1. General formula of carbohydrate = (CH20)n
2. Following are monosaccharides
   1. Glucose
   2. Fructose
   3. Galactose
3. NON REDUCING SUGARS = trehalose
4. REDUCING SUGAR = Maltose, lactose and cellobiose
5. Pentose sugar present in heart cells = lyxose
6. Monoscaarchirde glucose forms a part of the disaccharide sucrose 
7. GALACTOSE
   1. not an oligosaccharide
   2. Monosaccharide with a maximum rate of absorption in intestine 
8. SUCROSE 
   1. sugar characterised by its non-reducing property. It is also called cane sugar and table sugar 
   2. It cannot be metabolised 
   3. Invertase catalyzes the hydrolysis of = Sucrose into fructose and glucose**
9. FRUCTOSE
   1. In hereditary fructose intolerance, one can see intolerance to = Fructose and Sucrose 
   2. A patient with hereditary fructose intolerance is deficient in = Aldolase enzyme
   3. Highest concentrations of fructose are found in = Seminal fluid
10. LACTOSE 
    1. Milk sugar
    2. Hydrolysis of lactose yields glucose and galactose 
    3. Beta 1.4 glycosidic bond is present in = Lactose
11. GLUCOSE
    1. Glucose, Maltose and Lactose = Exhibit inversion 
    2. Malatose
       1. is dissacride of = Glucose and glucose
       2. Glycosidic linkage = alpha 1 – 4 
    3. Epimeric Pair = D Glucose and D Galactose 
    4. Glucose monomers in glycogen are held by = Alpha 1-4 bonds, alpha 1-6 bonds
    5. Only sugar absorbed against concentration gradient = Glucose
    6. True blood sugar level measures the levels of = Glucose + Fructose
    7. Abnormal constituents of urine = Ketone + Glucose
    8. Renal threshold of glucose = 180 mg/dl 
    9. In prolonged starvation, the main energy source of brain = Ketone bodies
    10. GLUCOSE can be synthesised from = Glutamate, Asparate and Alanine
    11. The uptake of glucose by the liver increases followed by carbohydrate meal because = increase in phosphorylation of glucose by glucokinase
    12. Apart from liver, glucokinase is present in = Pancreatic islet cells
    13. Glucokinase = It is a Inducible enzyme
    14. In glucose solution at equilibrium, mutarotation results in a fixed optical rotation of = 52.5*
    15. Form of glucose predominatly seen is as = Beta D Glucopyranose
    16. Glycemic index is highest for = Glucose
    17. Amount of asymmetric carbon atoms in glucose = FOUR
    18. Number of stereoisomers of glucose is = 16
    19. Substrate used by RBC in fasting state = Glucose
    20. Important precursors of glucose in animals
        1. Pyruvate
        2. Lactate
        3. Glycerol 
    21. Major factor that determine weather glucose is oxidized by aerobic or anaerobic glycolysis = NADH and ATP/ADP Ratio
    22. Potassium Oxalate and Sodium Fluoride = added to the blood sample to estimate glucose
    23. Muscle cannot release glucose from glycogen because of the deficiency of = Glucose 6 phosophatase 
12. GLYCOGEN
    1. Starch and Glycogen are polymers of = Alpha Glucose
    2. Amylose and amylopectin are constitutes of = Starch
    3. CARBOHYDRATE RESERVE OF THE BODY = glycogen 
    4. Glycogen breakdown = Glucose and Lactic acid
    5. Tissue with highest glycogen content = Liver
    6. An essential for the conversion of glucose to glycogen in the liver = UTP
    7. Muscle glycogen is mainly utilized for supplying energy to = Liver
13. Ditery fiber is rich in = Cellulose
14. The rate of absorption of sugars is highest for = Hexoses 
15. Proteins and carbohydrates of glycoproteins are held by = Glycosidic bonds 
16. Sialic acids are acetylated derivatives of = Neuraminic acid 
17. GLYCOLYSIS
    1. The oxidation of glucose or glycogen to pyruvate and lactate by the EMF pathway is called = Glycolysis
    2. EMF pathway reaction takes place outside the mitochondria 
    3. Phosphofructokinase is the key rate-limiting enzyme of = Glycolysis 
