Increased BRAF Heterodimerization Is the Common Pathogenic Mechanism for Noonan Syndrome-Associated RAF1 Mutants
出版年份 2012 全文链接
标题
Increased BRAF Heterodimerization Is the Common Pathogenic Mechanism for Noonan Syndrome-Associated RAF1 Mutants
作者
关键词
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出版物
MOLECULAR AND CELLULAR BIOLOGY
Volume 32, Issue 19, Pages 3872-3890
出版商
American Society for Microbiology
发表日期
2012-07-24
DOI
10.1128/mcb.00751-12
参考文献
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注意:仅列出部分参考文献,下载原文获取全部文献信息。- Mutational Patterns and Novel Mutations of the BRAF Gene in a Large Cohort of Korean Patients with Papillary Thyroid Carcinoma
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- MEK-ERK pathway modulation ameliorates disease phenotypes in a mouse model of Noonan syndrome associated with the Raf1L613V mutation
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- Cyclosporine attenuates cardiomyocyte hypertrophy induced by RAF1 mutants in Noonan and LEOPARD syndromes
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- Cardiac fibroblasts are essential for the adaptive response of the murine heart to pressure overload
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- Impact of Feedback Phosphorylation and Raf Heterodimerization on Normal and Mutant B-Raf Signaling
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- C-Raf Inhibits MAPK Activation and Transformation by B-RafV600E
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- Mutation of SHOC2 promotes aberrant protein N-myristoylation and causes Noonan-like syndrome with loose anagen hair
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- A restricted spectrum of NRAS mutations causes Noonan syndrome
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- Noonan syndrome cardiac defects are caused by PTPN11 acting in endocardium to enhance endocardial-mesenchymal transformation
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- The RAS/MAPK syndromes: novel roles of the RAS pathway in human genetic disorders
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- CRAF Autophosphorylation of Serine 621 Is Required to Prevent Its Proteasome-Mediated Degradation
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- MicroRNA-21 contributes to myocardial disease by stimulating MAP kinase signalling in fibroblasts
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