Brain development in mice lacking L1-L1 homophilic adhesion.
Brain development in mice lacking L1-L1 homophilic adhesion.
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DOI：
10.1083/jcb.200312107
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发表时间：
2004-04
期刊：
影响因子：
--
通讯作者：
Lemmon V
中科院分区：
文献类型：
--
作者：
Itoh K;Cheng L;Kamei Y;Fushiki S;Kamiguchi H;Gutwein P;Stoeck A;Arnold B;Altevogt P;Lemmon V
一个新的小鼠品系已经产生，其中第六IG结构域的L1细胞粘附分子已被删除。尽管有相当大的缺失，L1表达仍保持在正常水平。体外实验表明，L1-L1同嗜性结合丧失，沿着丧失L1-α5β1整联蛋白结合。然而，L1-neurocan和L1-neuropilin结合被保留，并且sema 3a反应是完整的。令人惊讶的是，在L1基因敲除小鼠中存在的许多轴突导向缺陷，如异常皮质脊髓束和胼胝体，没有观察到。然而，当在C57 BL/6品系上回交时，观察到严重的脑积水，并且在几代之后，变成胚胎致死。这些结果表明，L1与L1、TAG-1或F3的结合以及L1-α5β1整联蛋白的结合对于各种轴突通路的正常发育不是必需的，并表明L1-L1同嗜性结合在X连锁脑积水的产生中是重要的。
A new mouse line has been produced in which the sixth Ig domain of the L1 cell adhesion molecule has been deleted. Despite the rather large deletion, L1 expression is preserved at normal levels. In vitro experiments showed that L1–L1 homophilic binding was lost, along with L1-α5β1 integrin binding. However, L1–neurocan and L1–neuropilin binding were preserved and sema3a responses were intact. Surprisingly, many of the axon guidance defects present in the L1 knockout mice, such as abnormal corticospinal tract and corpus callosum, were not observed. Nonetheless, when backcrossed on the C57BL/6 strain, a severe hydrocephalus was observed and after several generations, became an embryonic lethal. These results imply that L1 binding to L1, TAG-1, or F3, and L1-α5β1 integrin binding are not essential for normal development of a variety of axon pathways, and suggest that L1–L1 homophilic binding is important in the production of X-linked hydrocephalus.
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影响因子：
4.8
作者：
Kalus, I;Schnegelsberg, B;Schachner, M
通讯作者：
Schachner, M
影响因子：
4.8
作者：
Bearer, CF;Swick, AR;Cheng, GH
通讯作者：
Cheng, GH
DOI：
10.1016/s0165-3806(00)00129-2
发表时间：
2001-01-31
期刊：
DEVELOPMENTAL BRAIN RESEARCH
影响因子：
--
作者：
Demyanenko, GP;Shibata, Y;Maness, PF
通讯作者：
Maness, PF
DOI：
10.1006/bbrc.2001.4334
发表时间：
2001-02-16
影响因子：
3.1
作者：
Fukamauchi, F;Aihara, O;Iwakura, Y
通讯作者：
Iwakura, Y
影响因子：
11.4
作者：
Castellani, V;De Angelis, E;Rougon, G
通讯作者：
Rougon, G