CCN3 and calcium signaling.

Cell Commun Signal

Laboratoire d'Oncologie Virale et Moléculaire, Tour 54, Case 7048, Université Paris 7-D,Diderot, 2 Place Jussieu 75005 PARIS, France.

Published: August 2003

The CCN family of genes consists presently of six members in human (CCN1-6) also known as Cyr61 (Cystein rich 61), CTGF (Connective Tissue Growth Factor), NOV (Nephroblastoma Overexpressed gene), WISP-1, 2 and 3 (Wnt-1 Induced Secreted Proteins). Results obtained over the past decade have indicated that CCN proteins are matricellular proteins, which are involved in the regulation of various cellular functions, such as proliferation, differentiation, survival, adhesion and migration. The CCN proteins have recently emerged as regulatory factors involved in both internal and external cell signaling. CCN3 was reported to physically interact with fibulin-1C, integrins, Notch and S100A4. Considering that, the conformation and biological activity of these proteins are dependent upon calcium binding, we hypothesized that CCN3 might be involved in signaling pathways mediated by calcium ions.In this article, we review the data showing that CCN3 regulates the levels of intracellular calcium and discuss potential models that may account for the biological effects of CCN3.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC244900PMC
http://dx.doi.org/10.1186/1478-811X-1-1DOI Listing

Publication Analysis

Top Keywords

ccn proteins
8
ccn3
5
proteins
5
ccn3 calcium
4
calcium signaling
4
signaling ccn
4
ccn family
4
family genes
4
genes consists
4
consists presently
4

Similar Publications

Stage-Dependent Fibrotic Gene Profiling of WISP1-Mediated Fibrogenesis in Human Fibroblasts.

Cells

December 2024

Biotherapeutics Enabling Biology, Lilly Research Laboratories, Eli Lilly and Company, Indianapolis, IN 46225, USA.

Idiopathic pulmonary fibrosis (IPF) is the most common interstitial lung disease with unknown etiology, characterized by chronic inflammation and tissue scarring. Although, Pirfenidone and Nintedanib slow the disease progression, no currently available drugs or therapeutic interventions address the underlying cause, highlighting the unmet medical need. A matricellular protein, Wnt-1-induced secreted protein 1 (WISP1), also referred to as CCN4 (cellular communication network factor 4), is a secreted multi-modular protein implicated in multi-organ fibrosis.

View Article and Find Full Text PDF

Unlocking the therapeutic potential of WISP-1: A comprehensive exploration of its role in age-related musculoskeletal disorders.

Int Immunopharmacol

January 2025

Department of Orthopedics, Xiangya Hospital, Central South University, Changsha 410008, China; National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha 410008, China. Electronic address:

As the global population ages, the incidence of age-related musculoskeletal diseases continues to increase, driven by numerous complex and poorly understood factors. WNT-1 inducible secreted protein 1 (WISP-1), a secreted matrix protein, plays a critical role in the growth and development of the musculoskeletal system, including chondrogenesis, osteogenesis, and myogenesis. Numerous in vivo and in vitro studies have demonstrated that WISP-1 is significantly upregulated in age-related musculoskeletal conditions, such as osteoarthritis, osteoporosis, and sarcopenia, suggesting its involvement in the pathogenesis of these diseases.

View Article and Find Full Text PDF

CCN1 Promotes Mesenchymal Phenotype Transition Through Activating NF-κB Signaling Pathway Regulated by S100A8 in Glioma Stem Cells.

CNS Neurosci Ther

December 2024

Department of Neurosurgery, Qilu Hospital, Cheeloo College of Medicine and Institute of Brain and Brain-Inspired Science, Shandong University, Jinan, Shandong, China.

Background: The presence of glioma stem cells (GSCs) and the occurrence of mesenchymal phenotype transition contribute to the miserable prognosis of glioblastoma (GBM). Cellular communication network factor 1 (CCN1) is upregulated within various malignancies and associated with cancer development and progression, while the implications of CCN1 in the phenotype transition and tumorigenicity of GSCs remain unclear.

Methods: Data for bioinformatic analysis were obtained from The Cancer Genome Atlas (TCGA) and Chinese Glioma Genome Atlas (CGGA) databases.

View Article and Find Full Text PDF
Article Synopsis
  • The study analyzed how specific mutations at Asp187 and Ser188 in the protease cocoonase (CCN) affect its ability to recognize substrates and carry out enzymatic activity.
  • Mutations at Asp187 significantly reduced enzymatic activity, highlighting its key role, while changes at Ser188 had a lesser impact but still contributed to substrate recognition.
  • Substituting Asp187 with other residues resulted in new substrate specificities, suggesting that the structure of the precursors remains stable, which may affect how the enzyme interacts with substrates and its overall catalytic function.
View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!