    4. During the conversation of glycerol to pyruvic acid, the first glycolytic intermediate to form = Dihydroxy acetone phosphate 
    5. Allosteric inhibition with ATP effects and rate-limiting enzyme is = Phosphofructokinase**
    6. The enzyme involved in the first committed step of glycolysis = Hexokinase 
    7. Enzyme phosphofructokinase 1 is strongly activated by = Fructose 2,6 bisphosphate 
    8. Enzyme Phosphofructokinase is allosterically inhibited by = Citrate
    9. Whenever the cells ATP supply is depleted =  Phosphofructokinase enzyme activity is increased
    10. ATP is produced by the following enzyme = Pyruvate Kinase 
    11. Glycolysis enzyme inhibited by fluoride is = Enolase
    12. ENOLASE = Catalyzes the reversible degradation of 2 – phosphoglycerate to phosphoenolpyruvate 
    13. For glucose estimation in blood, the mode of transportation from primary health care to the laboratory is done by the addition of = Sodium Fluoride 
    14. Insulin acts on which enzyme = Glucokinase 
    15. Inhibition of glycolysis in the presence of oxygen is called as = Pasteur Effect 
    16.  The reverse of Pasteur effect = Crabtree effect 
    17. The main pathways of metabolism in the brain are = Glycolysis and Citric Acid Cycle 
    18. The end product of glycolysis under anaerobic conditions is = Lactic acid 
    19. Number of ATP molecules generated in the conversion of glycogen to lactate = 2 
    20. Following exercise, the level of lactic acid in blood during ventilation = Decreases 
    21. Ion which is important in the glycolysis = Magnesium 
    22. Pyruvate dehydrogenase and Alpha-ketoglutarate dehydrogenase = Multienzymee complex 
    23. Pyruvate Dehydrogenase complex contains = NAD, FAD, Co-A
    24. The enzyme which provides a link between glycolysis and citric acid cycle = Pyruvate Dehydrogenase
    25. Increase in pyruvate and lactate is seen in = Thiamine deficiency 
    26. Unique by product of lycolysis in RBC = 2,3 biphosphoglycerate
    27. Glycerol enters glycolysis via = Dihydroxyacetone phosphate
    28. Glycolytic pathway is located in = CYTOSOL
    29. Glycolysis is always anaerobic in = Erthrocytes
    30. Enzyme responsible for the conversion of glucose 1 phosphate to glucose 6 phosphate = Phosphoglucomutase
    31. Irreversible step of glycolysis involves
        1. Phosphofructokinase
        2. Pyruvate kinase
        3. Hexokinase 
    32. True statements regarding anaerobic glycolysis
        1. End product is lactic acid
        2. Net production of ATP is 2 
        3. Occurs in places like eyes, lens and RBC’s 
    33. In the glycolysis cycle, substrate-level phosphorylation takes place in = pyruvate kinase 
    34. Generation of ATP upt pyruvate in aerobic glycolysis = 7
    35. Cancer cells derive energy mainly from = Glycolysis 
18. CITRIC ACID CYCLE 
    1. Enzymes concerned with the citric acid cycle are found in = Mitochondria 
    2. Kreb cycle occurs in = Aerobic conditions 
    3. Kreb cycle doesn’t occur in = RBC due to absence of mitochondria 
    4. In the TCA cycle, what is formed first = Citrate 
    5. In the TCA cycle, citrate is immediately converted into = Cisaconitate, after losing molecule of H20
    6. Acid formed in = Oxaloacetic acid 
    7. The correct sequential order of enzymatic reaction of kreb cycle when molecule acetyl-CoA enters the cycle = Citrate, ketoglutarate and oxaloacetate 
    8. In the TCA cycle, substrate-level phosphorylation takes place in = Succinyl CoA to succinate
    9. The enzyme involved in substrate-level phosphorylation = Succinyl CoA Synthetase 
    10. In the TCA cycle, substrate-level phosphorylation occurs at = Thiokinase
    11. High energy phosphate compound that is formed via substrate-level phosphorylation = GTP
    12. Succinyl CoA to Succinate = 1 ATP
