Biochemistry Flashcards
Vitamin D
*Purpose?:
*Acquired from:
*Storage & Active form?
*Purpose: Proper intestinal absorption of calcium & phosphate
- Estt’l for bone and teeth growth
- Stimulates osteoblastic activity
*Acquired from Sun + Food
*Storage: 25-OH-D3 (in liver)
*Active form: 1,25-OH2(D3) (in kidney)
Vitamin D XS
Stones, Thrones, Groans, Psychiatric Overtones
Tx: Saline + Calcitonin
Calcitonin
*Produced by what?
*A hormone produced by parafollicular C cells
in the thyroid
- Inhibits osteoclast activity and renal reabsorption of Ca2+ & phosphate to reduce serum Ca2+
Vitamin D Deficiency
- Osteomalacia
- Rickets
Rickets
*What?
*Findings
*What?: Genetic Defect in renal absorption of phosphate, leads to deficiency in vitamin D
*Findings: Bowing of legs
Osteomalacia
*What?:
*Findings?:
*What?: Deficiency of Vit. D
*Findings: bone + joint pain, muscle weakness, gait difficulties, muscle spasm/cramping
*Tx: Vit. D Supplement
Vitamin E
*What enzymes does it help with?
*Role in what function?
*Deficiency:
*XS:
*Glutathione pathway to make NADPH
*Role in neurologic function
- Deficiency = dec. proprioception, dec. vibration
*Deficiency:
- Dec. proprioception, Dec. Vibration
- Presents similar to Vitamin B12
*XS: Enterocolitis
Warfarin
- MOA:
- Reverse effects
- Monitor:
- MOA: Inhibits Vitamin K dependent Co-factors: 2, 7, 9, 10
- Reverse effects: Fresh frozen plasma & Vitamin K
- Monitor: PT
Heparin
- MOA:
- Monitor:
- MOA: Inhibits antithrombin 3 and activated factor X
- Reverse effects:
- Monitor: PTT
Factor V Leiden
*Description
*Mutation
*Clotting factor amplifies the production of thrombin
*Mutation: uncontrolled clotting
Vitamin A
*Role
*XS
*Deficiency
*Tx
*Role:
- Helps with vision
- Helps epithelial cells differentiate into specialized cells
*XS:
- N/V
- Dizziness
- Alopecia, Dry Skin,Liver toxicity, hyperlipidemia, renal failure
- Teratogenic effects
*Deficiency:
- Poor skin health
- Bitot spots (keratin spots in the eye)
- Dec. CSF production
*Tx:
- Help treat AML!
Pseudotumor Cerebri
*Cause:
*Findings:
*Cause: XS CSF Production
*Finding: Papilledema (increased intracranial pressure that leads to eye issues)
- Headache
- CT Scan demonstrates enlargement of ventricles
*Tx: Carbonic Anhydrase Inhibitors
Vitamin B1 (Thiamine)
*Reactions?:
*Deficiency
*Reactions: Dehydrogenase reactions
*Deficiency: seen in alcoholics
- Dry Beriberi : Peripheral neuropathy
- Wet Beriberi: Neurologic findings + Cardiac Findings (CHF, edema, cardiomegaly)
- Wernicke Korsakoff Syndromes:
Acutely: Wernicke – Ophthalmoplegia, Nystagmus, Ataxia
Chronically: Korsakoff – Memory loss, confabulations, nystagmus, ataxia
Vitamin B2 (Riboflavin)
*What Co-Factor is this?
*Deficiency
*What co-factor is this?: FAD
*Deficiency: Chelitis, Photosensitivity, Skin Dryness
Vitamin B3 (Niacin)
*Precursor to?:
*Treatment
*Deficiency
*Precursor to NAD, NADH, NADPH, NADP
*Tx: Can treat dyslipidemia = increases HDL, dec. VLDL, TGs,
*Deficiency:
- Pellagra: (4D’s) Dementia, Dermatitis, Diarrhea, Death
- Fatigue, restlessness, irritability, decreased concentration, anxiety, depression
Hartnup Disease
*Mutation?
*What is it?:
*Mutation in SCL6A19
- Gene encodes for neutral amino acid transporter
*Loss of Neutral amino acids in the urine = dec. amount of tryptophan leads to dec. niacin –> pellagra
- shift of remaining tryptophan produces XS serotonin
Vitamin B5 (Pantathoic Acid)
*Role?
