Cardiac-specific deletion of mkk4 reveals its role in pathological hypertrophic remodeling but not in physiological cardiac growth.
about
Signaling effectors underlying pathologic growth and remodeling of the heartMitogen-activated protein kinase signaling in the heart: angels versus demons in a heart-breaking tale.miR-92a inhibits vascular smooth muscle cell apoptosis: role of the MKK4-JNK pathwayPregnancy protects against antiangiogenic and fibrogenic effects of angiotensin II in rat heartsPak1 as a novel therapeutic target for antihypertrophic treatment in the heartExercise training reduces resting heart rate via downregulation of the funny channel HCN4Targeted deletion of ERK2 in cardiomyocytes attenuates hypertrophic response but provokes pathological stress induced cardiac dysfunction.Augmented cardiac hypertrophy in response to pressure overload in mice lacking ELTD1.Mkk4 is a negative regulator of the transforming growth factor beta 1 signaling associated with atrial remodeling and arrhythmogenesis with age.Distinct signaling properties of mitogen-activated protein kinase kinases 4 (MKK4) and 7 (MKK7) in embryonic stem cell (ESC) differentiation.Regulator of G protein signalling 14 attenuates cardiac remodelling through the MEK-ERK1/2 signalling pathway.DUSP8 Regulates Cardiac Ventricular Remodeling by Altering ERK1/2 Signaling.Parsing good versus bad signaling pathways in the heart: role of calcineurin-nuclear factor of activated T-cells.Therapeutic regulation of cardiac fibroblast function: targeting stress-activated protein kinase pathways.Regulation of cardiac hypertrophy and remodeling through the dual-specificity MAPK phosphatases (DUSPs).Murine Electrophysiological Models of Cardiac Arrhythmogenesis.The p21-activated kinase 1 (Pak1) signalling pathway in cardiac disease: from mechanistic study to therapeutic exploration.Metabolic stress-induced cardiomyopathy is caused by mitochondrial dysfunction due to attenuated Erk5 signaling.Targeted deletion of the extracellular signal-regulated protein kinase 5 attenuates hypertrophic response and promotes pressure overload-induced apoptosis in the heart.Protein kinase g iα inhibits pressure overload-induced cardiac remodeling and is required for the cardioprotective effect of sildenafil in vivo.Diet-induced obesity promotes altered remodeling and exacerbated cardiac hypertrophy following pressure overload.Mitogen-activated protein kinase kinase 4 deficiency in cardiomyocytes causes connexin 43 reduction and couples hypertrophic signals to ventricular arrhythmogenesis.
P2860
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P2860
Cardiac-specific deletion of mkk4 reveals its role in pathological hypertrophic remodeling but not in physiological cardiac growth.
description
2009 nî lūn-bûn
@nan
2009年の論文
@ja
2009年学术文章
@wuu
2009年学术文章
@zh
2009年学术文章
@zh-cn
2009年学术文章
@zh-hans
2009年学术文章
@zh-my
2009年学术文章
@zh-sg
2009年學術文章
@yue
2009年學術文章
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name
Cardiac-specific deletion of m ...... physiological cardiac growth.
@en
Cardiac-specific deletion of m ...... physiological cardiac growth.
@nl
type
label
Cardiac-specific deletion of m ...... physiological cardiac growth.
@en
Cardiac-specific deletion of m ...... physiological cardiac growth.
@nl
prefLabel
Cardiac-specific deletion of m ...... physiological cardiac growth.
@en
Cardiac-specific deletion of m ...... physiological cardiac growth.
@nl
P2093
P50
P1433
P1476
Cardiac-specific deletion of m ...... n physiological cardiac growth
@en
P2093
Arthur H Weston
Elizabeth J Cartwright
Jiawei Jin
Ludwig Neyses
Tomomi E Kimura
P304
P356
10.1161/CIRCRESAHA.108.188292
P577
2009-03-05T00:00:00Z