The DOI matches its Crossref record; 6 of the 6 references it cites were found in a registry or an index.
Reduced Affinity to and Inhibition by DKK1 Form a Common Mechanism by Which High Bone Mass-Associated Missense Mutations in LRP5 Affect Canonical Wnt Signaling
Open accessAbstract
The low-density-lipoprotein receptor-related protein 5 (LRP5), a coreceptor in the canonical Wnt signaling pathway, has been implicated in human disorders of low and high bone mass. Loss-of-function mutations cause the autosomal recessive osteoporosis-pseudoglioma syndrome, and heterozygous missense mutations in families segregating autosomal dominant high bone mass (HBM) phenotypes have been identified. We expressed seven different HBM-LRP5 missense mutations to delineate the mechanism by which they alter Wnt signaling. None of the mutations caused activation of the receptor in the absence of ligand. Each mutant receptor was able to reach the cell surface, albeit at differing amounts, and transduce exogenously supplied Wnt1 and Wnt3a signal. All HBM mutant proteins had reduced physical interaction with and reduced inhibition by DKK1. These data suggest that HBM mutant proteins can transit to the cell surface in sufficient quantity to transduce Wnt signal and that the likely mechanism for the HBM mutations' physiologic effects is via reduced affinity to and inhibition by DKK1.
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Cites
High Bone Density Due to a Mutation in LDL-Receptor–Related Protein 5
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“Additionally, yeast two-hybrid experiments identified Axin, a cytoplasmic component of the canonical signaling cascade, as being an LRP5-interacting partner (24).”
BackgroundNovel mechanism of Wnt signalling inhibition mediated by Dickkopf-1 interaction with LRP6/Arrow
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Essential role of β-catenin in postnatal bone acquisition.
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Self-citationMesd Encodes an LRP5/6 Chaperone Essential for Specification of Mouse Embryonic Polarity
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Cited by
Wnt/β-Catenin Signaling: Components, Mechanisms, and Diseases
MacDonald, B. T., Tamai, K., & He, X. (2009) · Developmental Cell · doi:10.1016/j.devcel.2009.06.016 · Cited by 5,583
Wnt/β-catenin signaling and disease
Clevers, H., & Nusse, R. (2012) · Cell · doi:10.1016/j.cell.2012.05.012 · Cited by 5,554
WNT signaling in bone homeostasis and disease: From human mutations to treatments
Baron, R., & Kneissel, M. (2013) · Nature Medicine · doi:10.1038/nm.3074 · Cited by 2,093
Regulation of bone mass by Wnt signaling
Krishnan, V. (2006) · Journal of Clinical Investigation · doi:10.1172/jci28551 · Cited by 1,407
Osteocytes, mechanosensing and Wnt signaling
Bonewald, L. F., & Johnson, M. L. (2008) · Bone · doi:10.1016/j.bone.2007.12.224 · Cited by 1,076
Metadata
- Authors
- Ai, M., Holmen, S. L., Van Hul, W., Williams, B. O., & Warman, M. L.
- Venue
- Molecular and Cellular Biology
- Publisher
- Informa UK Limited
- Published
- 2005-06-01
- Volume
- 25
- Issue
- 12
- Pages
- 4946-4955
- ISSN
- 0270-7306 (ISSN-L)
- 1098-5549
- OpenAlex
- W2118390249
- Cited by
- 253
- References
- 6
- FWCI
- 6.91
- Type
- journal article
- Language
- en
- Open access
- green
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- Ai, M., Holmen, S. L., Van Hul, W., Williams, B. O., & Warman, M. L. (2005). Reduced Affinity to and Inhibition by DKK1 Form a Common Mechanism by Which High Bone Mass-Associated Missense Mutations in LRP5 Affect Canonical Wnt Signaling. Molecular and Cellular Biology. https://doi.org/10.1128/mcb.25.12.4946-4955.2005
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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