    13.  1 molecule of glucose forms = 2 molecules of pyruvate 
    14. 1 molecule of acetyl CoA enzyme gives rise to = 12 ATP 
    15. Alpha Ketoglutarate = Metabolite which is used in the detoxification of ammonia in the brain 
    16. Acetly CoA can be converted into
        1. Fatty acids
        2. Cholesterol
        3. Ketone bodies
    17. Total Number of dehydrogenase = 4
    18. Final common pathway for the oxidation of carbohydrate, lipids and protein in human body is = TCA cycle 
19. INSULIN
    1. Glycogen synthesis is increased by = Insulin 
    2. Insulin increases the following pathway
       1. Glycogen synthesis 
       2. Fatty acid synthesis 
       3. Protein synthesis 
    3. Insulin causes lipogenesis by
       1. Increasing acetyl CoA carboxylase activity 
       2. Increases the transport of glucose into the cells
       3. Decreases the intracellular cAMP level 
    4. Glucose transporter which is stimulated by insulin is located in = Skeletal muscle and adipose tissue 
    5. Activity of which of the following enzyme is not affected by insulin = Hexokinase
    6. Insulin = not polymer of glucose
    7. Homopolysaccharide made up of fructose is = Insulin
20. GLYCOGENEIS 
    1. It requires
       1. Uridine diphosphate
       2. Glycogen synthetase
       3. Branching enzyme
21. GLYCOGENOLYISIS 
    1. Hypoglycaemia is corrected by increasing the rate of live glycogenolysis = GLUCAGON
    2. The first product of glycogenolysis = Glucose 1 phosphate 
    3. Rate limiting step of glycogenolysis = Glycogen Phosphorylase 
    4. A deficiency of Phosphorylase = would impair the body’s ability to maintain blood glucose concentration during the first 24 hours 
    5. The conversation of glucose 6 P to G 1 P = example of isomerization 
    6. Adrenaline acts on the enzyme = phosphorylase
    7. Glycogenolysis in muscle does not raise blood sugar due to lack of = H-6-phosphatase
    8. Glucose can be synthesized from
       1. Tryptophan and Phenylalanine
       2. Glycerol
       3. Lactic acid and propionic acid 
22. GLUCONEOGENSIS
    1. Mainly occurs in = Mainly in Liver and partly in Kidney, not in muscles**
    2. Liver and Muscle = involved in Cahill Cycle
    3. Substance for gluconeogenesis = Glycerol
    4. The key enzyme of gluconeogenesis = Pyruvate carboxylase 
    5. The compound that can give rise to glucose by gluconeogenesis = Lactate
    6. Amino acids that enter TCA cycle for gluconeogenesis = Phenylalanine, Tyrosine and Tryptophan 
    7. Glycerol is converted to glucose in = Liver 
    8. Major contribution towards hepatic gluconeogenesis = Lactate
    9. Hepatic gluconeogenesis is stimulated by = Glucagon and Epinephrine
    10. 
        1. X = Aspartate
        2. Y = Oxaloacetate 
    11. Major contribution towards gluconeogenesis is by = Alanine and Glutamine
    12. Malate shuttle –  is important in = Gluconeogensis and Glycolysis 
    13. Substrates of gluconeogensis =
        1. Glucogenic amino acids
        2. Lactate
        3. Glycerol
23. HMP Pathway 
    1. TRUE STATEMENTS
       1. HMP shunt is an alternative pathway for oxidation of glucose that occurs in the cytosol 
       2. It is characterized by the absence of production of ATP 
       3. It is active in the adipose tissue, liver and gonads 
       4. Oxidative phase generate NADPH 
       5. Non oxidative phase generates ribose precursors 
    2. Sites where HMP shunts can occur include
       1. Liver
       2. WBC
       3. Lactating mammary gland 
       4. Testes 
    3. Step in HMP pathway requiring TPP = Transketolase 
    4. HMP shunt is of great importance in cellular metabolism because it produces = NADPH 
    5. Dehydrogenases of HMP Shunt are specific for = NADP
    6. NADPH is the product of = HMP pathway 
    7. Enzymes which used NADP as coenzyme = Glucose 6 phosphate dehydrogenase = regulartory enzyme in HMP shunt
