共查询到10条相似文献,搜索用时 109 毫秒
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Kook H Yung WW Simpson RJ Kee HJ Shin S Lowry JA Loughlin FE Yin Z Epstein JA Mackay JP 《Biochemistry》2006,45(35):10584-10590
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Asanoma K Kato H Yamaguchi S Shin CH Liu ZP Kato K Inoue T Miyanari Y Yoshikawa K Sonoda K Fukushima K Wake N 《The Journal of biological chemistry》2007,282(33):24065-24074
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Hop is an unusual homeobox gene that modulates cardiac development 总被引:19,自引:0,他引:19
Chen F Kook H Milewski R Gitler AD Lu MM Li J Nazarian R Schnepp R Jen K Biben C Runke G Mackay JP Novotny J Schwartz RJ Harvey RP Mullins MC Epstein JA 《Cell》2002,110(6):713-723
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Molly Brunner Angélique Millon-Frémillon Genevieve Chevalier Inaam A. Nakchbandi Deane Mosher Marc R. Block Corinne Albigès-Rizo Daniel Bouvard 《The Journal of cell biology》2013,201(4):643-656
Dysbindin is an established schizophrenia susceptibility gene thoroughly studied in the context of the brain. We have previously shown through a yeast two-hybrid screen that it is also a cardiac binding partner of the intercalated disc protein Myozap. Because Dysbindin is highly expressed in the heart, we aimed here at deciphering its cardiac function. Using a serum response factor (SRF) response element reporter-driven luciferase assay, we identified a robust activation of SRF signaling by Dysbindin overexpression that was associated with significant up-regulation of SRF gene targets, such as Acta1 and Actc1. Concurrently, we identified RhoA as a novel binding partner of Dysbindin. Further phenotypic and mechanistic characterization revealed that Dysbindin induced cardiac hypertrophy via RhoA–SRF and MEK1–ERK1 signaling pathways. In conclusion, we show a novel cardiac role of Dysbindin in the activation of RhoA–SRF and MEK1–ERK1 signaling pathways and in the induction of cardiac hypertrophy. Future in vivo studies should examine the significance of Dysbindin in cardiomyopathy. 相似文献
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