ArticleFrontiers in cell and developmental biology2020
Conditional Knockout of PKC-δ in Osteoclasts Favors Bone Mass Accrual in Males Due to Decreased Osteoclast Function.
Article in Frontiers in cell and developmental biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed, 9 citations in OpenAlex.
- Review
- RUFY4 deletion prevents pathological bone loss by blocking endo-lysosomal trafficking of osteoclasts.Bone research · 2024Article
- Recent Advances in Osteoclast Biological Behavior.Frontiers in cell and developmental biology · 2021Review
- Functional proteomic analysis reveals roles for PKCδ in regulation of cell survival and cell death: Implications for cancer pathogenesis and therapy.Advances in biological regulation · 2020Article
- Sexual Dimorphism in Osteoclasts.Cells · 2020Review
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Authors and funding
11 authors at 5 institutions in 2 countries.
Funding
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Abstract
Protein kinase C delta (PKC-δ) functions as an important regulator in bone metabolism. However, the precise involvement of PKC-δ in the regulation of osteoclasts remains elusive. We generated an osteoclast specific PKC-δ knockout mouse strain to investigate the function of PKC-δ in osteoclast biology. Bone phenotype was investigated using microcomputed tomography. Osteoclast and osteoblast parameters were assessed using bone histomorphometry, and analysis of osteoclast formation and function with osteoclastogensis and hydroxyapatite resorption assays. The molecular mechanisms by which PKC-δ regulated osteoclast function were dissected by Western Blotting, TUNEL assay, transfection and transcriptome sequencing. We found that ablation of PKC-δ in osteoclasts resulted in an increase in trabecular and cortical bone volume in male mice, however, the bone mass phenotype was not observed in female mice. This was accompanied by decreased osteoclast number and surface, and Cathepsin-K protein levels
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