*Deficiency:
*Role:
- Helps synthesize fatty acids, amino acids, cholesterol, steroids, plays a role in 1st step of citric acid cycle
*Deficiency:
- Burning feet syndrome (5 toes = burning feet)
- Disruption of vitamin, cholesterol, amino acids
- Impaired Heme Synthesis
Vitamin B6 (Pyridoxine)
*Rxns?:
*Deficiency
*Role in decarboxylation rxn’s
*Helps synthesize neurotransmitters, sphingolipids, converts tryptophan to niacin, homocysteine –> Cysteine
*Deficiency: isoniazid causes B6 deficiency & peripheral neuropathy
Vitamin B9 (Folic Acid)
*Reactions:
*Esst’l for?
*Deficiency
*Reactions: Can make tetrahydrofolate
*Esst’l for neural tube development
*Deficiency: can cause megloblastic anemia
Vitamin B12 Deficiency what acids are elevated?
Elevated Homocysteine & methylmalonyl CoA Levels
Vitamin B12
*Reactions
*Failure to reabsorb B12 leads to?
*Reactions:
- Helps odd-chain FA recycling, when it’s deficient causes issues with myelin = issues w/ corticospinal & dorsal columns
- Needed to produce mehionine & THF
*Pernicious Anemia
Vitamin C (Ascorbic Acid)
*What?:
*Vitamin C needed for hydroxylation of lysin & proline
How do you treat Iron XS
Deferoxamine
Hypokalemia
*Cause
*Signs + Sx’s
*Caused:
- Vomiting, diarrhea, Diuretic use, Renal disease
*Sx’s:
- Fatigue
- Muscle weakness
- Constipation
- Cardiac Arrhythmia
- Paralysis
Bartter Syndrome
*Defect in TAL, NKCC2 co-transporter (looks like Loop diuretic)
- Loss of NaCl —> aldosterone stimulation –> loss of K+ and H+
- Causes Metabolic Alkalosis
Digoxin MOA
*What does Digoxin compete w/?
Inhibits the Na+/K+ ATPase, traps Na+ reverse the Na+/ Ca2+ exchangers, increases intracellular Ca2+ = slows HR and ^ contractility
- Digoxin competes with K+ for the same site on the ATPase,
- So ^ Digoxin = ^ K+ levels
What can you get hyperkalemia from?
- How can you treat hyperkalemia
*Acidosis, burns, leukocytosis, crush injury, lack of insulin
*Treat:
- Insulin
- Glucose
- Beta-2 Agonist
- Thiazide diuretics
- Loop diuretics
- Cation exchange resin
- Metabolic acidosis: give Na+ Bicarb
-
Cell Cycle
- What makes up metaphase?
- What inhibits metaphase?
Interphase: G1 (protein), S (DNA synthesis), G2 (make more proteins), M (mitosis)
*Mitosis = prophase, metaphase, anaphase, telophase
- Inhibited by: vincristine, vinblastine, colchicine
Prophase, Metaphase, Anaphase, Telophase, Cytokinesis
*Prophase: Chromosomes pair up
*Metaphase: Chromosomes line up at the midline plate
*Anaphase: Chromosomes pull apart
*Telophase: Chromosomes start to create membrane
*Cytokineses: Separate cell membranes are made
PCR
*Use
*Steps
*Use: Amplifies DNA
*Steps: (1) Denatures protein– strand separation
(2) Annealing–binding of primers upon cooling
(3) Elongation (DNA polymerase works in 5’ –> 3’ direction)
What is on th 5’ end?
- What does it require?
7-methylguanosine cap
- GTP
What is on the 3’ end?
- What does it require?
Poly-A tail
- ATP
Glycine
*Size
*Charge
*MOA
*Size: Small
*Charge: Negative
*MOA: Opens chloride channels & leads to the influx of chloride channels
What does the restriction enzyme, chymotrypsin, recognize?
Aromatic Amino Acids: Phenylalanine, Tryptophan, Tyrosine
Tryptophan is a precursor for…
Niacin and Serotonin
(5HTP –> serotonin needs Vit. B6)
- Serotonin can be converted into melatonin
Basic AA’s
*Move towards anode or cathode?
Lysine & Arginine
- Move towards cathode
Acidic AA’s
*Move towards anode or cathode?
