![]() In epithelial cells, adherens junctions are formed by calcium-dependent homotypic interactions between E-cadherins on the surface of opposing cells. ![]() Furthermore, a pool of phosphorylated JNK is localized in focal adhesions (14), where it promotes cell migration by phosphorylating the focal adhesion protein paxillin (15).Ĭell-cell adhesion is crucial to many aspects of multicellular existence, including morphogenesis, tissue integrity, and differentiation (16). In mammalian cells, JNK is phosphorylated only in cells at the edge of the wound, and inhibition of JNK pathway blocks migration and lamellipodia extension (13). Subsequent studies suggested that JNK signaling may also be important in movement of epithelial sheets (5, 6), wound healing (7), apoptosis (8, 9, 10), cell survival (11), and tumor development (12). ![]() JNKs were originally identified by their ability to phosphorylate c-jun in response to stress induced by a variety of stimuli, such as TNF-α (3) or UV radiation (4). The c-Jun N-terminal kinases (JNKs), also known as stress-activated protein kinases, belong to the mitogen-activated protein kinase (MAPK) group of serine threonine protein kinases (1, 2).
0 Comments
Leave a Reply. |
AuthorWrite something about yourself. No need to be fancy, just an overview. ArchivesCategories |