18015, USA.

出版信息

FEBS Lett. 2007 Jul 10;581(17):3297-302. doi: 10.1016/j.febslet.2007.06.030. Epub 2007 Jun 21.

Abstract

Mutations in the zebrafish connexin43 (cx43) gene cause the short fin phenotype, indicating that direct cell-cell communication contributes to bone length. Three independently generated cx43 alleles exhibit short segments of variable sizes, suggesting that gap junctional intercellular communication may regulate bone growth. Dye coupling assays showed that all alleles are capable of forming gap junction channels. However, ionic coupling assays revealed allele-specific differences in coupling efficiency and gating. For instance, oocyte pairs expressing the weakest allele exhibited much higher levels of coupling than either of the strong alleles. Therefore, measurable differences in Cx43 function may be correlated with the severity of defects in bone length.

摘要

斑马鱼连接蛋白43(cx43)基因的突变会导致短鳍表型,这表明直接的细胞间通讯对骨骼长度有影响。三个独立产生的cx43等位基因表现出大小可变的短片段,这表明间隙连接细胞间通讯可能调节骨骼生长。染料偶联试验表明,所有等位基因都能够形成间隙连接通道。然而,离子偶联试验揭示了偶联效率和门控方面的等位基因特异性差异。例如,表达最弱等位基因的卵母细胞对表现出比任何一个强等位基因都高得多的偶联水平。因此,Cx43功能的可测量差异可能与骨骼长度缺陷的严重程度相关。

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Life cycle of connexins in health and disease.连接蛋白在健康与疾病中的生命周期。
Biochem J. 2006 Mar 15;394(Pt 3):527-43. doi: 10.1042/BJ20051922.
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Connexin-based gap junction hemichannels: gating mechanisms.基于连接蛋白的间隙连接半通道:门控机制。
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