*Stimulate what type of receptor?
Glutamate or aspartate (have COOH-)
- Move towards anode
- NMDA receptor (leads to Ca2+ influx) – glutamate stimulates NMDA stronger
Sulfur AA’s
- Help build?
Cysteine & Methionine
- Help build: Insulin, GH, prolactin, inhibin
Nitrogen contining AA’s
Glutamine + Asparagine
- Helps build muscle
What is maple syrup urine disease?
Absence of Branched-chain alpha-keto acid DH, causes body to not be able to break down branched chain AA’s
Methylmalonic Acidemia
Occurs with Vitamin B12 or Methylmalonyl CoA defficiency! Can’t make Succinyl CoA.
Tyrosine is a precuror to…
NE, E (does have a methyl group), Dopamine
Ketogenic AA’s
Lysine + Leucine
- Broken down to yield Acetyl CoA –> Ketones
GLucogenic + Ketogenic AA’s
PITTT:
- Phenylalanine
- Isoleucine
- Tyrosine
- Tryptophan
- Threonine
Essential AA’s
PVT TIM HALL
*Phenylalanine
*Valine
*Threonine
*Tryptophan
*Isoleucine
*Methionine
*Histidine
*Arginine
*Lysine
*Leucine
PKU
*Involves?
*Deficiency of?
*Involves?: Phenylalanine
*Deficiency of?: Phenylalanine Hydroxylase (can’t make tyrosine)
Albinism
*Involves?
*Deficiency of?
*Involves?: Tyrosine
*Deficiency of?: Tyrosinase
Alkaptonuria
*Involves?
*Deficiency of?
*Involves?: Tyrosine & Phenylalanine
*Deficiency of?: Homogentistic Acid Oxidase
- AR
- Blue/Black discoloration of CT
Maple Syrup Urine Disease
*Involves?
*Deficiency of?
*Involves?: Build up of branched-chain AA’s
- Maple trees have branches = branched chain AA’s
*Deficiency of?:
- Branched chain Alpha Keto Acid DH
G-protein S activates what? (say whole cascase)
Gs –> Adenylyl cyclase –> cAMP –> Protein Kinase A
- Protein Kinase A: phosphorylates serine & threonine
- Magnesium = Co-Factor
Gq cascade
Gq –> phospholipase C –> PIP2 –> DAG & IP3 –> allows movement of Ca2+ into cytosol –> actions
Receptors & their G-Proteins & Receptors action
“qiss & qiq siq sqs” = kiss & kick until you’re sick of sex
Alpha1
Alpha2
Beta1
Beta 2
M1
M2
M3
D1
D2
H1
H2
V1
V2
Alpha1: Gq ; SM contraction
Alpha2: Gi; Dec. NE release from pre-synpatic membrane
Beta1: Gs; ^ CO, HR, SV, Renin Release
Beta 2: Gs; SM relaxation
M1: Gq; Autonomic ganglia, CNS & Gastric Glands
M2: Gi; Heart & CNS
M3: Gq; SM of eye, viscera, exocrine glands + epithelium
D1: Gs; CNS
D2: Gi; Brain + Periphery
H1: Gq; SM, Vascular endothelial cells, heart, CNS
H2: Gs; Heart, CNS, PMN’s, vascular SM, Parietal Cells
V1: Gq; Vascular SM, platelets, heart, kidneys
V2: Gs; Kidney
Nitrates MOA
Increase cyclic GMP –> vasodilation, intracellular cGMP = vascular relaxation
*Veins & Arteries both dilate = decrease preload
Collagen Types
4 Types:
SCAB
- Type 1: Skin
- Type 2: Cartilage / Connective Tissue
- Type 3: Arteries
- Type 4: Basement Membrane
What is needed for collagen production?
*Lysine + Proline (Vitamin C)
*Copper
Glycosylation
Occurs in Golgi
Hydroxylation
Occurs in RER
Wound contractions happens with what?
