lecture 1.1 summary

Ion channels

Mechanism: proteins embedded in cell membranes that form pores

examples: Sodium channels. Charged particles like sodium cannot cross lipid bilayers without help. Channels facilitate their passage

Therapeutic relevance: Modulating ion channels can alter cell function. For neurons, sodium channel activation leads to depolarization, which can be beneficial (cognition, wakefulness) or detrimental (seizures)

Types: Ligand-gated, voltage-gated

G Protein-Coupled Receptors (GPCRs)

Prevalence:The majority of currently approved drugs amplifies the signal

Mechanism: Involve a cascade(G protein activation) that amplifies the signal

G protein Subtypes:

• G alpha S: stimulatory (eg. activates adenylyl cyclase)

• G alpha I: inhibitory

• G alpha Q: Activates different pathways

Significance: The cascade effect allows for single drug molecule to have a powerful and rapid impact on the cell.

Enzymatic Receptors

Prevalence:Only about 3% of current drugs affect enzymatic targets

Types:

Receptor Tyrosine Kinase (RTKs):Ligand binding causes dimerization and activation of an enzyme that phosphorylates tyrosine amino acids

Phosphates Receptors

Kinase Function: kinases are enzymes that add phospahte groups to molecules

Intracellular receptors

Mechanism:Drugs must be lipophilic enough to cross the cell membrane to bind these receptors, which are located in the cytosol or nucleus

Outcome: Binding typically leads to changes in DNA transcription and the production of new proteins.

Examples: Steroid hormones like testosterone can affect muscle protein production.

ion channel picture

GPCR picture

enzymatic picture

intracellular picture