Evaluation of the therapeutic potential of a CNP analog in a Fgfr3 mouse model recapitulating achondroplasia - Wikidata - awgldk - TriplyDB

Evaluation of the therapeutic potential of a CNP analog in a Fgfr3 mouse model recapitulating achondroplasia

Evaluation of the therapeutic potential of a CNP analog in a Fgfr3 mouse model recapitulating achondroplasia

http://www.wikidata.org/entity/Q34314761

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Short and tall stature: a new paradigm emerges Fibroblast growth factor signaling in skeletal development and disease Optimal management of complications associated with achondroplasia Regulation of intraocular pressure by soluble and membrane guanylate cyclases and their role in glaucoma Mechanisms and models of endoplasmic reticulum stress in chondrodysplasia A pathway to bone: signaling molecules and transcription factors involved in chondrocyte development and maturation Advances in Skeletal Dysplasia Genetics Meclozine facilitates proliferation and differentiation of chondrocytes by attenuating abnormally activated FGFR3 signaling in achondroplasia Protective effects of C-type natriuretic peptide on linear growth and articular cartilage integrity in a mouse model of inflammatory arthritis Final adult height in long-term growth hormone-treated achondroplasia patients.Recent research on the growth plate: Recent insights into the regulation of the growth plate The Fibroblast Growth Factor signaling pathway A human skeletal overgrowth mutation increases maximal velocity and blocks desensitization of guanylyl cyclase-B.New therapeutic targets in rare genetic skeletal diseases.FGFR3/fibroblast growth factor receptor 3 inhibits autophagy through decreasing the ATG12-ATG5 conjugate, leading to the delay of cartilage development in achondroplasia Tyrosine kinase inhibitor NVP-BGJ398 functionally improves FGFR3-related dwarfism in mouse model.Inhibition of fibroblast growth factor receptor 3-dependent lung adenocarcinoma with a human monoclonal antibody.Meckel's and condylar cartilages anomalies in achondroplasia result in defective development and growth of the mandible.Knock-in human FGFR3 achondroplasia mutation as a mouse model for human skeletal dysplasia.Fibroblast growth factor (FGF) signaling in development and skeletal diseases.Advances in treatment of achondroplasia and osteoarthritis.Therapeutic effect of CNP on renal osteodystrophy by antagonizing the FGF-23/MAPK pathway.Skeletal Dysplasias: What Every Bone Health Clinician Needs to Know.Clinical dosage of meclozine promotes longitudinal bone growth, bone volume, and trabecular bone quality in transgenic mice with achondroplasia.Short Anabolic Peptides for Bone Growth.The ras-GTPase activity of neurofibromin restrains ERK-dependent FGFR signaling during endochondral bone formation.Achondroplasia: Development, pathogenesis, and therapy.Genetics of Short Stature.Mouse models for the study of cranial base growth and anomalies.Height outcome of short children with hypochondroplasia after recombinant human growth hormone treatment: a meta-analysis.Molecular therapeutic strategies for FGFR3 gene-related skeletal dysplasia.Skeletal Characterization of the Fgfr3 Mouse Model of Achondroplasia Using Micro-CT and MRI Volumetric Imaging.Meeting report of the 8th International Conference on cGMP "cGMP: generators, effectors, and therapeutic implications" at Bamberg, Germany, from June 23 to 25, 2017.Dephosphorylation of the NPR2 guanylyl cyclase contributes to inhibition of bone growth by fibroblast growth factor.Mutations in C-natriuretic peptide (NPPC): a novel cause of autosomal dominant short stature.Skeletal overgrowth-causing mutations mimic an allosterically activated conformation of guanylyl cyclase-B that is inhibited by 2,4,6,-trinitrophenyl ATP.HDAC6 deficiency or inhibition blocks FGFR3 accumulation and improves bone growth in a model of achondroplasia.Circulatory CNP Rescues Craniofacial Hypoplasia in Achondroplasia.Statin treatment rescues FGFR3 skeletal dysplasia phenotypes.Serum NT-proCNP levels increased after initiation of GH treatment in patients with achondroplasia/hypochondroplasia.

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Evaluation of the therapeutic potential of a CNP analog in a Fgfr3 mouse model recapitulating achondroplasia

http://www.wikidata.org/entity/Q34314761

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Evaluation of the therapeutic ...... recapitulating achondroplasia

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Evaluation of the therapeutic ...... recapitulating achondroplasia

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J.AJHG.2012.10.014

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American Journal of Human Genetics

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Evaluation of the therapeutic ...... recapitulating achondroplasia

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Arnold Munnich

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Charles A O'Neill

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Dan J Wendt

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Federico Di Rocco

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Florence Lorget

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Sean M Bell

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Sherry Bullens

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P2860

Fibroblast growth factor receptor 3 is a negative regulator of bone growth

Mutations in the transmembrane natriuretic peptide receptor NPR-B impair skeletal growth and cause acromesomelic dysplasia, type Maroteaux

A loss-of-function mutation in natriuretic peptide receptor 2 (Npr2) gene is responsible for disproportionate dwarfism in cn/cn mouse

Dwarfism and early death in mice lacking C-type natriuretic peptide

Fibroblast growth factor expression in the postnatal growth plate.

Mutations in the transmembrane domain of FGFR3 cause the most common genetic form of dwarfism, achondroplasia.

Genetic inactivation of ERK1 and ERK2 in chondrocytes promotes bone growth and enlarges the spinal canal

Constitutive activation of MEK1 in chondrocytes causes Stat1-independent achondroplasia-like dwarfism and rescues the Fgfr3-deficient mouse phenotype

Systemic administration of C-type natriuretic peptide as a novel therapeutic strategy for skeletal dysplasias

Achondroplasia: pathogenesis and implications for future treatment.

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Laurence Legeai-Mallet

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