v-akt murine thymoma viral oncogene homolog 3 (AKT3), also known as PKB-GAMMA, with AKT1/PKBalpha, AKT2/PKBbeta, are the memerbers of Akt kinase family, share extensive structural similarity and perform common as well as unique functions within cells. The Akt signaling cascade initiates at the cell surface when growth factors or other extracellular stimuli activate phosphoinositide 3-kinase (PI3K). AKT3 was discovered to be the predominant isoform activated in sporadic melanomas. Levels of activity increased during melanoma progression with metastatic melanomas having the highest activity. Although mechanisms of AKT3 activation remain to be fully characterized, overexpression of AKT3 and decreased PTEN activity play important roles in this process. Targeted reduction of AKT3 activity decreased survival of melanoma tumor cells leading to inhibition of tumor development, which may be therapeutically effective for shrinking tumors in melanoma patients. AKT2 and AKT3 play an important role in the viability of human malignant glioma cells. Targeting AKT2 and AKT3 may hold promise for the treatment of patients with gliomas.
Activated leukocyte cell adhesion molecule (ALCAM), also named as CD166 and MEMD, is a typeI transmembrane glycoprotein of immunoglobulin superfamily, which mediates homotypic and heterotypic interactions between cells. ALCAM interacts with high affinity with CD6 molecule but weaker homotypic (ALCAM–ALCAM) interactions have also been described. ALCAM–CD6 interactions play an important role in the maintenance of T cell activation, proliferation as well as in formation of immune synapse between antigen-presenting cell and lymphocytes. ALCAM is expressed on a wide variety of cells, particularly on activated lymphocytes, dendritic cells and monocytes, and on various epithelial cell types. It is also involved in multiple processes including embryogenesis, hematopoiesis, angiogenesis, and immune response. While expressed in a wide variety of tissues, ALCAM is usually restricted to subsets of cells in most adult tissues. Recently studies showed ALCAM has prognostic relevance in several human carcinomas, and it has been used as a biomarker for several tumor entities, including melanoma, gynecologic, urologic, and gastrointestinal cancers.
Activated leukocyte cell adhesion molecule (ALCAM)/Cluster of differentiation (CD166) is a type I transmembrane cell adhesion molecule belonging to the Ig superfamily and a ligand for CD6 that is expressed on T lymphocytes. The extracellular domain of ALCAM contains five Ig-like domains (three Ig-like C2-type domains and two Ig-like V-type domains), of which the amino-terminal V1 domain is essential for ligand binding and ALCAM-mediated cell aggregation. ALCAM mediates both heterophilic (ALCAM-CD6) and homophilic (ALCAM-ALCAM) cell-cell interactions. ALCAM/CD6 interaction plays a role in T cell development and T cell regulation, as well as in the binding of T- and B-cells to activated leukocytes. Recently, homophilic (ALCAM-ALCAM) adhesion was shown to play important roles in tight cell-to-cell interaction and regulation of stem cell differentiation. While expressed in a wide variety of tissues, ALCAM is usually restricted to subsets of cells involved in dynamic growth and/or migration, including neural development, branching organ development, hematopoiesis, immune response and tumor progression. And CD166 is regarded as a potential novel breast cancer indicator and therapeutic target.
Activin Receptor-Like Kinase 1 (ALK-1) is a type I cell-surface receptor for the TGF-β superfamily of ligands, which mediates signaling of BMP9 (bone morphogenetic protein) and BMP10. ALK1 signaling is necessary for angiogenesis during embryogenesis, wound healing, and tumor growth. ALK-1 has a high degree of similarity in serine-threonine kinase subdomains, a glycine and serine rich region preceding the kinase-domain, and a C-terminal tail with other activin receptor-like kinase proteins. ALK-1 is mainly expressed in endothelial cells regulating proliferation and migration in vitro and angiogenesis in vivo. Mutations in ALK-1 as well as in endoglin are associated with hereditary hemorrhagic telangiectasia (HHT), suggesting ALK-1 plays a critical role for in the control of blood vessel development or repair.
Activin A receptor, type II-like 1 (ACVRL1), also known as ALK-1 (activin receptor-like kinase 1), is an endothelial-specific type I receptor of the TGF-beta (transforming growth factor beta) receptor family of ligands. On ligand binding, a heteromeric receptor complex forms consisting of two type II and two type I transmembrane serine/threonine kinases. ACVRL1 protein is expressed in certain blood vessels of kidney, spleen, heart and intestine, serving as an important role during vascular development. Mutations in ACVRL1 gene are associated with hemorrhagic telangiectasia type 2, also known as Rendu-Osler-Weber syndrome 2 and vascular disease.
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