c-Jun N-terminal kinases (JNK) antagonize cardiac growth through cross-talk with calcineurin-NFAT signaling.
about
Direct interaction and reciprocal regulation between ASK1 and calcineurin-NFAT control cardiomyocyte death and growthSignaling effectors underlying pathologic growth and remodeling of the heartMitogen-activated protein kinase signaling in the heart: angels versus demons in a heart-breaking tale.Isogarcinol is a new immunosuppressantRegulation of Akt/PKB activity by P21-activated kinase in cardiomyocytesPak1 as a novel therapeutic target for antihypertrophic treatment in the heartThe AP-1 transcription factor c-Jun prevents stress-imposed maladaptive remodeling of the heart.Direct and indirect interactions between calcineurin-NFAT and MEK1-extracellular signal-regulated kinase 1/2 signaling pathways regulate cardiac gene expression and cellular growth.Pathway analysis of dilated cardiomyopathy using global proteomic profiling and enrichment maps.Regulation of calcineurin through transcriptional induction of the calcineurin A beta promoter in vitro and in vivo.Crosstalk between mitogen-activated protein kinases and mitochondria in cardiac diseases: therapeutic perspectivesActivity- and calcineurin-independent nuclear shuttling of NFATc1, but not NFATc3, in adult skeletal muscle fibers.c-Jun N-terminal kinase (JNK-1) confers protection against brief but not extended ischemia during acute myocardial infarction.Transfusion effects on cardiomyocyte growth and proliferation in fetal sheep after chronic anemiaSuccinate causes pathological cardiomyocyte hypertrophy through GPR91 activation.Uses for JNK: the many and varied substrates of the c-Jun N-terminal kinases.Re-employment of developmental transcription factors in adult heart diseaseGnRH regulation of Jun and Atf3 requires calcium, calcineurin, and NFAT.Orphan Nuclear Receptor Nur77 Inhibits Cardiac Hypertrophic Response to Beta-Adrenergic Stimulation.Targeting calcineurin and associated pathways in cardiac hypertrophy and failure.Lost in transgenesis: a user's guide for genetically manipulating the mouse in cardiac research.Novel roles of PAK1 in the heart.Nuclear factor of activated T cells balances angiogenesis activation and inhibition.Pathogenesis of hypertrophic cardiomyopathy caused by myozenin 2 mutations is independent of calcineurin activityHeart failure with preserved ejection fraction: chronic low-intensity interval exercise training preserves myocardial O2 balance and diastolic function.Disease mechanisms and emerging therapies: protein kinases and their inhibitors in myocardial disease.Systems analysis reveals down-regulation of a network of pro-survival miRNAs drives the apoptotic response in dilated cardiomyopathy.Mitogen-activated protein kinases in heart development and diseasesDUSP8 Regulates Cardiac Ventricular Remodeling by Altering ERK1/2 Signaling.Understanding the role of transforming growth factor-beta signalling in the heart: overview of studies using genetic mouse models.Stretch-induced regulation of angiotensinogen gene expression in cardiac myocytes and fibroblasts: opposing roles of JNK1/2 and p38alpha MAP kinasesMAPK signalling in cardiovascular health and disease: molecular mechanisms and therapeutic targets.Parsing good versus bad signaling pathways in the heart: role of calcineurin-nuclear factor of activated T-cells.Cdc42 is an antihypertrophic molecular switch in the mouse heart.Therapeutic regulation of cardiac fibroblast function: targeting stress-activated protein kinase pathways.Role of the Wnt-Frizzled system in cardiac pathophysiology: a rapidly developing, poorly understood area with enormous potential.Heterodimerization of β2 adrenergic receptor and somatostatin receptor 5: Implications in modulation of signaling pathway.Wnt-5a/Ca2+-induced NFAT activity is counteracted by Wnt-5a/Yes-Cdc42-casein kinase 1alpha signaling in human mammary epithelial cells.Systems biological approaches to the cardiac signaling network.Dual-specificity phosphatase 14 protects the heart from aortic banding-induced cardiac hypertrophy and dysfunction through inactivation of TAK1-P38MAPK/-JNK1/2 signaling pathway.
P2860
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P2860
c-Jun N-terminal kinases (JNK) antagonize cardiac growth through cross-talk with calcineurin-NFAT signaling.
description
2003 nî lūn-bûn
@nan
2003年の論文
@ja
2003年論文
@yue
2003年論文
@zh-hant
2003年論文
@zh-hk
2003年論文
@zh-mo
2003年論文
@zh-tw
2003年论文
@wuu
2003年论文
@zh
2003年论文
@zh-cn
name
c-Jun N-terminal kinases (JNK) ...... th calcineurin-NFAT signaling.
@en
c-Jun N-terminal kinases
@nl
type
label
c-Jun N-terminal kinases (JNK) ...... th calcineurin-NFAT signaling.
@en
c-Jun N-terminal kinases
@nl
prefLabel
c-Jun N-terminal kinases (JNK) ...... th calcineurin-NFAT signaling.
@en
c-Jun N-terminal kinases
@nl
P2093
P2860
P356
P1433
P1476
c-Jun N-terminal kinases (JNK) ...... th calcineurin-NFAT signaling.
@en
P2093
Benjamin J Wilkins
Chia-Yi Kuan
Orlando F Bueno
Qiangrong Liang
P2860
P304
P356
10.1093/EMBOJ/CDG474
P407
P577
2003-10-01T00:00:00Z