Control

we don't want pathways running all te time--> we turn them on and off

• 1) allosteric control (most rapid method)
• 2) reversible covalent modification (phosphorylation)
• --> longer because you have to take in a kinase
• 3) control amount of enzyme; level of transcription (slowest response)

• hexokinase
• phosphofructokinase: the most important step because it is committed (on/off)
• pyruvate kinase
• hexokinase and pyruvate kinase are regulatory

• controlled allosterically; responds to high ATP levels
• Also, due to lower pH as a result of lactic acid, aTP turns i off.

ATP binds to allosteric sights on phosphofructokinase, causing a conformational change in which the enzyme has a lower affinity for the substrate. There's a lot of energy.

• reversed by high levels of AMP
• adenylate kinase can take two ADP molecules and convert it into ATP and AMP.

This occurs when a cell is desperate for ATP

AMP turns it on

• The flow into glycolysis (controlled by hexokinase)
• the flow out of glycolysis (controlled by pyruvate kinase)

A buildup of fructose 6-phosphate causes a buildup of glucose 6-phosphate, which it is in equilibrium with. This clogs up the active site of hexokinase, turning it off (in muscle)

Glucose that gets into muscle cells can now get back out and go to other places

it is inhibited by high levels of ATP--> slow down the enzyme

An amino acid made from pyruvate  is alanine. If in high concentration, pyruvate kinase slows down

It never deals with pH change

• inhibited by ATP in the same way
• Also inhibited by citrate in CAC, which can lead into the cytoplasm, signifying that building blocks are present, enhancing ATP production

fructose 2,6-bisphosphate (F-2,6-BP)

Glucose levels high in bloodstream; buildup of fructose 2,6-bisphosphate; activates phosphofructokinase in liver

glucokinase

can't be inhibited by own product. It'll keep churning out G6P--> goes to be converted to glycogen

• in liver there is the L type
• reversible phosphorylation
• blood glucose levels low--> phosph kinase--> turn it off in liver--> glucose can escape and be used elsewhere

glucose high--> dephosphorylation--> glucose doesn't get away

• pyruvate
• pyruvate
• Acetyl CoA

• CO2
• lipids

control is in this area by the pyruvate dehydrogenase complex

• Enzyme E1 can be reversibly phosphorylated. 
• Kinases activate it by high levels of NADH, acetyl CoA, and ATP; all three say that energy content in the cell is okay
• shut off the omplex--> let pyruvate do something else

• Isocitrate dehydrogenase
• alpha-ketoglutrate dehydrogenase complex

allosteric changes from ATP and NADH 

high ATP and NADH turns it off

high ADP turns it on

responds to same as pyruvate dehydrogenase complex

• NADH, ATP, or its production 
• high levels shut off

they measure O2 consumption for results

control oxidative phosphorylation; flow of e- through ETC dependent on ADP levels

once ADP is added, O2 consumed at large rates

need for ATP controls oxidative phosphorylation

high ATP leads to flow of electrons in ETC

adipose cells with a lot of mitochondrion in them; found in animals that like to hibernate

these mitochondria produce Hydrogen gradient

if you're hibernating, proton gradient not used for ATP. You need to stay warm

A group of proteins (UCP)= uncoupling proteins

they uncouple the link ebtween electron transport and use of hydrogen gradient to make ATP

allows buildup an flow of Hydrogen ion, making heat

• flagellar rotation
• active transport
• electron potential
• heat production
• NADPH synthesis
• ATP