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Ligand Gated Ion Channels

Receptors are found on the surface of cells and have numerous functions. They act as binding sites or antigens to antibodies and other ligands and can communicate signals within a cell or between cells and even allow for transport of molecules into and out of the cell. Receptors are made of proteins and act as ligands to other proteins, molecules, drugs or toxins. Basically, the ligand will bind to the receptor and form a ligand-receptor complex. Certain ligands can activate a receptor. These are called agonists. Other ligands will deactivate or block the receptor from having a certain action. These are called antagonists. Antibodies can serve as binding materials and can also be agonists or antagonists. Receptor structure varies depending on the classification of the certain receptor. There are receptors that merely sit on the surface of cells and receptors that go across the external cellular membrane. These include G-protein coupled receptors and ligand- gated ion channels. Neuroreceptors are receptors for neurotransmitters in the brain. These receptors are activated solely by neurotransmitters like serotonin, dopamine, norepinephrine, and histamine. Some of these receptors are ligand-gated ion channels. Ligand-gated ion channels are transmembrane ion channels which can either be opened or closed in response to the binding of the chemical ligand.

The anti-clusterin antibody attaches to the clusterin protein. The first isoform is a chaperone protein that stops nonnative proteins from attaching to the cell. In actuality, this prevents the aggregation of blood plasma proteins from attaching during stress- induced situations. This protein does not require ATP to function. When this protein is secreted by cells it prevents the apoptosis process. There are other nuclear forms of clusterin that promote apoptosis. The notch 2 protein is a receptor on the membrane of cells and binds to ligands and anti-notch 2 antibodies. These proteins regulate the fate of the cell by influencing processes including differentiation, proliferation, and apoptosis specifically of osteoclasts or bone cells. Defects in NOTCH2 cause Alagille syndrome type 2 and Hajdu-Cheney syndrome (HJCYS). HJCYS is a skeletal disorder. Affected individuals have facial defects, osteoporosis, acro-osteolysis, and periodontal disease.


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