• Publications
  • Influence
NOV (nephroblastoma overexpressed) and the CCN family of genes: structural and functional issues
  • B. Perbal
  • Biology
    Molecular pathology : MP
  • 1 April 2001
The variety of biological functions attributed to the CCN proteins has led to the proposal of a model in which physical interactions between the amino and carboxy portions of the CCNs modulate their biological activity and ensure a proper balance of positive and negative signals through interactions with other partners.
Proviral rearrangements and overexpression of a new cellular gene (nov) in myeloblastosis-associated virus type 1-induced nephroblastomas.
It is established that increasing levels of proviral rearrangement were associated with tumor progression and that 22 individual tumors, representative of different developmental stages, did not contain any common MAV1 integration site.
Proposal for a unified CCN nomenclature
A proposal is put forth to unify the nomenclature of the CCN family of secreted, cysteine rich regulatory proteins that regulate cell adhesion, migration, proliferation, survival, and differentiation through integrin mediated mechanisms.
Regulatory T cells promote myelin regeneration in the Central Nervous System
Findings reveal a new regenerative function of Treg in the CNS, distinct from immunomodulation, and identify CCN3 as a Treg-derived mediator of oligodendrocyte differentiation and myelination in vitro.
CCN3 (NOV) Interacts with Connexin43 in C6 Glioma Cells
Evidence is reported for an interaction of CCN3 with the C terminus of Cx43, which could play an important role in mediating growth control induced by specific gap junction proteins.
A structural approach to the role of CCN (CYR61/CTGF/NOV) proteins in tumourigenesis
The current data regarding the involvement of CCN proteins in tumourigenesis is reviewed and structural basis for the stimulatory and inhibitory functions of the full length and truncatedCCN proteins that are expressed in various tumour tissues are attempted.
CCN3 (NOV) is a negative regulator of CCN2 (CTGF) and a novel endogenous inhibitor of the fibrotic pathway in an in vitro model of renal disease.
Both CCN2 and CCN3 appear to act in a yin/yang manner to regulate ECM metabolism, which may serve to naturally limit fibrosis in vivo and provide opportunities for novel, endogenous-based therapeutic treatments.