ArticleEndocrinology2010
Nephroblastoma overexpressed (Nov) inactivation sensitizes osteoblasts to bone morphogenetic protein-2, but nov is dispensable for skeletal homeostasis.
Article in Endocrinology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 34 citations in OpenAlex.
- CCN Proteins as Matricellular Regulators of Bone in Aging and Disease.Current osteoporosis reports · 2025Review
- Why do humans need thrombospondin-1?Journal of cell communication and signaling · 2023Review
- Structural insights into regulation of CCN protein activities and functions.Journal of cell communication and signaling · 2023Review
- Myeloid CCN3 protects against aortic valve calcification.Cell communication and signaling : CCS · 2023Article
- Single-cell atlas of craniogenesis uncovers SOXC-dependent, highly proliferative, and myofibroblast-like osteodermal progenitors.Cell reports · 2022Article
- Differential intolerance to loss of function and missense mutations in genes that encode human matricellular proteins.Journal of cell communication and signaling · 2021Article
- CCN3 and DLL1 co-regulate osteogenic differentiation of mouse embryonic fibroblasts in a Hey1-dependent manner.Cell death & disease · 2018Article
- Connective tissue growth factor (CCN2) is a matricellular preproprotein controlled by proteolytic activation.The Journal of biological chemistry · 2018Article
- Nuclear factor of activated T cells 2 is required for osteoclast differentiation and function in vitro but not in vivo.Journal of cellular biochemistry · 2018Article
- Characterization of bone morphology in CCN5/WISP5 knockout mice.Journal of cell communication and signaling · 2018Article
- Periostin is required for matricellular localization of CCN3 in periodontal ligament of mice.Journal of cell communication and signaling · 2017Article
- WNT1-induced Secreted Protein-1 (WISP1), a Novel Regulator of Bone Turnover and Wnt Signaling.The Journal of biological chemistry · 2015Article
- Targeted mutation of NOV/CCN3 in mice disrupts joint homeostasis and causes osteoarthritis-like disease.Osteoarthritis and cartilage · 2015Article
- Nemo-like kinase regulates postnatal skeletal homeostasis.Journal of cellular physiology · 2014Article
- Sex and genetic factors determine osteoblastic differentiation potential of murine bone marrow stromal cells.PloS one · 2014Article
- CCN3 protein participates in bone regeneration as an inhibitory factor.The Journal of biological chemistry · 2013Article
- CCN3 modulates bone turnover and is a novel regulator of skeletal metastasis.Journal of cell communication and signaling · 2012Article
- Taking aim at the extracellular matrix: CCN proteins as emerging therapeutic targets.Nature reviews. Drug discovery · 2011Review
- CCN family 2/connective tissue growth factor (CCN2/CTGF) promotes osteoclastogenesis via induction of and interaction with dendritic cell-specific transmembrane protein (DC-STAMP).Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2011Article
- Nephroblastoma overexpressed (Nov) induces gremlin in ST-2 stromal cell lines by post-transcriptional mechanisms.Journal of cellular biochemistry · 2011Article
Corrections and comments
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Authors and funding
6 authors at 5 institutions in 1 country.
Funding
Abstract
Overexpression of nephroblastoma overexpressed (Nov), a member of the Cyr 61, connective tissue growth factor, Nov family of proteins, inhibits osteoblastogenesis and causes osteopenia. The consequences of Nov inactivation on osteoblastogenesis and the postnatal skeleton are not known. To study the function of Nov, we inactivated Nov by homologous recombination. Nov null mice were maintained in a C57BL/6 genetic background after the removal of the neomycin selection cassette and compared with wild-type controls of identical genetic composition. Nov null mice were identified by genotyping and absent Nov mRNA in calvarial extracts and osteoblast cultures. Nov null mice did not exhibit developmental skeletal abnormalities or postnatal changes in weight, femoral length, body fat, or bone mineral density and appeared normal. Bone volume and trabecular number were decreased only in 1-month-old female mice. In older mice, after 7 months of age, osteoblast surface and bone formation were increased in females, and osteoclast and eroded surfaces were increased in male Nov null mice. Calvarial osteoblasts from Nov null mice displayed enhanced alkaline phosphatase activity, alkaline phosphatase mRNA, and transactivation of a bone morphogenetic protein (BMP)/phosphorylated mothers against decapentaplegic reporter construct in response to BMP-2. Similar results were obtained after the down-regulation of Nov by RNA interference in ST-2 stromal and MC3T3 cells. Osteoclast number was increased in marrow stromal cell cultures from Nov null mice. Surface plasmon resonance demonstrated direct interactions between Nov and BMP-2. In conclusion, Nov sensitizes osteoblasts to BMP-2, but Nov is dispensable for the maintenance of bone mass.
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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.