    8. First pentose formed in HMP shunt = Ribulose 5 phosphate
    9. Metabolites in HMP shunt are
       1. Sedoheptulose 7 phosphate
       2. Glyceraldehyde 3 phosphate
       3. Xylulose 5 phosphate 
24. GLYCOGEN STORAGE DISORDERS
    1. Glucose 6 phosphate deficiency
       1. is seen in = Von Gierke’s disease = autosomal recessive 
       2. Defective cori cycle and increased mobilization of glycogen from liver is seen
       3. Hyper-ureicemia is feature of = type 1 glycogen disorder (Von Gierke’s disease)
    2. Type 2 glycogen disorder is due to deficiency of =
       1. 4 and 1,6 – glucosidase
       2. lysosomal alpha 1 
    3. McArdles disease is due to deficiency of = Myophosphorylase (Type 5)
    4. Beta Galactosidase is deficient in = Krabbe’s disease
    5. Limit detrin accumulate in cytosol = Type 3 – Cori’s disease**
    6. Pompe’s disease is due to defieceny = Acid Malatase
25. Galactosaemia commonly is due to deficiency of = galactose 1 phosphate uridyl transferase
26. Cytochromes are = iron containing porphyrins
27. Main enzyme responsible for the activation of xenobiotics = Cytochrome P-450
28. Most lipogenic = fructose
29. Xylitol is = Natural five carbon sugar
30. Glucose transporters present in the Beta cells of the islets of langerhans is = GLUT 2
31. GLUT 4
    1. Is present in adipose tissue
    2. Facilitates diffusion of glucose
    3. Transferred from cytosol to the cell membrane by insulin
    4. Glucose transporter in myocyte stimulated by insulin is = GLUT4
32. Prolonged carbohydrate deficiency leads to = Ketoacidosis 
33. Glutathione
    1. Tripeptide
    2. Conjugates xenobiotics
    3. Co factor of various enzymes
34. Sphingosine is present in = Ceramide
35. Haworth structures refer to = Pyran and Furan forms of sugars 
36. Glycosaminoglycan present in cornea as = Keratan Sulphate and Dermatan Sulphate
37. Enantiomers – non superimposbale images of one another
    1. D mannose and L mannose 
    2. D Glucose and L glucose
38. Specific rotation of beta D glucopyranose = +19*
39. Hetropolysccaride among the following = Heparin
40. Lactate formed in muscles can be utilized through = Cori cycle 
41. Alpha Lactone is = Vitamin C
42. Most prominent carbohydrate component of hemicelllulose = Arabinoxylan 
43. Rothera’s test is for = Ketones
44. Bacterial Glutamine synthethase = Enzyme catalyzes a reaction in which reduced nitrogen is introduced into cellular metabolism 
45. When velocity of enzyme activity is plotted against substrate concentration = HYPERBOLIC CURVE 
46. Glycoproteins = are important for white blood cell recognition
47. Cytochrome C = recieves flavoproteins
48. Anabolism and Catbolism are chemically linked in the form of = ATP
49. Factors determining the activity of an enzyme
    1. Association with regulatory protein
    2. Sequestration
    3. Allosteric regulation 
50. 6 – phosphogluconate dehydrogenase = catalyses the first step in the pentose phosphate pathway 
51. Flux control coefficient = measure of the effect of an enzyme’s concentration on flux through a multi enzyme pathway 
52. Frutose 2,6 bisphosphate = compounds are responsible for the coordinated regulation of glucose and glycogen metabolism 
53. Elasticity Coefficent = measure of how responsive the enzyme is to changes in the concentration of metabolite 
54. After Overnight fasting, levels of glucose transporters are reduced in = Adipocytes 
55. Isomerase = enzyme that catalyzes the conversion of an aldose sugar to a ketose sugar 
56. Insulin stimulated glucose uptake takes place in via GLUT 4 which is insulin dependent
    1. Heart 
    2. Skelteal Muscle
    3. Adipose tissue
57. Transport of glucose in Liver = GLUT 2 = Insulin independent 
58. Decrease BMR is seen in = Starvation 
59. Caloric Value of Alcohol = 7Kcal/g

