Molecular Physiology and Pathophysiology of Tight Junctions - I. Tight junction structure and function: lessons from mutant animals and proteins
Molecular Physiology and Pathophysiology of Tight Junctions - I. Tight junction structure and function: lessons from mutant animals and proteins
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DOI：
10.1152/ajpgi.2000.279.2.g250
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发表时间：
2000-08-01
影响因子：
4.5
通讯作者：
Anderson, JM
中科院分区：
文献类型：
--
作者：
Mitic, LL;van Itallie, CM;Anderson, JM
紧密连接形成上皮组织中的主要细胞旁屏障。屏障密封性能在电阻、溶质和水通量以及电荷选择性方面在电池类型之间变化很大。这种变异性的分子解释似乎更接近以下跨膜蛋白occludin和claudin多基因家族的成员的鉴定。例如，claudin-16突变的人类表型表明，它创建了一个通道，允许镁通过肾脏紧密连接扩散。类似地，敲除claudin-11的小鼠揭示了其在睾丸中髓鞘和支持细胞之间紧密连接形成中的作用。对其他claudins的研究有望阐明它们在所有上皮组织中形成连接结构和生理学的贡献。
Tight junctions form the major paracellular barrier in epithelial tissues. Barrier-sealing properties are quite variable among cell types in terms of electrical resistance, solute and water flux, and charge selectivity. A molecular explanation for this variability appears closer following identification of the transmembrane proteins occludin and members of the claudin multigene family. For example, the human phenotype of mutations in claudin-16 suggests that it creates a channel that allows magnesium to diffuse through renal tight junctions. Similarly, a mouse knockout of claudin-11 reveals its role in formation of tight junctions in myelin and between Sertoli cells in testis. The study of other claudins is expected to elucidate their contributions to creating junction structure and physiology in all epithelial tissues.