- Abnormal connective tissue healing causes:
*Myofibrils & Fibrils
- Abnormal Healing: *Keloids & Desmoplasia
Scurvy
*Cause
*Sx’s
*Results of Vitamin C deficiency
- Leads to inability to hydroxylate proline + lysine in RER
*Sx’s: Gingival bleeding, petechiae, ecchymoses, perifollicular hemorrhage, poor wound healing
Ehler’s Danlos
*Cause
*Sx’s
*Cause: Faulty collagen synthesis
- Deficiencies of lysyl hydroxylase or pro-collagen peptidases
*Sx’s: Highly stretchable skin, hypermobile joints, easy bruising
Osteogenesis Imperfecta
*Abnormal collagen type 1 production
- leads to brittle bones
*Sx’s
- Skin gets SO thin you can see through it
- See choroidal veins
Keratin
*Proteinaceous structure rich in cysteine
- provides tensile strength to tissue
*Found in hair, nails, outer skin, cornea
*Epithelial cells:
- Tumors that stain (+) Keratin:
- Carcinomas, mesotheliomas, thymomas, sarcomas, trophoblastic tumors, desmoplastic small round cell tumors
Elastin
*Needed for stretching and recoiling properties
*Contains Hydroxyproline
*Contains smallest amino acid glycine
Anabolic Pathways take place in?
Cytoplasm/Cytosol
Catabolic Pathways take place in?
*What pathway is the exception?
*Break down pathways
*Mitochondria
- Controlled by epinephrine & glucagon
*Glycolysis: cytosol
What 3 pathways occur in cytoplasm & mitochondria?
(1) Heme Synthesis
(2) Gluconeogenesis
(3) Urea cycle
Types of energy used by different structures?
*Brain: Glucose (normal conditions), glucose (stress conditions), ketones (extreme stress)
*Heart: Lipids
*Muscle: Glucose, Fatty Acids, FA’s
*RBC: Glucose
Glucokinase
- Where does it work?
- Km
- Where does it work?: Works in the liver + beta islet cells in the pancreas
- Km: High Km, Low affinity
Hexokinase
- Where does it work?
- Km
- Where does it work?: Other tissues
- Km: LOW Km, High affinity for glucose
Rate limiting step of glycolysis
PFK-1
*Converts F-6-P —PFK-1—> F-1,6-BP
2,3 BPG
Causes a conformational change in hemoglobin molecule and forces it to release oxygen
Glycolysis produces how many net ATP’s? net NADH’s?
2 ATP’s ; 2 NADH’s/glucose
Last step in glycolysis
Phosphenylpyruvate —pyruvate kinase–> Pyruvate
2 methods for getting NADH into mitochondria
(1) Malate aspartate shuttle
- Alpha-KG–>OAA—-NADH-NAD+ & Malate DH—> Malate crosses mitochondria Malate –> OAA —> Alpha KG
(2) 3-phosphoglycerate shuttle (req. 2 ATP’s)
Gluconeogenesis
*4 Uni-directional enzymes
(1) Pyruvate Carboxykinase (Pyruvate –> OAA)
(2) PEP Carboxykinase (OAA –> PEP)
(3) Fructose-1-6-Bisphophatase (Fructose-1,6-BP –> Fructose-6-P) Rate limiting enzyme
(4) Glucose-6-P (glucose-6-P –> glucose)
The Cori Cycle
Shuttles lactate from muscle –> liver to make lactate –> pyruvate –> glucose
Galactosemia
*What is the rate-limiting enzyme?
*Inheritance
*Sx’s
*Seen w/?
*Enzyme: Galactose-1-Phosphate Uridyltransferase Deficiency
*Inheritance: AR
*Sx’s: lethargy, N/V, failure to thrive, jaundice, hepatomegaly, intellectual disability, cataracts
*Seen in between bottle feedings
Galactokinase Deficiency
*Galactokinase = kinder
Galactose accumulates
-Sx’s: see infantile cataracts
Essential fructosuria
*Deficiency?
*Deficient enzyme: Fructokinase
Fructosemia
*Enzyme deficiency?
*Seen when?
*Sx’s
*Enzyme deficiency: Aldose B deficiency
- Accumulation of F-1-P
*Seen w/ baby started on fruits
*Sx’s: hypoglycemia, jaundice, cirrhosis, vomiting
Pyruvate –> Acetyl CoA
- Requires: 5 Co-Factors
*B Vitamins 1 - 5
Antidote to methanol or ethylene glycol poisoning?
Fomepizole
Citric Acid Cycle
*Mnemonic
*Main goal?