ENZYME CHARACTERISTICS

• Increase rate of reaction by lowering activation energy
• Most are proteins
• Specific – conversion of one specific substance to one product
• May require cofactors or coenzymes
• Carefully regulated

ΔG = free energy

• Free energy of the product minus the free energy of the reactants
• ΔG is negative for enzymatic reaction because energy is released (exergonic reaction)

ΔEa = activation energy

• Energy barrier that must be overcome for a reaction to proceed
• Enzymes lower activation energy of a reaction by stabilizing transition state
• Energy required to get to equilibrium (rate of forward and reverse reactions are the same) correlates with ΔG and is unchanged in the presence or absence of enzyme
• Enzyme doesn’t dictate whether reaction will proceed but determines speed of reaction

ENZYME ACTIVE SITE

• 3D structure produces active site
• Shaped so that substrate fits in
• Product of an enzymatic reaction has lower affinity for binding site: exits binding site and is released

COFACTORS AND COENZYMES

• Bind cofactor binding site (distinct from active site)
• Some enzymes inactive without cofactor or coenzyme
• Many are vitamin-derived, metal ions, or other smaller organic molecules

PHENYLKETONURIA

Pathophysiology: Toxic Metabolites of Phenylalanine

To understand the pathophysiology of phenylketonuria, show that when phenylalanine accumulates at toxic levels, it transaminates into:

• Phenylpyruvate (aka phenyl ketone); hence, “phenylketonuria” describes the presence of phenylpyruvate, phenylalanine, and two key other derivatives in the urine and blood:
  • Phenylacetate which has a distinct “must/mousy odor”.
  • Phenyllactate.

Phenylalanine Excess / Tyrosine Deficiency

• Thus, overall indicate that in phenylketonuria, there is an:
  • Excess of phenylalanine
  • Deficiency of tyrosine

So the goal of therapy is to reduce phenylalanine intake and to supplement tyrosine deficiency via the diet. Remember the sparing action of tyrosine on the requirements of phenylalanine

Clinical Presentation of PKU

• Hypopigmentation
  • Indicate that hypopigmentation (of the skin and iris) is a finding in this disorder (remember: melanin is a derivative of tyrosine and tyrosine is deficient in PKU).
• Neuropsychiatric disorder
  • And because the toxic levels of phenylalanine and its derivatives are neurotoxic, this disorder causes tremo r, psychosis, seizures, and cognitive dysfunction.

PHEOCHROMOCYTOMA

Clinical Presentation of Pheochromocytoma

• Symptoms
  • Spontaneous severe anxiety: palpitations, sweating, panic
• Physical Exam Signs
  • Tachycardia (Rapid heart rate)
  • Hypertension (High blood pressure)

Biochemical Pathophysiology

As a simplification…

• Dopamine
  • We can attribute the agitation and possible psychosis to the surge in Dopamine.
• Norephine & Epinephrine
  • The sympathetic nervous system “fight or flight” symptoms relate to the surge in norepinephrine and epinephrine.

Laboratory Testing

• We test for pheochromocytoma in patients with unexplained episodic hypertension (high blood pressure) with blood and urine collection of:
  • Catecholamine metabolite levels
  • Metanephrine levels

• Specifically, we typically order:
  • Urine and plasma free metanephrines
  • Urine and plasma free catecholamines
  • Urine homovanillic acid (HVA)
  • Urine vanillylmandelic acid (VMA)

• The tests are highly sensitive, which leads to false positives. As anticipated, causes of false positives include:
  • Sympathetic nervous system agitation (ie, psychophysiological stress)
  • Exogenous triggers of catecholamines: pharmaceuticals, tobacco, caffeine, and illicit drugs.

Tumor Appearance

• Pheochromocytomas are black staining tumors (remember this was the color of melanin, another tyrosine derivative, as well) that classically grow out of the medullary layer of the adrenal gland.
  • For a better understanding of the difference between the adrenal medulla and the adrenal cortex, see adrenal gland hormone production.
• Paragangliomas are essentially extra-adrenal pheochromocytomas
  • They derive from cancerous autonomic nervous system tissue.
  • True to the anatomy of the autonomic nervous system – head/neck ANS paragangliomas are parasympathetic whereas thorax and abdominal paragangliomas are sympathetic.

PHARMACOTHERAPEUTICS IN PARKINSON’S DISEASE

Parkinson’s disease (and for that matter, all Parksinonism syndromes) are Dopamine deficiency syndromes within the brain.

