ArticleMolecular and cellular biology2005
WISP3, the gene responsible for the human skeletal disease progressive pseudorheumatoid dysplasia, is not essential for skeletal function in mice.
Article in Molecular and cellular biology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 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
40 citing papers in PubMed, 65 citations in OpenAlex.
- From farm to lab: gene-edited sheep transforming bone research.JBMR plus · 2026Review
- CCN Proteins as Matricellular Regulators of Bone in Aging and Disease.Current osteoporosis reports · 2025Review
- A monoallelic variant in CCN2 causes an autosomal dominant spondyloepimetaphyseal dysplasia with low bone mass.Bone research · 2024Article
- Dual roles of cellular communication network factor 6 (CCN6) in the invasion and metastasis of oral cancer cells to bone via binding to BMP2 and RANKL.Carcinogenesis · 2023Article
- Why do humans need thrombospondin-1?Journal of cell communication and signaling · 2023Review
- Significance of CCNs in liver regeneration.Journal of cell communication and signaling · 2023Review
- Temperal and spatial expression of CCN1, CCN3, CCN4, CCN5 and CCN6 proteins in the developing postnatal teeth.Journal of cell communication and signaling · 2023Article
- Fibroblast Growth Factors and Cellular Communication Network Factors: Intimate Interplay by the Founding Members in Cartilage.International journal of molecular sciences · 2022Review
- CCN proteins in the musculoskeletal system: current understanding and challenges in physiology and pathology.Journal of cell communication and signaling · 2021Review
- Differential intolerance to loss of function and missense mutations in genes that encode human matricellular proteins.Journal of cell communication and signaling · 2021Article
- Novel homozygous variant inClinical case reports · 2020Article
- Skeletal phenotype/genotype in progressive pseudorheumatoid chondrodysplasia.Clinical rheumatology · 2020Article
- Matricellular CCN6 (WISP3) protein: a tumor suppressor for mammary metaplastic carcinomas.Journal of cell communication and signaling · 2018Review
- Genes uniquely expressed in human growth plate chondrocytes uncover a distinct regulatory network.BMC genomics · 2017Article
- MMTV-cre;Ccn6 knockout mice develop tumors recapitulating human metaplastic breast carcinomas.Oncogene · 2017Article
- Emerging roles of CCN proteins in vascular development and pathology.Journal of cell communication and signaling · 2016Article
- WISP3 mutational analysis in Indian patients diagnosed with progressive pseudorheumatoid dysplasia and report of a novel mutation at p.Y198.Bone & joint research · 2016Article
- Del1 Knockout Mice Developed More Severe Osteoarthritis Associated with Increased Susceptibility of Chondrocytes to Apoptosis.PloS one · 2016Article
- Emerging role of CCN family proteins in tumorigenesis and cancer metastasis (Review).International journal of molecular medicine · 2015Review
- A homozygous deletion of exon 1 in WISP3 causes progressive pseudorheumatoid dysplasia in two siblings.Human genome variation · 2015Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
In humans, loss-of-function mutations in WISP3 cause the autosomal recessive skeletal disease progressive pseudorheumatoid dysplasia (PPD) (Online Mendelian Inheritance in Man database number 208230). WISP3 encodes Wnt1-inducible signaling protein 3, a cysteine-rich, multidomain, secreted protein, whose paralogous CCN (connective tissue growth factor/cysteine-rich protein 61/nephroblastoma overexpressed) family members have been implicated in diverse biologic processes including skeletal, vascular, and neural development. To understand the role of WISP3 in the skeleton, we targeted the Wisp3 gene in mice by creating a mutant allele comparable to that which causes human disease. We also created transgenic mice that overexpress human WISP3 in cartilage. Surprisingly, homozygous Wisp3 mutant mice appear normal and do not recapitulate any of the morphological, radiographic, or histological abnormalities seen in patients with PPD. Mice that overexpress WISP3 are also normal. We conclude, that in contrast to humans, Wisp3 is not an essential participant during skeletal growth or homeostasis in mice.
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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.