Biochemistry Mini1 Part2

• irreversible acetylcholinesterase
• overactivation of the parasympatheic pathway
• similar to organo-phosphate poisioning

• Xanithine Oxidase inhibitor
• Prevent the breakdown of hypoxanthine to Urate
• Allievation of gout/uric acid poisoning

• Competitive inhibitor of succinate dehydrogenase
• displacing succinic acid

competitive inhibitor of alcohol dehydrogenase for methanol

• competitive inhibitor of alcohol dehydrogenase
• used for methanol and ethanol poisoning
• does not produce formaldehyde products which are poisonous to occular nerve

• the lower the Ki(Km of inhibitor) compared to the Km of the original (k-1/k1) substrate the more competitive the drug is for the inhibition of the ES complex
• instead forms EI complex

Km change in competitive and Vmax change in none competitive

• substrate binding changes the enzyme kinetics
• hemoglobin binding to oxygen is considered homotropic

• breaks NAM-NAG repeats in bacterial wall
• lysis of glycosidic bonds (2 sugars in this case)
• Glutamate and Aspartate catalytic peptides

• Serine-protease (serine lead bond breaking)
• his, asp, ser catalytic triad
• break down peptide bonds
• trypsin and elastase in the same family

• H₂O+CO₂<--> H₂CO₃
• bicarbonate buffer system
• binds metals
• conversion of CO2 to carbonic acid (intermediate)
• inhibitor Acetazolamide can treat glacoma and respiratory alkidosis by increasing CO2 levels in body

• Cholesterol biosynthesis
• end stage of beta hydroxylation
• over production of cholesteral in familial hypercholesterolemia
• Inhibitor of statin

• gets ride of your aceytlchoine into choline and acetate with water
• inhibitors are poisons (organophosphates fasciculin-II, diisopropyl phosphofluridate)

• Cyclin D+ CDK4/6 act.
• Cyclin E+ CDK2 act
• S - phase

• Cdc25 act
• CDK1
• Cyclin A+CDK1 act
• Cyclin B
• Cyclin B + CDK1 act
• Mitosis Promoting Factor

• Sister chromatid seperation using seperase
• Cdc20 act
• APC tagging
• securin for ubiquitinalytion
• seperase free to cut cohesin

• PFK1 phosphorolates fructose 6-phosphate
• committs sugar to glycolytic pathway
• add the 2nd ATP to the sugar molecue

• adds first ATP to sugar
• hexos version does all sugars with low Km
• Gluco version in liver is only for glucose and has high Km compared to hexos, will not be saturated and only kicks in when there is EXCESS glucose

• Adds 1 PiH to each of the two glyceraldehyde 3-phosphate WITHOUT using ATP
• produces 1,3 bisphospholycerate
• NAD+ is reduced to NADH
• NADH is used eithe rin oxidative phosphorylation or anarobic respiration of pryruvate to lactic acid
• 3rd and last Pi addition to sugar substrate
• now you have 2 bisphosphates each with 2 Pi's

• PGK - produces the first ATP of glycolysis
• taking the Pi that we just put on with GAPDH
• first pay off

2nd and last substrate level phosphorylation (not linked to eletrcon transport chain)

• 2ATP (added 4Pi but only 2 cost ATPs and took off 4Pi)
• 2NADH
• 2 pyruvate

• Gluconeogensis at liver
• makes glucose from lactate

• PFK-1 negativly regulated by ATP allocsticly
• increases Km while not affecting Vmax
• AMP lowers Km

• negative for PFK and PK - ATP
• pos for PFK and PK - AMP

• F2,6BP regulates PFK-1 by reducing its Km
• insulin/glucogon --> phosphorylation of PFK-2 --> phosphorylates F6P to F2,6BP(not a part of glycolysis) --> decreases Km for PFK-1

• Results from alcohol metabolism
• inhibits citric acid cycle, gluconeogensis and fatty acid oxidation
• promotes fatty acid synthesis in liver

• Alcohol dehydrogenase
• aldehyde dehydrogenase
• produce high energy NADH and acetate
• drive motabosim towards ketone bodies and fatty acids

• Control molecues
• ↓insulin ↑cAMP ↑PKA↑PFK-2 activity ↓F2,6BP↓PFK-1 activity ↓ glycolysis

vise versa

similar ↑ cAMP will ↑PKA BUUUT ↑ PFK-2 KINASE activity ↑F2,6BP ↑PFK-1

• PKA phosphorylation to change activity
• phosphorylate --> phosphatase in liver cells
• phosphorylate --> kinase in cardiac muscles

• ↑ATP/Ala ↓ PK
• ↑PEP ↑PK
• ↑F-1,6,P2 ↑PK
• ↑cAMP ↑PKA ↓PK -similar to liver glycolysis to conserve glucose during fasting or energy need

hexokinase deficiency in erythrocyte

• hemolytic anemia, pallor, jaundice, ulcers
• due to hemolytic issues, enlarged speen, low RBC
• low ATP with elevated 2,3,BPG
• genetic disorder for isozyme of PK in RBC

• grows
• inactive E2F-Rb form
• activated by CyclinD+Cdk4/6
• E2f free form produces Cyclin E

• promoted by free E2F
• with Cdk2 -> goes into S phase

• chromatid stress produced
• activates APC
• with cdc14 dephosphorylate seperase to activate

• APC ubiquitinalytes securin
• releases seperase
• seperase still phosphorylated(inactive, needs Cdc 20/14)

• regulated by amount of Cdc20 through APC
• inactive bound to securin
• active cleave cohesin --> anaphase

• Cdk 1 activity:
• activated by Cdc25 and deactivated by WEE-1

• Cdk-1 + Cyclin B
• Cdk activation by Cdc25
• Cyclin B activation by Cdk1+Cyclin A

• p53 kills (tumor necrosis factor)
• inactive if bound to mdm2
• alone it promots apoptosis

• Alcohol dehydrogenase (requires NAD+)
• --> acetal-adyhyde
• Acetalaldyhyde dehydrogenase
• -->acetic acid

• Alcohol degradation eats up NAD+ and pyruvate
• Both are needed for pyruvate carboxylase, rate limiting step of gluconeogenisis