MiR-221 promotes cardiac hypertrophy in vitro through the modulation of p27 expression. - Wikidata - awgldk - TriplyDB

MiR-221 promotes cardiac hypertrophy in vitro through the modulation of p27 expression.

MiR-221 promotes cardiac hypertrophy in vitro through the modulation of p27 expression.

http://www.wikidata.org/entity/Q51438277

about

Overview of MicroRNAs in Cardiac Hypertrophy, Fibrosis, and Apoptosis Human miR-221/222 in Physiological and Atherosclerotic Vascular Remodeling MicroRNAs in heart failure: Small molecules with major impact miR-185 plays an anti-hypertrophic role in the heart via multiple targets in the calcium-signaling pathways MiR-451 is decreased in hypertrophic cardiomyopathy and regulates autophagy by targeting TSC1.MicroRNA signatures differentiate preserved from reduced ejection fraction heart failure MicroRNA-221 inhibits autophagy and promotes heart failure by modulating the p27/CDK2/mTOR axis.MiRNA inhibition in tissue engineering and regenerative medicine.The altered expression profile of microRNAs in cardiopulmonary bypass canine models and the effects of mir-499 on myocardial ischemic reperfusion injury.ANGPTL2 activity in cardiac pathologies accelerates heart failure by perturbing cardiac function and energy metabolism.Comparative mRNA and MicroRNA Profiling during Acute Myocardial Infarction Induced by Coronary Occlusion and Ablation Radio-Frequency Currents.Role of microRNAs in Vascular Remodeling.The therapeutic potential of miRNAs regulated in settings of physiological cardiac hypertrophy.Therapeutic targeting of autophagy in myocardial infarction and heart failure.miR-30a downregulation aggravates pressure overload-induced cardiomyocyte hypertrophy.MicroRNA regulation in heart and skeletal muscle over the freeze-thaw cycle in the freeze tolerant wood frog.Hydrogen sulfide alleviates myocardial fibrosis in mice with alcoholic cardiomyopathy by downregulating autophagy.Exacerbation of diabetic cardiac hypertrophy in OVE26 mice by angiotensin II is associated with JNK/c-Jun/miR-221-mediated autophagy inhibition.Identification and analysis of a key long non-coding RNAs (lncRNAs)-associated module reveal functional lncRNAs in cardiac hypertrophy.Gender and cardiovascular disease: are sex-biased microRNA networks a driving force behind heart failure with preserved ejection fraction in women?Differential microRNA expression profiles and bioinformatics analysis between young and aging spontaneously hypertensive rats.The effects of subacute inhaled multi-walled carbon nanotube exposure on signaling pathways associated with cholesterol transport and inflammatory markers in the vasculature of wild-type mice Commentary: MicroRNA-221/222 Family Counteracts Myocardial Fibrosis in Pressure Overload-Induced Heart Failure

P2860

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P2860

MiR-221 promotes cardiac hypertrophy in vitro through the modulation of p27 expression.

http://www.wikidata.org/entity/Q51438277

description

2012 nî lūn-bûn

@nan

2012年の論文

@ja

2012年学术文章

@wuu

2012年学术文章

@zh

2012年学术文章

@zh-cn

2012年学术文章

@zh-hans

2012年学术文章

@zh-my

2012年学术文章

@zh-sg

2012年學術文章

@yue

2012年學術文章

@zh-hant

name

MiR-221 promotes cardiac hypertrophy in vitro through the modulation of p27 expression.

@en

MiR-221 promotes cardiac hypertrophy in vitro through the modulation of p27 expression.

@nl

type

label

MiR-221 promotes cardiac hypertrophy in vitro through the modulation of p27 expression.

@en

MiR-221 promotes cardiac hypertrophy in vitro through the modulation of p27 expression.

@nl

prefLabel

MiR-221 promotes cardiac hypertrophy in vitro through the modulation of p27 expression.

@en

MiR-221 promotes cardiac hypertrophy in vitro through the modulation of p27 expression.

@nl

P1433

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P2860

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P698

Q51438277-9E0A76D1-BCBC-447E-B7FA-B0E4235D829D

P356

P1433

Journal of Cellular Biochemistry

P1476

MiR-221 promotes cardiac hypertrophy in vitro through the modulation of p27 expression.

@en

P2093

Changxin Wang

http://www.w3.org/2001/XMLSchema#string

Jizheng Wang

http://www.w3.org/2001/XMLSchema#string

Lei Song

http://www.w3.org/2001/XMLSchema#string

Peng Zhao

http://www.w3.org/2001/XMLSchema#string

Rutai Hui

http://www.w3.org/2001/XMLSchema#string

Shuiyun Wang

http://www.w3.org/2001/XMLSchema#string

Xiaojian Wang

http://www.w3.org/2001/XMLSchema#string

Yilu Wang

http://www.w3.org/2001/XMLSchema#string

Yubao Zou

http://www.w3.org/2001/XMLSchema#string

P2860

miR-9 and NFATc3 regulate myocardin in cardiac hypertrophy

Expression of microRNAs is dynamically regulated during cardiomyocyte hypertrophy

MicroRNAs: genomics, biogenesis, mechanism, and function

Analyzing real-time PCR data by the comparative C(T) method

MicroRNA-directed cleavage of HOXB8 mRNA

Regulation by let-7 and lin-4 miRNAs results in target mRNA degradation

NFATc4 is negatively regulated in miR-133a-mediated cardiomyocyte hypertrophic repression

Suppression of proliferation and cardiomyocyte hypertrophy by CHAMP, a cardiac-specific RNA helicase

Control of stress-dependent cardiac growth and gene expression by a microRNA

Prognostic implications of echocardiographically determined left ventricular mass in the Framingham Heart Study

P304

2040-2046

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P31

scholarly article

P356

10.1002/JCB.24075

http://www.w3.org/2001/XMLSchema#string

P433

6

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P478

113

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P577

2012-06-01T00:00:00Z

http://www.w3.org/2001/XMLSchema#dateTime

P698

22275134

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