Cell adhesion

[4] Alterations in cell adhesion can disrupt important cellular processes and lead to a variety of diseases, including cancer[5][6] and arthritis.

[8][9] CAMs are classified into four major families: integrins, immunoglobulin (Ig) superfamily, cadherins, and selectins.

Intracellular domains of cadherins are also highly conserved, as they bind to proteins called catenins, forming catenin-cadherin complexes.

[10][11][12] Interactions with actin filaments can also promote clustering of cadherins, which are involved in the assembly of adherens junctions.

[15] Tight junction is formed by transmembrane proteins, including claudins, occludins and tricellulins, that bind closely to each other on adjacent membranes in a homophilic manner.

[17] Selectins are a family of specialised CAMs involved in transient cell–cell adhesion occurring in the circulatory system.

[25] Hemidesmosomes are important in maintaining structural stability of epithelial cells by anchoring them together indirectly through the extracellular matrix.

In focal adhesions, integrins attach fibronectins, a component in the extracellular matrix, to actin filaments inside cells.

[24] Adapter proteins, such as talins, vinculins, α-actinins and filamins, form a complex at the intracellular domain of integrins and bind to actin filaments.

[27] Molecules that are either nutrients or signals required for growth are transported, either passively or selectively, between plant cells through plasmodesmata.

[27] Protozoans express multiple adhesion molecules with different specificities that bind to carbohydrates located on surfaces of their host cells.

An example of a pathogenic protozoan is the malarial parasite (Plasmodium falciparum), which uses one adhesion molecule called the circumsporozoite protein to bind to liver cells,[29] and another adhesion molecule called the merozoite surface protein to bind red blood cells.

Pathogenic species such as Escherichia coli and Vibrio cholera possess flagella to facilitate adhesion.

[33] Adhesins can recognise a variety of ligands present on the host cell surfaces and also components in the extracellular matrix.

Loss of cell–cell adhesion in metastatic tumour cells allows them to escape their site of origin and spread through the circulatory system.

[38] This leads to reduced expression of β2 integrin heterodimers, which are required for leukocytes to firmly attach to the endothelial wall at sites of inflammation in order to fight infections.

[40] Pathogenic microorganisms, including bacteria, viruses and protozoans, have to first adhere to host cells in order to infect and cause diseases.

Anti-adhesion therapy can be used to prevent infection by targeting adhesion molecules either on the pathogen or on the host cell.