desmoglein

They are made of two specialized cadherins, desmoglein and desmocollin.

Desmoglein 3 has been shown to interact with PKP3.

Disruption of function: In this case, the antibody blocks the desmoglein 1 from being formed into a desmosome.

Desmoglein 1, the protein that is destroyed by the autoantibody, is only found in the top dry layer of the skin.

Milder forms of pemphigus (like foliacious and erythematoses) are more desmoglein 1 heavy.

The autoimmune disease pemphigus vulgaris results from autoantibodies to desmoglein and other normal body proteins.

In pemphigus, autoantibodies form against desmoglein.

Desmoglein 1 is a protein that in humans is encoded by the DSG1 gene.

Exfoliating toxins are serine proteases that specifically bind to and cleave desmoglein 1 (Dsg1).

Steric hindrance of the desmoglein 1: The antibody caps off the site for intracellular binding to another keratinocyte.

The severity of the disease, as well as the mucosal lesions, is believed to be directly proportional to the levels of desmoglein 3.

If there is an autoimmune IgG buildup in the epidermis, then nearly almost all of the antibodies are aimed against desmoglein 1.

Toxins are produced by S. aureus and target desmoglein, which is a desmosomal cell-cell adhesion molecule that is found in the upper levels of the epidermis.

Other features that have been reported include the abnormal deposition of laminin and heparan sulfate proteoglycan within the basement membrane and increased expression of desmoglein.

The cell adhesion proteins of the desmosome, desmoglein and desmocollin, are members of the cadherin family of cell adhesion molecules.

A very similar non-infectious condition is seen in the autoimmune skin disorder pemphigus vulgaris in which there is an IgG antibody against the cadherin desmoglein 3.

Exfoliatins are glutamate-specific serine proteases highly specific to the cadherin desmoglein I, an adhesion protein in the desmosomes of the stratum granulosum that facilitates intracelluar adhesion between keratinocytes.

Blistering diseases such as Pemphigus vulgaris and Pemphigus foliaceus are autoimmune diseases in which auto-antibodies target the proteins desmoglein 3 and desmoglein 1 respectively.

A characteristic of EMT is loss of the epithelial markers (E-cadherin, cytokeratins, claudin, occluding, desmoglein, desmocolin) and gain of mesenchymal markers (N-cadherin, vimentin, fibronectin) .

The extracellular domain of the desmosome is called the Extracellular Core Domain (ECD) or the Desmoglea, and is bisected by an electron-dense midline where the desmoglein and desmocollin proteins bind to each other.

It is an autoimmune disease caused by antibodies directed against both desmoglein 1 and desmoglein 3 resulting in the loss of cohesion between keratinocytes in the epidermis, classified as a type II hypersensitivity reaction.