Daniel J Wendt, Melita Dvorak-Ewell, Sherry Bullens, Florence Lorget, Sean M Bell, Jeff Peng, Sianna Castillo, Mika Aoyagi-Scharber, Charles A O'Neill, Pavel Krejci, William R Wilcox, David L Rimoin, Stuart Bunting. J Pharmacol Exp Ther 2015
Times Cited: 59
Times Cited: 59
Times Cited
Times Co-cited
Similarity
Evaluation of the therapeutic potential of a CNP analog in a Fgfr3 mouse model recapitulating achondroplasia.
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Overexpression of CNP in chondrocytes rescues achondroplasia through a MAPK-dependent pathway.
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Systemic administration of C-type natriuretic peptide as a novel therapeutic strategy for skeletal dysplasias.
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Dwarfism and early death in mice lacking C-type natriuretic peptide.
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Statin treatment rescues FGFR3 skeletal dysplasia phenotypes.
Akihiro Yamashita, Miho Morioka, Hiromi Kishi, Takeshi Kimura, Yasuhito Yahara, Minoru Okada, Kaori Fujita, Hideaki Sawai, Shiro Ikegawa, Noriyuki Tsumaki. Nature 2014
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Mutations in the transmembrane natriuretic peptide receptor NPR-B impair skeletal growth and cause acromesomelic dysplasia, type Maroteaux.
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Postnatal soluble FGFR3 therapy rescues achondroplasia symptoms and restores bone growth in mice.
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Meclozine promotes longitudinal skeletal growth in transgenic mice with achondroplasia carrying a gain-of-function mutation in the FGFR3 gene.
Masaki Matsushita, Satoru Hasegawa, Hiroshi Kitoh, Kensaku Mori, Bisei Ohkawara, Akihiro Yasoda, Akio Masuda, Naoki Ishiguro, Kinji Ohno. Endocrinology 2015
Masaki Matsushita, Satoru Hasegawa, Hiroshi Kitoh, Kensaku Mori, Bisei Ohkawara, Akihiro Yasoda, Akio Masuda, Naoki Ishiguro, Kinji Ohno. Endocrinology 2015
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Mutations in the transmembrane domain of FGFR3 cause the most common genetic form of dwarfism, achondroplasia.
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Tyrosine kinase inhibitor NVP-BGJ398 functionally improves FGFR3-related dwarfism in mouse model.
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Interaction of fibroblast growth factor and C-natriuretic peptide signaling in regulation of chondrocyte proliferation and extracellular matrix homeostasis.
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Overexpression of the C-type natriuretic peptide (CNP) is associated with overgrowth and bone anomalies in an individual with balanced t(2;7) translocation.
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Meclozine facilitates proliferation and differentiation of chondrocytes by attenuating abnormally activated FGFR3 signaling in achondroplasia.
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C-type natriuretic peptide plasma levels are elevated in subjects with achondroplasia, hypochondroplasia, and thanatophoric dysplasia.
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Advances in treatment of achondroplasia and osteoarthritis.
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A novel FGFR3-binding peptide inhibits FGFR3 signaling and reverses the lethal phenotype of mice mimicking human thanatophoric dysplasia.
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A novel tyrosine kinase inhibitor restores chondrocyte differentiation and promotes bone growth in a gain-of-function Fgfr3 mouse model.
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Graded activation of fibroblast growth factor receptor 3 by mutations causing achondroplasia and thanatophoric dysplasia.
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A mouse model for achondroplasia produced by targeting fibroblast growth factor receptor 3.
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A novel homozygous mutation in FGFR3 causes tall stature, severe lateral tibial deviation, scoliosis, hearing impairment, camptodactyly, and arachnodactyly.
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A cluster of translocation breakpoints in 2q37 is associated with overexpression of NPPC in patients with a similar overgrowth phenotype.
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Heterozygous mutations in natriuretic peptide receptor-B (NPR2) gene as a cause of short stature.
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Co-cited is the co-citation frequency, indicating how many articles cite the article together with the query article. Similarity is the co-citation as percentage of the times cited of the query article or the article in the search results, whichever is the lowest. These numbers are calculated for the last 100 citations when articles are cited more than 100 times.