*Rate limiting step
*Mnemonic: Citrate is krebs starting substrate for making oxaloacetate
*Main goal: Produce NADH for ETC to make ATP
- NADH2 = 2.5 ATPs
- FADH2 = 1.5 ATPs
*Rate limiting step = isocitrate DH
Do saturated fats have double bonds?
No
Do unsaturated fats contain double bonds?
Yes
How does fatty acid synthesis begin?
- Where does it get it’s NADPH’s from?
*Begins from citrate accumulation due from inhibition of PFK-1,
*Acetyl-CoA –ATP (via ACoA Carboxylase)—> Malonyl CoA
*NADPH’s come from HMP Shunt
of rounds to make certain length of chain =
Number of NADPH’s needed / round =
Number of rounds to make certain length of chain =
# of ATP’s needed to make entire FA =
Number of FA breakdown to release NADH, FADH2, ACoA =
of rounds to make certain length of chain = (#C / 2) -1
Number of NADPH’s needed / round = # of carbons - 2
Number of roounds to make certain length of chain = (#C / 2 ) - 1
# of ATP’s needed to make entire FA = #C - 1
Number of FA breakdown to release NADH, FADH2, ACoA = (#C / 2 ) -1
Fatty Acid synthesis steps
Acetyl CoA —–Acetyl CoA Carboxylase——> Malolnyl CoA —> Decarboxylation –> Addition of NADPH + Addition of NADPH
How does fatty acid catabolism being?
- What is needed?
- Fatty acids > 12 carbons need?
- Steps of catabolism
Glucagon stimulates hormone sensitive lipase
- 2 ATP’s needed
- Fatty acids > 12 carbons need CAT-1 (cytosol) and CAT-2 (mito) to be transported
- Steps of catabolism:
Oxidation, hydrolysis, oxidation, thiolysis
Deficiency of Cat-1 causes:
Adrenoleukodystrophy (X-linked Rec)
- Disrupts leydig cells, CNS , adrenal cortex
What do you need in dealing with Odd chain fatty acids?
Propionate + Succinyl CoA –> TCA intermediate
Ketone Synthesis
*What is the Rate Limiting Enzyme?
*What is the Reaction?
*Rate Limiting Enzyme?: HMG-COA Synthase
*Reaction:
Acetyl CoA –Thiolase–> Acetoacetyl CoA —–HMG-CoA Synthase–> Hydroxy-beta-methylglutaryl CoA —HMG-CoA Lyase–> Acetoacetate —D-Beta-hydroxybutyrate DH—> Acetone + CO2 & D-Beta-Hydroxybutyrate
The phospholipid pathway
Phospholipids —> Arachidonic Acid —*–> COX1 & COX2
COX1 –> Homeostatic Functions
COX2 –> Inflammation
COX 1 & COX 2 –> Prostacyclin (PGI2), Thromboxane (TXA2), Prostaglandins (PGD2, PGE2)
*Can be inhibited by NSAIDs
Phospholipids —> Arachidonic Acid —> 5-Lipoxygenase –> 5-HPETE –> Lipoxin A4/B4
5-HPETE –> Leukkotrienes –> Vasoconstriction, ^ Vascular permeability, Bronchospasm
(1) What irreversibly inhibits cox1 & cox 2?
(2) What reversibly inhibits cox1 & 2?
(3) What inhibits the cox enzyme?
(4) What reversibly inhibits Cox-2?
(1) Aspirin
(2) NSAIDs: Ibuprodfen & Naproxen
(3) Acetominophen
(4) Celecoxib
What is the rate limiting enzyme of glycogen synthesis?
- What elongates the chain?
*Glycogen Synthase
- Chain elongates in alpha-1,4 direction & links via Alpha-1,6 linkage
Von Gierke Disease
*Inheritance:
*Enzyme Defect:
*Clinical Findings:
*Inheritance: AR
*Enzyme Defect: Glucose-6-phosphatase
*Clinical Findings:
- Hepatomegaly
- Hypoglycemia (severe)
- Hyperlipidemia
- Hyperuricemia
- Failure to Thrive
Pompe’s Disease
*Inheritance:
*Enzyme Defect:
*Clinical Findings:
*Inheritance: AR
*Enzyme Defect: Alpha-glucosidase
*Clinical Findings:
- Cardiorespiratory Failure
What does ABCD stand for in terms of glycogen storage diseases?
