Reengineering inducible cardiac-specific transgenesis with an attenuated myosin heavy chain promoter.
about
Gq/11-mediated signaling and hypertrophy in mice with cardiac-specific transgenic expression of regulator of G-protein signaling 2Cardiac regulation by phosphoinositide 3-kinases and PTENSingle-stranded DNA-binding proteins PURalpha and PURbeta bind to a purine-rich negative regulatory element of the alpha-myosin heavy chain gene and control transcriptional and translational regulation of the gene expression. Implications in the repPlasma membrane Ca2+-ATPase isoform 4 antagonizes cardiac hypertrophy in association with calcineurin inhibition in rodentsA thrombospondin-dependent pathway for a protective ER stress responseCIB1 is a regulator of pathological cardiac hypertrophyProtein kinase cascades in the regulation of cardiac hypertrophyGene therapy for cardiovascular disease: advances in vector development, targeting, and delivery for clinical translationThe ubiquitin-proteasome system and cardiovascular diseaseAberrant sodium influx causes cardiomyopathy and atrial fibrillation in miceCardiomyocyte GATA4 functions as a stress-responsive regulator of angiogenesis in the murine heartThe transcription factor GATA-6 regulates pathological cardiac hypertrophyGSK-3alpha directly regulates beta-adrenergic signaling and the response of the heart to hemodynamic stress in miceMutual antagonism between IP(3)RII and miRNA-133a regulates calcium signals and cardiac hypertrophyNetwork reconstruction and systems analysis of cardiac myocyte hypertrophy signaling.Imaging cellular signals in the heart in vivo: Cardiac expression of the high-signal Ca2+ indicator GCaMP2.Protective effect of geranylgeranylacetone via enhancement of HSPB8 induction in desmin-related cardiomyopathy.Inducible cardiomyocyte-specific gene disruption directed by the rat Tnnt2 promoter in the mouseTEAD-1 overexpression in the mouse heart promotes an age-dependent heart dysfunction.Genetic manipulation of the cardiac mitochondrial phosphate carrier does not affect permeability transition.Mitsugumin 29 regulates t-tubule architecture in the failing heart.Calcineurin protects the heart in a murine model of dilated cardiomyopathy.Glycogen synthase kinase-3beta regulates post-myocardial infarction remodeling and stress-induced cardiomyocyte proliferation in vivoConstitutive glycogen synthase kinase-3alpha/beta activity protects against chronic beta-adrenergic remodelling of the heart.Reversal of amyloid-induced heart disease in desmin-related cardiomyopathy.Overexpression of junctophilin-2 does not enhance baseline function but attenuates heart failure development after cardiac stress.Enhanced basal contractility but reduced excitation-contraction coupling efficiency and beta-adrenergic reserve of hearts with increased Cav1.2 activity.The IP3 receptor regulates cardiac hypertrophy in response to select stimuli.Cardiac-specific expression of the tetracycline transactivator confers increased heart function and survival following ischemia reperfusion injuryReceptor-independent cardiac protein kinase Calpha activation by calpain-mediated truncation of regulatory domains.Reversibility of PRKAG2 glycogen-storage cardiomyopathy and electrophysiological manifestations.Transgenic rabbit model for human troponin I-based hypertrophic cardiomyopathy.Cardioprotection of controlled and cardiac-specific over-expression of A(2A)-adenosine receptor in the pressure overloadβ-Adrenergic stimulation increases Cav3.1 activity in cardiac myocytes through protein kinase ACardiac-specific elevations in thyroid hormone enhance contractility and prevent pressure overload-induced cardiac dysfunction.Cardiac-specific NRAP overexpression causes right ventricular dysfunction in miceLeft ventricular dysfunction in murine models of heart failure and in failing human heart is associated with a selective decrease in the expression of caveolin-3.Targeting GSK-3 family members in the heart: a very sharp double-edged sword.The PDZ motif of the α1C subunit is not required for surface trafficking and adrenergic modulation of CaV1.2 channel in the heart.Transgenic knockdown of cardiac sodium/glucose cotransporter 1 (SGLT1) attenuates PRKAG2 cardiomyopathy, whereas transgenic overexpression of cardiac SGLT1 causes pathologic hypertrophy and dysfunction in mice.
P2860
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P2860
Reengineering inducible cardiac-specific transgenesis with an attenuated myosin heavy chain promoter.
description
2003 nî lūn-bûn
@nan
2003年の論文
@ja
2003年学术文章
@wuu
2003年学术文章
@zh
2003年学术文章
@zh-cn
2003年学术文章
@zh-hans
2003年学术文章
@zh-my
2003年学术文章
@zh-sg
2003年學術文章
@yue
2003年學術文章
@zh-hant
name
Reengineering inducible cardia ...... d myosin heavy chain promoter.
@en
Reengineering inducible cardia ...... d myosin heavy chain promoter.
@nl
type
label
Reengineering inducible cardia ...... d myosin heavy chain promoter.
@en
Reengineering inducible cardia ...... d myosin heavy chain promoter.
@nl
prefLabel
Reengineering inducible cardia ...... d myosin heavy chain promoter.
@en
Reengineering inducible cardia ...... d myosin heavy chain promoter.
@nl
P2093
P1433
P1476
Reengineering inducible cardia ...... d myosin heavy chain promoter.
@en
P2093
Atsushi Sanbe
Hanna Osinska
James Gulick
Jeffrey Robbins
Mark C Hanks
Qiangrong Liang
P304
P356
10.1161/01.RES.0000065442.64694.9F
P577
2003-03-06T00:00:00Z