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Convergence of protein kinase C and JAK-STAT signaling on transcription factor GATA-4 总被引:4,自引:0,他引:4
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Wang J Paradis P Aries A Komati H Lefebvre C Wang H Nemer M 《Molecular and cellular biology》2005,25(22):9829-9844
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The transcription factors GATA4 and GATA6 regulate cardiomyocyte hypertrophy in vitro and in vivo 总被引:16,自引:0,他引:16
Liang Q De Windt LJ Witt SA Kimball TR Markham BE Molkentin JD 《The Journal of biological chemistry》2001,276(32):30245-30253
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Chandrasekar B Mummidi S Valente AJ Patel DN Bailey SR Freeman GL Hatano M Tokuhisa T Jensen LE 《The Journal of biological chemistry》2005,280(28):26263-26277
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The antiapoptotic gene mcl-1 is up-regulated by the phosphatidylinositol 3-kinase/Akt signaling pathway through a transcription factor complex containing CREB. 总被引:22,自引:0,他引:22
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Ju-Ming Wang Jyh-Rong Chao Wannhsin Chen Min-Liang Kuo Jeffrey J.-Y. Yen Hsin-Fang Yang-Yen 《Molecular and cellular biology》1999,19(9):6195-6206
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Hey basic helix-loop-helix transcription factors are repressors of GATA4 and GATA6 and restrict expression of the GATA target gene ANF in fetal hearts 总被引:4,自引:0,他引:4
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Fischer A Klattig J Kneitz B Diez H Maier M Holtmann B Englert C Gessler M 《Molecular and cellular biology》2005,25(20):8960-8970
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Jinjing Yang Yu Nie Fang Wang Jianfeng HouXiangfeng Cong Shengshou HuXi Chen 《Biochimica et Biophysica Acta (BBA)/Molecular and Cell Biology of Lipids》2013,1831(8):1386-1394
Earlier, our study demonstrated that lysophosphatidic acid (LPA) receptor mediated cardiomyocyte hypertrophy. However, the subtype-specific functions for LPA1 and LPA3 receptors in LPA-induced hypertrophy have not been distinguished. Growing evidence indicates that microRNAs (miRNAs) are involved in the pathogenesis of cardiac hypertrophy by down-regulating target molecules. The present work therefore aimed at elucidating the functions mediated by different subtypes of LPA receptors and investigating the modulatory role of miRNAs during LPA induced hypertrophy. Experiments were done with cultured neonatal rat cardiomyocytes (NRCMs) exposed to LPA and we showed that knockdown of LPA1 by small interfering RNA (siRNA) enhanced LPA-induced cardiomyocyte hypertrophy, whereas LPA3 silencing repressed hypertrophy. miR-23a, a pro-hypertrophic miRNA, was up-regulated by LPA in cardiomyocytes and its down-regulation reduced LPA-induced cardiomyocyte hypertrophy. Importantly, luciferase reporter assay confirmed LPA1 to be a target of miR-23a, indicating that miR-23a is involved in mediating the LPA-induced cardiomyocyte hypertrophy by targeting LPA1. In addition, knockdown of LPA3, but not LPA1, eliminated miR-23a elevation induced by LPA. And PI3K inhibitor, LY294002, effectively prevented LPA-induced miR-23a expression in cardiomyocytes, suggesting that LPA might induce miR-23a elevation by activating LPA3 and PI3K/AKT pathway. These findings identified opposite subtype-specific functions for LPA1 and LPA3 in mediating cardiomyocyte hypertrophy and indicated LPA1 to be a target of miR-23a, which discloses a link between miR-23a and the LPA receptor signaling in cardiomyocyte hypertrophy. 相似文献
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