Four receptor families: G-protein coupled receptors (GPCRs), receptor tyrosine kinases (RTKs), ligand-gated ion channels, and intracellular receptors for lipid-soluble ligands. Steroid and thyroid hormones cross the membrane and act directly as transcription factors — slow but long-lasting.
GPCRs and Second Messengers
Ligand binding makes Gα swap GDP for GTP: Gs activates adenylyl cyclase (cAMP up, PKA on), inhibits it, activates phospholipase C to make (releases ER ) and DAG (activates PKC).
Start by reading the study notes and working through the examples on this page. Then use the flashcards to test your recall. Regular review and active practice are key to retention.
Is this Cell Signaling study guide free?▾
Yes — all study notes, flashcards, and practice problems for Cell Signaling on Study Mondo are free to access. No account is needed.
What course covers Cell Signaling?▾
Cell Signaling is part of the MCAT Prep course on Study Mondo, specifically in the Biological & Biochemical Foundations section. You can explore the full course for more related topics and practice resources.
Gi
Gq
IP3
Ca2+
Cholera toxin locks Gs on and pertussis toxin locks Gi off — both raise cAMP. Caffeine and sildenafil inhibit phosphodiesterases, prolonging cAMP or cGMP signals.
RTKs, Amplification, and NO
RTKs dimerize and autophosphorylate tyrosines, recruiting adapters into the Ras-MAPK growth cascade; constitutively active RTKs (HER2, EGFR) and GTPase-dead Ras drive cancer.
Each cascade step multiplies the signal: 1 ligand→many G-proteins→many cAMP→millions of products
Nitric oxide diffuses through membranes, activates guanylyl cyclase, raises cGMP, and relaxes smooth muscle.
Key Takeaways
Know what each Gα subtype does and which second messengers result.
RTKs signal growth via dimerization and Ras-MAPK — no G-proteins involved.
Amplification explains why hormones act at nanomolar concentrations.
Desensitization (arrestin, internalization, downregulation) explains drug tolerance.