ArticlePeptides2008
Reduced ability of C-type natriuretic peptide (CNP) to activate natriuretic peptide receptor B (NPR-B) causes dwarfism in lbab -/- mice.
Article in Peptides, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 21 citations in OpenAlex.
- Phosphorylation-Dependent Regulation of Guanylyl Cyclase (GC)-A and Other Membrane GC Receptors.Endocrine reviews · 2024Review
- Mutations in C-natriuretic peptide (NPPC): a novel cause of autosomal dominant short stature.Genetics in medicine : official journal of the American College of Medical Genetics · 2018Article
- Skeletal overgrowth-causing mutations mimic an allosterically activated conformation of guanylyl cyclase-B that is inhibited by 2,4,6,-trinitrophenyl ATP.The Journal of biological chemistry · 2017Article
- Heterozygous mutations in natriuretic peptide receptor-B (NPR2) gene as a cause of short stature.Human mutation · 2015Article
- Guanylyl cyclases A and B are asymmetric dimers that are allosterically activated by ATP binding to the catalytic domain.Science signaling · 2012Article
- ATP potentiates competitive inhibition of guanylyl cyclase A and B by the staurosporine analog, Gö6976: reciprocal regulation of ATP and GTP binding.The Journal of biological chemistry · 2011Article
- Regulation and therapeutic targeting of peptide-activated receptor guanylyl cyclases.Pharmacology & therapeutics · 2011Review
- NPR-C: a component of the natriuretic peptide family with implications in human diseases.Journal of molecular medicine (Berlin, Germany) · 2010Review
- C-type natriuretic peptide (CNP) is a bifurcation factor for sensory neurons.Proceedings of the National Academy of Sciences of the United States of America · 2009Article
- Systemic administration of C-type natriuretic peptide as a novel therapeutic strategy for skeletal dysplasias.Endocrinology · 2009Article
- Natriuretic peptides: their structures, receptors, physiologic functions and therapeutic applications.Handbook of experimental pharmacology · 2009Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
C-type natriuretic peptide (CNP) stimulates endochondrial ossification by activating the transmembrane guanylyl cyclase, natriuretic peptide receptor-B (NPR-B). Recently, a spontaneous autosomal recessive mutation that causes severe dwarfism in mice was identified. The mutant, called long bone abnormality (lbab), contains a single point mutation that converts an arginine to a glycine in a conserved coding region of the CNP gene, but how this mutation affects CNP activity has not been reported. Here, we determined that 30-fold to greater than 100-fold more CNP(lbab) was required to activate NPR-B as compared to wild-type CNP in whole cell cGMP elevation and membrane guanylyl cyclase assays. The reduced ability of CNP(lbab) to activate NPR-B was explained, at least in part, by decreased binding since 10-fold more CNP(lbab) than wild-type CNP was required to compete with [125I][Tyr0]CNP for receptor binding. Molecular modeling suggested that the conserved arginine is critical for binding to an equally conserved acidic pocket in NPR-B. These results indicate that reduced binding to and activation of NPR-B causes dwarfism in lbab(-/-) mice.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.