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How do drugs actually ( )? Scientists in the early 20th century realized that in order for a drug to exert its ( )( ), human cells must have a site for the recognition and acceptance of a ( ) type of drug. This site of drug action is termed a ( ), and drug-receptor interactions have now become the focus of research for new drugs and
are important in ( ) settings.
Receptors which are the primary targets of the majority of drugs are biological ( ) that have evolved specifically for ( ) communication to maintain life. Basically, the biological function of these receptors is to respond to the body's own chemical messengers such as ( ) or neurotransmitters. When binding takes place,
it triggers a series of biochemical and physiological changes known as a response.
Drugs which bind with receptors and mimic the effects of hormones or neurotransmitters are called ( ). Drugs which bind to the receptors but do not have the unique structural ( ) necessary to activate them are called ( ). Since antagonists occupy the binding site of the receptors, they prevent ( ) by agonists.
Based on their locations, receptors are classified into two groups: membrane and ( ) receptors. While membrane receptors are located on the cell ( ), intracellular receptors are located in the ( ). The intracellular receptors are separated into two classes and both are called ( ) receptors. Class I nuclear receptors are located in the cytoplasm, and after ( ) bind to them, receptor-ligand complexes migrate into the nucleus and bind to DNA, resulting in up- or down-regulation of gene ( ). Class II nuclear receptors are located in the nucleus ( ) to DNA and upon ligand binding, they are activated to regulate the expression of specific ( ).
genes bound expressions ligands nuclear cytoplasm membrane intracellular activation features
antagonists agonists hormones intercellular macromolecules clinical receptor specific
elective action work