- alpha B-Crystallin Suppresses Pressure Overload Cardiac Hypertrophy
[作者：Kumarapeli, ARK; Su, HB; Huang, W; Tang, MX; Zheng, HQ; Horak, KM; Li, MX; Wang, XJ,期刊：Circulation Research, 页码：1473-1482 , 文章类型： Article，,卷期：2008年103-12]
- alpha B-Crystallin (CryAB) is the most abundant small heat shock protein (HSP) constitutively expressed in cardiomyocytes. Gain- and loss-of-function studies demonstrated that CryAB can protect against myocardial ischemi...
- Homozygous Missense N629D hERG (KCNH2) Potassium Channel Mutation Causes Developmental Defects in the Right Ventricle and Its Outflow Tract and Embryonic Lethality
[作者：Teng, GQ; Zhao, X; Lees-Miller, JP; Quinn, FR; Li, P; Rancourt, DE; London, B; Cross, JC; Duff, HJ,期刊：Circulation Research, 页码：1483-U270 , 文章类型： Article，,卷期：2008年103-12]
- Loss-of-function mutations in the human ERG1 potassium channel (hERG1) frequently underlie the long QT2 (LQT2) syndrome. The role of the ERG potassium channel in cardiac development was elaborated in an in vivo model of ...
- O-Linked GlcNAc Modification of Cardiac Myofilament Proteins
[作者：Ramirez-Correa, GA; Jin, WH; Wang, ZH; Zhong, X; Gao, WD; Dias, WB; Vecoli, C; Hart, GW; Murphy, AM,期刊：Circulation Research, 页码：1354-U30 , 文章类型： Article，,卷期：2008年103-12]
- In addition to O-phosphorylation, O-linked modifications of serine and threonine by beta-N-acetyl-D-glucosamine (GlcNAc) may regulate muscle contractile function. This study assessed the potential role of O-GlcNAcylation...
- Loss of Bmx Nonreceptor Tyrosine Kinase Prevents Pressure Overload-Induced Cardiac Hypertrophy
[作者：Mitchell-Jordan, SA; Holopainen, T; Ren, SX; Wang, SJ; Warburton, S; Zhang, MJ; Alitalo, K; Wang, YB; Vondriska, TM,期刊：Circulation Research, 页码：1359-U43 , 文章类型： Article，,卷期：2008年103-12]
- Bmx nonreceptor tyrosine kinase has an established role in endothelial and lymphocyte signaling; however, its role in the heart is unknown. To determine whether Bmx participates in cardiac growth, we subjected mice defic...
- S-Endoglin Expression Is Induced in Senescent Endothelial Cells and Contributes to Vascular Pathology
[作者：Blanco, FJ; Grande, MT; Langa, C; Oujo, B; Velasco, S; Rodriguez-Barbero, A; Perez-Gomez, E; Quintanilla, M; Lopez-Novoa, JM; Bernabeu, C,期刊：Circulation Research, 页码：1383-U91 , 文章类型： Article，,卷期：2008年103-12]
- Senescence of endothelial cells (ECs) may contribute to age-associated cardiovascular diseases, including atherosclerosis and hypertension. The functional and gene expression changes associated with cellular senescence a...
- Platelet-Derived Growth Factor Receptor beta Signaling Is Required for Efficient Epicardial Cell Migration and Development of Two Distinct Coronary Vascular Smooth Muscle Cell Populations
[作者：Mellgren, AM; Smith, CL; Olsen, GS; Eskiocak, B; Zhou, B; Kazi, MN; Ruiz, FR; Pu, WT; Tallquist, MD,期刊：Circulation Research, 页码：1393-U120 , 文章类型： Article，,卷期：2008年103-12]
- The epicardium plays an essential role in coronary artery formation and myocardial development, but signals controlling the development and differentiation of this tissue are not well understood. To investigate the role ...
