[4] The intracellular portion of classical cadherins interacts with a complex of proteins that allows connection to the actin cytoskeleton.

The major function of desmoplakins is to bind to intermediate filament by interacting with plakoglobin, which attach to the ICS of desmogleins, desmocollins and plakophilins.

[10] Cadherins are synthesized as polypeptides and undergo many post-translational modifications to become the proteins which mediate cell-cell adhesion and recognition.

[12]  Because cadherins are Ca2+ dependent, they have five tandem extracellular domain repeats that act as the binding site for Ca2+ ions.

During development, their behavior assists at properly positioning cells: they are responsible for the separation of the different tissue layers and for cellular migration.

[16] Conversely, the expression of the N-cadherins remains unchanged in other regions of the neural tube that is located on the anterior-posterior axis of the vertebrate.

They participate greatly in keeping the ability of the structured heart due to pumping and release blood.

Because of the contribution of N-cadherins adhering strongly between the cardiomyocytes, the heart can overcome the fracture, deformation, and fatigue that can result from the blood pressure.

[1] After development, cadherins play a role in maintaining cell and tissue structure, and in cellular movement.

[18] The E-cadherin–catenin complex plays a key role in cellular adhesion; loss of this function has been associated with increased invasiveness and metastasis of tumors.

[19] The suppression of E-cadherin expression is regarded as one of the main molecular events responsible for dysfunction in cell-cell adhesion, which can lead to local invasion and ultimately tumor development.

[20] Additionally, the overexpression of type 5, 6, and 17 cadherins alone or in combination can lead to cancer metastasis, and ongoing research aims to block their ability to function as ligands for integral membrane proteins.

[21] It has been discovered that cadherins and other additional factors are correlated to the formation and growth of some cancers and how a tumor continues to grow.

[22] The loss of the cell adhesion molecules, E cadherins, is causally involved in the formation of epithelial types of cancers such as carcinomas.

E-cadherins, on the surface of all epithelial cells, are linked to the actin cytoskeleton through interactions with catenins in the cytoplasm.

In epithelial cell cancers, disrupted cell-cell adhesion that might lead to metastases can result from abnormalities in the expression of E-cadherin or its associated catenins.

The levels of these molecules increase during the luteal phase while their expression is regulated by progesterone with endometrial calcitonin.

[24] There are said to be over 100 different types of cadherins found in vertebrates, which can be classified into four groups: classical, desmosomal, protocadherins, and unconventional.

[26][27] These large amount of diversities are accomplished by having multiple cadherin encoding genes combined with alternative RNA splicing mechanisms.