ArticlePloS one2010
Negative regulation of bone formation by the transmembrane Wnt antagonist Kremen-2.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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
34 citing papers in PubMed, 64 citations in OpenAlex.
- Ablation of the pro-apoptotic protein Bax protects mice from glucocorticoid-induced bone growth impairment.PloS one · 2012Trial
- Sox8 is essential for vertebrate gastrulation.EMBO reports · 2025Article
- Genetic Variants in theInternational journal of molecular sciences · 2024Article
- Wnt/β-catenin signaling components and mechanisms in bone formation, homeostasis, and disease.Bone research · 2024Review
- LINC01638 sustains human mesenchymal stem cell self-renewal and competency for osteogenic cell fate.Scientific reports · 2023Article
- Nanocomposite orthopaedic bone cement combining long-acting dual antimicrobial drugs.Biomaterials advances · 2023Article
- Wnt signaling: Essential roles in osteoblast differentiation, bone metabolism and therapeutic implications for bone and skeletal disorders.Genes & diseases · 2023Review
- Kremen2 drives the progression of non-small cell lung cancer by preventing SOCS3-mediated degradation of EGFR.Journal of experimental & clinical cancer research : CR · 2023Article
- Increased Kremen2 predicts worse prognosis in colon cancer.Pathology oncology research : POR · 2023Article
- Spine Metastases in Immunocompromised Mice after Intracardiac Injection of MDA-MB-231-SCP2 Breast Cancer Cells.Cancers · 2022Article
- Review
- The WNT1Bone research · 2021Article
- Lack of Pituitary Adenylate Cyclase-Activating Polypeptide (PACAP) Disturbs Callus Formation.Journal of molecular neuroscience : MN · 2021Article
- Glucocorticoids Influencing Wnt/β-Catenin Pathway; Multiple Sites, Heterogeneous Effects.Molecules (Basel, Switzerland) · 2020Review
- Knockdown of Kremen2 Inhibits Tumor Growth and Migration in Gastric Cancer.Frontiers in oncology · 2020Article
- DKK1 and Kremen Expression Predicts the Osteoblastic Response to Bone Metastasis.Translational oncology · 2018Article
- Wnt Pathway in Bone Repair and Regeneration - What Do We Know So Far.Frontiers in cell and developmental biology · 2018Review
- Identification of novel genes associated with fracture healing in osteoporosis induced by Krm2 overexpression or Lrp5 deficiency.Molecular medicine reports · 2017Article
- Structure of the Dual-Mode Wnt Regulator Kremen1 and Insight into Ternary Complex Formation with LRP6 and Dickkopf.Structure (London, England : 1993) · 2016Article
- Serum levels of sclerostin, Dickkopf-1, and secreted frizzled-related protein-4 are not changed in individuals with high bone mass causing mutations in LRP5.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2014Article
Corrections and comments
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Authors and funding
18 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Wnt signalling is a key pathway controlling bone formation in mice and humans. One of the regulators of this pathway is Dkk1, which antagonizes Wnt signalling through the formation of a ternary complex with the transmembrane receptors Krm1/2 and Lrp5/6, thereby blocking the induction of Wnt signalling by the latter ones. Here we show that Kremen-2 (Krm2) is predominantly expressed in bone, and that its osteoblast-specific over-expression in transgenic mice (Col1a1-Krm2) results in severe osteoporosis. Histomorphometric analysis revealed that osteoblast maturation and bone formation are disturbed in Col1a1-Krm2 mice, whereas bone resorption is increased. In line with these findings, primary osteoblasts derived from Col1a1-Krm2 mice display a cell-autonomous differentiation defect, impaired canonical Wnt signalling and decreased production of the osteoclast inhibitory factor Opg. To determine whether the observed effects of Krm2 on bone remodeling are physiologically relevant, we analyzed the skeletal phenotype of 24 weeks old Krm2-deficient mice and observed high bone mass caused by a more than three-fold increase in bone formation. Taken together, these data identify Krm2 as a regulator of bone remodeling and raise the possibility that antagonizing KRM2 might prove beneficial in patients with bone loss disorders.
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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.