- Toll-Like Receptor 2 Mediates Apolipoprotein CIII-Induced Monocyte Activation
[作者：Kawakami, A; Osaka, M; Aikawa, M; Uematsu, S; Akira, S; Libby, P; Shimokado, K; Sacks, FM; Yoshida, M,期刊：Circulation Research, 页码：1402-U132 , 文章类型： Article，,卷期：2008年103-12]
- Apolipoprotein (apo) CIII predicts risk for coronary heart disease. We recently reported that apoCIII directly activates human monocytes. Recent evidence indicates that toll-like receptor (TLR)2 can contribute to atherog...
- MEKK3 Initiates Transforming Growth Factor beta(2)-Dependent Epithelial-to-Mesenchymal Transition During Endocardial Cushion Morphogenesis
[作者：Stevens, MV; Broka, DM; Parker, P; Rogowitz, E; Vaillancourt, RR; Camenisch, TD,期刊：Circulation Research, 页码：1430-U188 , 文章类型： Article，,卷期：2008年103-12]
- Congenital heart defects occur at a rate of 5% and are the most prevalent birth defects. A better understanding of the complex signaling networks regulating heart development is necessary to improve repair strategies for...
- P53 Impairs Endothelium-Dependent Vasomotor Function Through Transcriptional Upregulation of P66shc
[作者：Kim, CS; Jung, SB; Naqvi, A; Hoffman, TA; DeRicco, J; Yamamori, T; Cole, MP; Jeon, BH; Irani, K,期刊：Circulation Research, 页码：1441-U202 , 文章类型： Article，,卷期：2008年103-12]
- The transcription factor, p53, and the adaptor protein, p66shc, both play essential roles in promoting oxidative stress in the vascular system. However, the relationship between the two in the context of endothelium-depe...
- Long QT Syndrome-Associated Mutations in KCNQ1 and KCNE1 Subunits Disrupt Normal Endosomal Recycling of I-Ks Channels
[作者：Seebohm, G; Strutz-Seebohm, N; Ureche, ON; Henrion, U; Baltaev, R; Mack, AF; Korniychuk, G; Steinke, K; Tapken, D; Pfeufer, A; Kaab, S; Bucci, C; Attali, B; Merot, J; Tavare, JM; Hoppe, UC; Sanguinetti, MC; Lang, F,期刊：Circulation Research, 页码：1451-U217 , 文章类型： Article，,卷期：2008年103-12]
- Physical and emotional stress is accompanied by release of stress hormones such as the glucocorticoid cortisol. This hormone upregulates the serum-and glucocorticoid-inducible kinase (SGK)1, which in turn stimulates I-Ks...
- Differential Structure of Atrial and Ventricular K-ATP Atrial K-ATP Channels Require SUR1
[作者：Flagg, TP; Kurata, HT; Masia, R; Caputa, G; Magnuson, MA; Lefer, DJ; Coetzee, WA; Nichols, CG,期刊：Circulation Research, 页码：1458-U228 , 文章类型： Article，,卷期：2008年103-12]
- The isoform-specific structure of the ATP-sensitive potassium (K-ATP) channel endows it with differential fundamental properties, including physiological activation and pharmacology. Numerous studies have convincingly de...
- Redox Modification of Ryanodine Receptors Contributes to Sarcoplasmic Reticulum Ca2+ Leak in Chronic Heart Failure
[作者：Terentyev, D; Gyorke, I; Belevych, AE; Terentyeva, R; Sridhar, A; Nishijima, Y; de Blanco, EC; Khanna, S; Sen, CK; Cardounel, AJ; Carnes, CA; Gyorke, S,期刊：Circulation Research, 页码：1466-U252 , 文章类型： Article，,卷期：2008年103-12]
- Abnormal cardiac ryanodine receptor (RyR2) function is recognized as an important factor in the pathogenesis of heart failure (HF). However, the specific molecular causes underlying RyR2 defects in HF remain poorly under...
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