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WISP-3/CCN6 has a role in inhibiting apoptosis by regulating caspase pathway after hyperoxia in lung epithelial cells
WISP3 gene was associated with developmental dysplasia of the hip (DDH) in Chinese Han population. GGCGG haplotype might be a biomarker for DDH.
analysis of WISP3 mutations causing progressive pseudorheumatoid dysplasia in Jammu and Kashmir-India
we found that WISP-3 induced VEGF-A expression and subsequently promoted angiogenesis and tumor growth in human chondrosarcoma cells via suppressing miR-452 through the c-Src and p38 signaling cascades.
These results demonstrate that CCN6 regulates epithelial and mesenchymal states transition and tumor initiating cells programs in breast cancer
two WISP3 mutations have been identified in two affected siblings by targeted NGS, thus permitting the clinical diagnosis of PPD. This case supports the utility of NGS in the genetic characterization of skeletal dysplasias, which in turn may aid their clinical care, permit predictive screening, and to provide genetic counselling to families.
CCN6 acts as a molecular brake, which is appropriately balanced by Nrf2, in regulating mitochondrial function.
Studies indicate that the CYR61 CTGF NOV matricellular proteins (CCN family of proteins) comprises the members CCN1, CCN2, CCN3, CCN4, CCN5 and CCN6 and have been identified in various types of cancer.
WISP3 harbored not only frameshift mutation but also mutational intratumoral heterogeneity and loss of expression, which together might play a role in tumorigenesis of GC and CRC with MSI-H by inhibiting tumor suppressor functions of WISP3.
WISP3 variant leads to the diagnosis of SEDT-PA.
Novel and recurrent mutations in WISP3 and an atypical phenotype have been described in Indian families with progressive pseudorheumatoid dysplasia.
A novel mutation c.667T>G (p.Cys223Gly) and the c.857C>G (p.Ser286*) mutation were detected in three Chinese patients with PPD.
This study identified 3 different WISP3 mutations in 2 unrelated Chinese families with spondyloepiphyseal dysplasia tarda with progressive arthropathy.
Suggest WISP3-Wnt/beta-catenin axis may have role in regulating gastric cancer cell proliferation and metastasis.
Novel C223G and C252X mutations in exon 4 of the WISP3 gene are responsible for progressive pseudorheumatoid dysplasia in Chinese patients.
Results are indicative of an operational WISP3-IGF1 regulatory loop whereby WISP3 preserves cartilage integrity by restricting IGF1-mediated hypertrophic changes in chondrocytes, at least partly, upon interaction with IGF1.
A report on 11 different homozygous mutations and one instance of compound heterozygosity in the WISP3 gene in patients with progressive pseudorheumatoid dysplasia.
These results reveal a novel function of the matricellular protein CCN6 and establish a mechanistic link between CCN6 and TbetaRIII in maintaining acinar organization in the breast.
Mutation analysis of WISP3 allowed the confirmation of the diagnosis in 63 out of 64 typical cases of progressive pseudorheumatoid dysplasia.
The data presented in this study reveal that CCN6 downregulation disrupts acinar morphogenesis and promotes invasion of mammary epithelial cells
One paralog of mammalian wisp3 was found in zebrafish.
Overexpression of zebrafish Wisp3 protein inhibited bone morphogenetic protein (BMP) and Wnt signaling in developing zebrafish.
This gene encodes a member of the WNT1 inducible signaling pathway (WISP) protein subfamily, which belongs to the connective tissue growth factor (CTGF) family. WNT1 is a member of a family of cysteine-rich, glycosylated signaling proteins that mediate diverse developmental processes. The CTGF family members are characterized by four conserved cysteine-rich domains: insulin-like growth factor-binding domain, von Willebrand factor type C module, thrombospondin domain and C-terminal cystine knot-like domain. This gene is overexpressed in colon tumors. It may be downstream in the WNT1 signaling pathway that is relevant to malignant transformation. Mutations of this gene are associated with progressive pseudorheumatoid dysplasia, an autosomal recessive skeletal disorder, indicating that the gene is essential for normal postnatal skeletal growth and cartilage homeostasis. Multiple transcript variants encoding different isoforms have been found for this gene.
CCN family member 6
, WNT1-inducible-signaling pathway protein 3
, WNT1 inducible signaling pathway protein 3
, WNT1-inducible-signaling pathway protein 3-like