Neurochondrin negatively regulates CaMKII phosphorylation, and nervous system-specific gene disruption results in epileptic seizure

被引：41

作者：

Dateki, M

Horii, T

Kasuya, Y

Mochizuki, R

Nagao, Y

Ishida, J

Sugiyama, F

Tanimoto, K

Yagami, K

Imai, H

Fukamizu, A ^{[1
]}

机构：

[1] Univ Tsukuba, Ctr Tsukuba Adv Res Alliance, Tsukuba, Ibaraki 3058577, Japan

[2] Kyoto Univ, Grad Sch Agr, Reprod Physiol Lab, Kyoto 6068502, Japan

[3] Chiba Univ, Grad Sch Med, Dept Mol Pharmacol & Biochem, Chiba 2608670, Japan

[4] Univ Tsukuba, Lab Anim Source Ctr, Tsukuba, Ibaraki 3058577, Japan

来源：

JOURNAL OF BIOLOGICAL CHEMISTRY | 2005年 / 280卷 / 21期

关键词：

D O I：

10.1074/jbc.M414033200

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 [生物化学与分子生物学]; 081704 [应用化学];

摘要：

Neurochondrin is a novel cytoplasmic protein and possibly involved in neurite outgrowth, chondrocyte differentiation, and bone metabolism. Our previous trial in disclosing its role by the loss of function in mice failed because of the lethality in utero. In this study, we eliminated the neurochondrin gene expression preferentially in the nervous system by the conditional knockout strategy. Our results showed that neurochondrin is a negative regulator of Ca2+/calmodulin-dependent protein kinase II phosphorylation and essential for the spatial learning process but not for the differentiation or neurite outgrowth of the neuron. In addition, the nervous system-specific homozygous gene disruption resulted in epileptic seizure.

引用

页码：20503 / 20508

页数：6

共 32 条

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Alzheimer's disease underlies some cases of complex partial status epilepticus - Clinical, radiologic, EEG, and pathologic correlations [J].