CCN2/CTGF Protein, Rhesus macaque (HEK293, His)

Cellular communication network factor 2 (CCN2) is a mitogen secreted by vascular endothelial cells and a cysteine-rich secreted matrix cell protein. CCN2 is involved in chondrocyte proliferation and differentiation, cell adhesion of multiple cell types, and in mesenchymal cells such as chondrocytes, osteoblasts, and fibroblasts under multiple types of mechanical stress, such as tensile stress, compressive stress, and highly expressed under shear stress). Furthermore, CCN2 expression is regulated by activation of various mechanosensory signaling pathways, such as mechanosensing ion channels, integrin-focal adhesion-actin dynamics, Rho GTPase family members, Hippo-YAP signaling, and G protein-coupled receptors. body. Certain polymorphisms in the CCN2 gene are associated with a higher incidence of systemic sclerosis. In the field of airway fibrotic asthma, CCN2 and fibronectin (FN) are classic epithelial-to-mesenchymal transition (EMT) and fibrosis markers. CCN2 and FN are upregulated in A549 cells in response to AREG stimulation. EGFR/JNK/AP-1 activation by AREG stimulation further mediates TGF-β-induced EMT in human lung epithelial cells. CCN2 is also associated with platelet-derived growth factor. Sunitinib (HY-10255A) induces autophagy through the TOLLIP (Toll-interacting protein)-mediated endosome-related pathway, leading to cardiomyocyte apoptosis and cardiac dysfunction. This maladaptive autophagy selectively degrades the cardiomyocyte survival mediator CCN2. Thus, sunitinib-induced cardiac dysfunction in vivo can be mimicked by the ability of adeno-associated virus serotype 9 (AAV9) to specifically knock down Ccn2.