ArticleExperimental & molecular medicine2019
Adaptor protein CrkII negatively regulates osteoblast differentiation and function through JNK phosphorylation.
Article in Experimental & molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
- Propofol-induced osteogenic differentiation in dental pulp stem cells: Modulation of MAPK signaling under inflammatory conditions.Journal of dental sciences · 2025Article
- The guanine nucleotide exchange factor DOCK5 negatively regulates osteoblast differentiation and BMP2-induced bone regeneration via the MKK3/6 and p38 signaling pathways.Experimental & molecular medicine · 2025Article
- MLK3 silence suppressed osteogenic differentiation and delayed bone formation via influencing the bone metabolism and disturbing MAPK signaling.Journal of orthopaedic translation · 2023Article
- Icariin promotes the repair of bone marrow mesenchymal stem cells in rabbit knee cartilage defects via the BMP/Smad pathway.Annals of translational medicine · 2022Article
- Crk adaptor proteins are necessary for the development of the zebrafish retina.Developmental dynamics : an official publication of the American Association of Anatomists · 2022Article
- Exercise improves bone formation by upregulating the Wnt3a/β-catenin signalling pathway in type 2 diabetic mice.Diabetology & metabolic syndrome · 2021Article
- Bifunctional Role of CrkL during Bone Remodeling.International journal of molecular sciences · 2021Article
- Circular RNAs in stem cell differentiation: a sponge-like role for miRNAs.International journal of medical sciences · 2021Review
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
The adaptor protein CrkII is involved in several biological activities, including mitogenesis, phagocytosis, and cytoskeleton reorganization. Previously, we demonstrated that CrkII plays an important role in osteoclast differentiation and function through Rac1 activation both in vitro and in vivo. In this study, we investigated whether CrkII also regulates the differentiation and function of another type of bone cells, osteoblasts. Overexpression of CrkII in primary osteoblasts inhibited bone morphogenetic protein (BMP) 2-induced osteoblast differentiation and function, whereas knockdown of CrkII expression exerted the opposite effect. Importantly, CrkII strongly enhanced c-Jun-N-terminal kinase (JNK) phosphorylation, and the CrkII overexpression-mediated attenuation of osteoblast differentiation and function was recovered by JNK inhibitor treatment. Furthermore, transgenic mice overexpressing CrkII under control of the alpha-1 type I collagen promoter exhibited a reduced bone mass phenotype. Together, these results indicate that CrkII negatively regulates osteoblast differentiation and function through JNK phosphorylation. Given that CrkII acts as a negative and positive regulator of osteoblast and osteoclast differentiation, respectively, the regulation of CrkII expression in bone cells may help to develop new strategies to enhance bone formation and inhibit bone resorption.
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