A: Anderson
B: Branching enzyme
C: Cori
D: Debranching Enzyme
Cori
*Inheritance:
*Enzyme Defect:
*Clinical Findings:
*Inheritance: AR
*Enzyme Defect:
- Debranching enzyme
*Clinical Findings:
- Similar to Von Gierke but less severe
Anderson
*Inheritance:
*Enzyme Defect:
*Clinical Findings:
*Inheritance: AR
*Enzyme Defect: Branching Enzyme
*Clinical Findings:
- Cirrhosis of liver
- Death by liver failure
McArdle
*Inheritance:
*Enzyme Defect:
*Clinical Findings:
*Inheritance: AR
*Enzyme Defect: Myophosphorylase
*Clinical Findings:
- Cramping during physical activity
Hers
*Inheritance:
*Enzyme Defect:
*Clinical Findings:
*Inheritance: AR
*Enzyme Defect: Liver Phosphorylase
- issue w/ glycogen synthesis
*Clinical Findings:
- Increased Amount
Pentose Phosphate Pathway
*Generates?
*Rate Limiting Enzyme?
*Occurs where?
*Two phases?
*Generates: NADPH & Ribose-5-Phosphate
*Rate Limiting Enzyme: Glucose-6-phosphate DH
*Occurs: Cytosol
*Two Phases: Oxidative & Non-Oxidative
Glucose-6-Phosphate DH Deficiency
- Inheritance
*NADPH used by RBC to maintain reduced glutathione to counteract free radicals
*Inheritance: X-linked recessive
Cholesterol Synthesis
*Rate-limiting enzyme:
*What acts at this enzyme?
*Pathway
*Rate-limiting enzyme: HMG-CoA Reductase
*What acts at this enzyme? Statins
*Pathway:
Acetoacetyl CoA + Acetyl CoA –> HMG-CoA –HMG-COA reductase–> Mevalonate –> Mevalonate –> Prequalene pyrophosphates –squalene synthase–> squalene –> Cholesterol
Niacin
*What Vitamin is it?
*What does it do?
*Vitamin B3
*Decreases VLDL production in the Liver, Best HDL-raising ability, Uncomfortable skin flushing
Urea Cycle (p. 125)
*What is it?
*Where does it work
*Rate limiting ezyme
*What is it?: Removes toxic ammonia that builds up during protein breakdown + makes urea
*Where does it work: cytosol & mitochondria
*Rate limiting enzyme: Carbamoyl phosphate synthetase 1 (CPS-1)
Arginase Deficiency
*What is arginase used for?
*Sx’s of deficiency
*Management:
*What is arginase used for?: makes urea
*Sx’s: spaticity
*Management:
- Lower protein intake and eleminiate arginine from diet
Liver Failure Tx
1. Management
2. Treatment
- Lower protein inake
- Lactulose: used to treat constipation + hepatic encephalopathy. Pulls in water to lumen, and traps ammonia
Rate Limiting Enzymes
Glycolysis RLE
RLE of glycolysis: Phosphfructokinase-1 (PFK-1)
Rate Limiting Enzymes
Gluconeogenesis RLE
RLE of gluconeogenesis: Fructose-1,6-Bisphosphatase
Rate Limiting Enzymes
Citric Acid Cycle
RLE of Citric Acid Cycle: Isocitrate DH
Rate Limiting Enzymes
Glycogen synthesis
RLE Glycogen Synthesis: Glycogen Synthase
Rate Limiting Enzymes
Glycogenolysis
RLE of Glycogenolysis: Glycogen Phosphorylase
Rate Limiting Enzymes
HMP Shunt
RLE HMP Shunt: G6PDH
Rate Limiting Enzymes
Urea Cycle
RLE Urea Cycle: Carbamoyl Phosphate Synthetase 1 (CPS-1)
Rate Limiting Enzymes
Fatty Acid Synthesis
Fatty Acid Synthesis RLE: Acetyl CoA Carboxylase
Rate Limiting Enzymes
Fatty Acid oxidation
Fatty Acid Oxidation RLE: Carnitine acyltransferase 1
Rate Limiting Enzymes
Ketogenesis
Ketogenesis RLE: HMG CoA Synthase
Rate Limiting Enzymes
Cholesterol Synthesis
Cholesterol Synthesis RLE: HMG-CoA Reductase
