2005
DOI: 10.1248/bpb.28.957
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Inactivation of 14-3-3 Protein Exacerbates Cardiac Hypertrophy and Fibrosis through Enhanced Expression of Protein Kinase C .BETA.2 in Experimental Diabetes

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Cited by 30 publications
(24 citation statements)
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“…14-3-3 proteins can interact with a vast array of different proteins and play a role in diverse functions like cell cycle regulation, signaling transduction and apoptosis [47]. A recent study revealed that inactivation of 14-3-3 proteins exacerbated cardiac hypertrophy and fibrosis in diabetic mice [48]. The role of 14-3-3 in asthma pathogenesis is unknown.…”
Section: Discussionmentioning
confidence: 99%
“…14-3-3 proteins can interact with a vast array of different proteins and play a role in diverse functions like cell cycle regulation, signaling transduction and apoptosis [47]. A recent study revealed that inactivation of 14-3-3 proteins exacerbated cardiac hypertrophy and fibrosis in diabetic mice [48]. The role of 14-3-3 in asthma pathogenesis is unknown.…”
Section: Discussionmentioning
confidence: 99%
“…In the context of hyperglycemia or insulin resistance, a model should exhibit (1) evidence of LV dysfunction such as 106,148,149 There are numerous models of enhanced cardiac fibrosis in the literature. Of relevance to diabetes are models with increased expression or activation of the renin-angiotensin signaling pathways.…”
Section: Minimal Criteria For Mouse Models Of Diabetic Cardiomyopathymentioning
confidence: 99%
“…The 14-3-3 proteins specifically bind to serine-phosphorylated proteins and interact with Raf-1, PI-3K, ASK-1, PKC or other protein kinases, regulating signalling pathways (18)(19)(20)(21). Previous studies demonstrated that the expression of 14-3-3 proteins β, γ, δ and θ is high in lung cancer tissue and are associated with malignant potential (22).…”
Section: Resultsmentioning
confidence: 99%