吴刘成,邵义祥.2011.Map3k1调控小鼠眼睑闭合的研究进展.动物学杂志,46(3):144-151. |
Map3k1调控小鼠眼睑闭合的研究进展 |
Map3k1 Regulation of Mouse Eyelid Closure |
投稿时间:2010-10-15 修订日期:2011-03-02 |
DOI: |
中文关键词: Map 3 k 1 基因调控 信号通路 眼睑闭合 |
英文关键词:Map 3 k 1 Gene regulation Signal pathway Eyelid closure |
基金项目:国家自然科学基金项目(No. 30671081),江苏省自然科学基金项目(No. BK2010279),南通大学研究生科技创新计划项目(No.YKC 10015); |
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中文摘要: |
小鼠( Mus musculus )眼睑发育需要协调细胞增殖、细胞形态改变、迁移及凋亡。 Map 3 k 1是MAPK家族中重要的一员, Map 3 k 1表达的蛋白质MEKK1是MAPK信号通路重要的节点。MEKK1-JNK信号通路活化c-jun,增强AP-1转录因子的转录活性,从而调控肌动蛋白纤维的形成和细胞的迁移。MEKK1还有可能通过c-jun与HB-EGF/EGFR-ERK信号通路相互作用。 Map 3 k 1基因敲除后,小鼠胚胎眼睑不能闭合,造成小鼠出生时眼睑开放,导致角膜病。因此,深入研究 Map 3 k 1基因功能将有可能为研究人类先天性眼睑缺陷及角膜病提供新的思路,为此类疾病的早期诊断、预防、治疗提供新的手段和途径。 |
英文摘要: |
The development of the eyelid requires coordinated processes of cell proliferation, morphology changes, migration and cell death. Map 3 k 1 is an important member of MAPK family and its protein, MEKK1, is a crucial cross-point in MAPK signal pathway. MEKK1-JNK signal pathway regulates actin filament formation and cell migration through enhancing the transcriptional activity of Ap-1.Moreover, MEKK1 has a possible interaction with HB-EGF/EGFR-ERK by c-jun. The Map 3 k 1 knockout mouse is defective in embryonic eyelid closure, and Map 3 k 1 mutant results in the postnatal corneal disease in mouse. Thus, study of Map 3 k 1 function provides a new perspective for human congenital eyelid defects and the corneal disease, and sheds the new light on early diagnosis, prevention, and therapy of this disease. |
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