The DOI matches its Crossref record; 21 of the 21 references it cites were found in a registry or an index.
Osteopetrosis in Src-deficient mice is due to an autonomous defect of osteoclasts.
Open accessAbstract
Osteopetrosis is a bone modeling disorder resulting in excessive accumulation of bone matrix due to defective function of osteoclasts, the cells that resorb bone. Mice carrying a targeted disruption of the gene Src that encodes pp60c-src (Src), a nonreceptor protein tyrosine kinase, develop this phenotype but do not exhibit other overt defects despite the fact that the kinase is normally present in a broad variety of cell types. Because Src is expressed in osteoblasts as well as in osteoclasts and both are required for normal bone resorption, the basic defect could occur in either cell type. In this study we have used in vitro approaches and fetal liver transplantation into irradiated Src- recipients to demonstrate that the inherent defect is with osteoclasts and autonomous of the bone marrow microenvironment. This result (i) identifies a cell type in which Src function is essential and cannot be replaced by other related kinases and (ii) should allow the isolation of a substrate that is specific to Src.
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Cites
Targeted disruption of the c-src proto-oncogene leads to osteopetrosis in mice
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Association between the PDGF receptor and members of the src family of tyrosine kinases
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pp59fyn mutant mice display differential signaling in thymocytes and peripheral T cells
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Self-citationRequirement of pp60c-src expression for osteoclasts to form ruffled borders and resorb bone in mice.
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Cited by
The molecular understanding of osteoclast differentiation
Asagiri, M., & Takayanagi, H. (2007) · Bone · doi:10.1016/j.bone.2006.09.023 · Cited by 1,363
Requirement for NF-κB in osteoclast and B-cell development
Franzoso, G., Carlson, L., Xing, L., Poljak, L., Shores, E. W., Brown, K. D., Leonardi, A., Tran, T., Boyce, B. F., & Siebenlist, U. (1997) · Genes & Development · doi:10.1101/gad.11.24.3482 · Cited by 996
Self-citationThe ligand for osteoprotegerin (OPGL) directly activates mature osteoclasts.
Burgess, T. L., Qian, Y.-X., Kaufman, S., Ring, B. D., Van, G., Capparelli, C., Kelley, M., Hsu, H., Boyle, W. J., Dunstan, C. R., et al. (1999) · The Journal of Cell Biology · doi:10.1083/jcb.145.3.527 · Cited by 689
Src and Syk kinases: key regulators of phagocytic cell activation
Berton, G., Mócsai, A., & Lowell, C. A. (2005) · Trends in Immunology · doi:10.1016/j.it.2005.02.002 · Cited by 214
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Metadata
- Authors
- Lowe, C., Yoneda, T., Boyce, B. F., Chen, H., Mundy, G. R., & Soriano, P.
- Venue
- Proceedings of the National Academy of Sciences
- Published
- 1993-05-15
- Volume
- 90
- Issue
- 10
- Pages
- 4485-4489
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- OpenAlex
- W2028638661
- Cited by
- 329
- References
- 21
- FWCI
- 5.37
- Type
- journal article
- Language
- en
- Open access
- green
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- CoChat. (2026). Citation check: Osteopetrosis in Src-deficient mice is due to an autonomous defect of osteoclasts. https://app.cochat.ai/papers/10.1073/pnas.90.10.4485
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- Lowe, C., Yoneda, T., Boyce, B. F., Chen, H., Mundy, G. R., & Soriano, P. (1993). Osteopetrosis in Src-deficient mice is due to an autonomous defect of osteoclasts. Proceedings of the National Academy of Sciences. https://doi.org/10.1073/pnas.90.10.4485
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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