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25 QA flashcards covering signaling, receptors, GPCR/RTK mechanisms, and mitochondrial/ETC biology.
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What are the four main types of cell signaling?
Autocrine (self), Paracrine (nearby), Endocrine (via blood, distant), Juxtacrine (direct contact).
Name the four receptor classes.
GPCR, RTK, Ion channel receptors, Intracellular/nuclear receptors.
Describe how a GPCR signals inside the cell.
Ligand binds; G-protein activated (GDP→GTP); second messengers produced (e.g., cAMP, IP3, DAG, Ca2+).
Give an example of GPCR dysfunction.
Cholera toxin locks Gαs on, increasing cAMP and causing massive fluid secretion/diarrhea.
Describe how an RTK signals.
Ligand binds (e.g., insulin); receptor dimerizes; autophosphorylation; downstream signaling cascade.
Give an example of RTK dysfunction.
Insulin receptor defect → diabetes (impaired glucose uptake).
What does cAMP do in signaling?
Activates protein kinase A (PKA).
What is the function of IP3 in signaling?
Causes release of Ca2+ from the endoplasmic reticulum.
What is the function of DAG in signaling?
Activates protein kinase C (PKC) in conjunction with Ca2+.
Describe the outer mitochondrial membrane.
Porous membrane containing porins.
Describe the inner mitochondrial membrane and its role.
Impermeable membrane that houses the ETC and ATP synthase; folded into cristae.
What is inside the mitochondrial matrix?
Krebs cycle enzymes, mitochondrial DNA, ribosomes, and production of NADH and FADH2.
Where do NADH and FADH2 donate electrons in the ETC?
NADH donates at Complex I; FADH2 donates at Complex II.
Outline the electron transport chain flow starting from NADH.
NADH → Complex I → CoQ → Complex III → Cyt C → Complex IV → O2.
What is the difference between NADH and FADH2 in terms of proton pumping and ATP yield?
NADH pumps more protons and yields ~2.5 ATP per NADH; FADH2 pumps fewer protons and yields ~1.5 ATP per FADH2.
How does ATP synthase make ATP?
Protons flow back into the matrix through ATP synthase; rotation drives ADP + Pi to ATP.
Define chemiosmosis.
Use of a proton gradient across the inner mitochondrial membrane to drive ATP synthesis.
Name common ETC inhibitors.
Rotenone (Complex I), Cyanide (Complex IV), Oligomycin (ATP synthase).
What is an uncoupler and give an example?
Uncouplers dissipate the proton gradient, producing heat instead of ATP; example: DNP.
Why do mitochondrial diseases affect muscles and neurons most?
These tissues have high energy demands; ATP shortages cause dysfunction (e.g., MELAS, LHON).
What happens when a cell runs out of ATP?
Ion pumps fail → cell swelling → necrosis (cell death).
Why is O2 essential in the ETC?
O2 is the final electron acceptor at Complex IV; without it, the ETC halts and no ATP is made.
How does FADH2 differ from NADH in the ETC?
FADH2 donates electrons at Complex II (bypassing Complex I); fewer protons are pumped, so less ATP is produced.
What is the role of porins in the outer mitochondrial membrane?
Porins form large channels allowing the passage of small solutes.
What happens to NADH and FADH2 after they donate electrons?
They are oxidized to NAD+ and FAD, respectively, and re-enter metabolic pathways.