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PFK
glycolysis committed step (F6P → F1,6-BP
Pyruvate kinases
glycolysis final step (PEP → pyruvate)
PDH complex
pyruvate → acetyl-CoA
CA cycle
oxidative decarboxylations
acetyl-CoA carboxylase
fatty acid synthesis committed step (acetyl-CoA → malonyl-CoA)
Acetyl-CoA carboxylase
anabolic (on when energy and building blocks are abundant, off when energy is low)
Catabolic enzymes
high ATP → inhibits, High AMP → activates
Anabolic enzymes
High ATP → activates, High AMP → inhibits
PFK
High ATP/citrate → inhibits, High AMP/F2-6BP→ activates
PFK two binding sites
active site - high affinity(low atp levels), allosteric - low affinity(high atp levels)
F2-6BP
pure signal, no metabolic role. Set by insulin/glucagon
Citrate effect on PFK vs Acetyl-CoA carboxylase
opposite affects, inhibits pfk and activates acetyl-coa
PDH complex
Activated by low energy (high atp, low adp) and pyruvate. Inhibited by ATP and acetyl-coA and NADH
Pyruvate Kinase (glycolysis step 10)
inhibited by ATP. Activated by F1-6BP.
feed-forward activation
upstream substrate or product activating a downstream enzyme. (1) f1-6bp activates pyruvate kinase (2) pyruvate activates PDH
CA Cycle
Activates from low energy (high adp/amp) inhibits from high atp and high nadh and succinyl-coA.
Acetyl-CoA Carboxylase
Activates from ATP , citrate , insulin. Inhibitors are AMP, palmitoyl-CoA (fatty acid abundance/ product) and catabolic hormones glucagon & epinephrine
high NADH inhibits catabolic pathways
shows the ETC is backed up, so point in making more reduced carriers so slows catabolism down
Glucagon & epinephrine
catabolism
Insulin
anabolism