Carbidopa

• Indicate that the pharmaceutical carbidopa is used to block the decarboxylation of DOPA to dopamine, peripherally, and increase the bioavailability of dopamine centrally (in the central nervous system – where it is intended to treat Parkinson’s disease).
• Dopamine cannot cross the blood brain barrier but DOPA can, so Dopamine is administered systemically as L-DOPA. However, if it were administered without a decarboxylase inhibitor (such as carbidopa) it would be decarboxylated peripherally into Dopamine and patients would simply become nauseated.
• In the presence of a peripheral decarboxylase inhibitor, DOPA is taken up in the CNS and THEN decarboxylated to Dopamine (in the basal ganglia where it serves to replenish the deficient stores of Dopamine). Carbidopa (itself) doesn’t cross the blood brain barrier.

Therapeutics

• Levodopa: Dopamine Precursor
  • So to treat a patient with Parkinson’s disease, let’s add levodopa as a Dopamine precursor.
• Carbidopa: DOPA decarboxylation Inhibitor
  • At the same time, we need to add Carbidopa to block the peripheral DOPA decarboxylation of DOPA – we need to ensure that the levodopa makes it through the systemic circulation and enters the brain, otherwise it will simply act like any catecholamine within the periphery and increase blood pressure and heart rate but fail to impact the central nervous system Dopamine deficiency state.
• Ropinirole & Pramipexole: Dopamine agonists
  • We can also add ropinirole or pramipexole, which are Dopamine agonists that optimize the release of Dopamine from the remaining Dopaminergic neurons within the substantia nigra.
• Entacapone: COMT Inhibitor
  • We can add entacapone, which is a COMT inhibitor to increase the circulation of the Dopamine that we’ve stimulated or replaced (ie, we can inhibit catecholamine metabolism).
• Selegeline or Rasagaline: MAO-B Inhibitors
• And we can add selegeline or rasagaline, which are MAO-B (specifically) inihibitors which also increase Dopamine but via MAO inhibition (catecholamine metabolism inhibition).
• The B subunit is specific to Dopamine catalysis, whereas the MAO-A enzyme is less specific and also metabolizes norepinephrine and serotonin, thus drugs that inhibit MAO-A are potentially much more hazardous to use.

HYPERTHYROIDISM

Clinical Presentation

• Hypermetabolic state that manifests with:
  • Weight loss, sweats, fevers, rapid heart rate.
• Skin and hair thinning
• Grave’s Ophthalmopathy
  • Ocular protrusion and reddening

ALKAPTONURIA

• Show alkaptonuria, which we can think of as a melanin-like substance in the urine and joints.

Pathogenesis

• It occurs from a deficiency in homogentisate 1,2 dioxygenase.
  • This results in a build-up of a melanin-like polymer called benzoquinone acetic acid (a product of the oxidation of homogentisic acid), which binds connective tissue and causes dark pigmentation or ochronosis (arthritis).
• Thus, we can think of alkaptonuria as the opposite of albinism + the build-up of acetic acid in the tissues irritates the joints and causes joint pain.

Presenting Symptoms

• Children: Dark Urine
  • The presenting manifestation in children is typically urine that darkens when it sits for awhile (not common now with disposable diapers). The darkening occurs from the excess homogentisate in the urine (5,000 mg vs 20-30mg (normally).
• Adults: Join Pain
  • In adults, the disease presents, typically, from joint pain from the build-up of acetic acid in the tissues, which irritates the joints.

TYROSINEMIA TYPE I

Pathogenesis: fumarylacetoacetate hydrolase deficiency

• Indicate that tyrosinemia type I (aka hereditary tyrosinemia, tyrosinosis) results from fumarylacetoacetate hydrolase deficiency.

Presenting symptom: “cabbage-like odor”

• Indicate that it characteristically causes a “cabbage-like odor” but importantly causes liver and kidney failure, polyneuropathy, and bone dysplasia (rickets), manifesting early-on with diarrhea, vomiting and tyrosine and its metabolites in the urine.
• Also consider that transient tyrosinemia (elevated blood levels of tyrosine) occurs in ~ 10% of newborns, most often due to vitamin C deficiency or immature liver enzymes due to premature birth.

STEPS OF VESICULAR BUDDING AND FUSION (+ PROTEINS INVOLVED)

• Cargo selection (cargo receptor, adaptor protein)
• Vesicular budding (adaptor proteins, coat proteins)
• Fission from donor membrane (dynamin)
• Vesicular coat dissociates
• Vesicular targeting and transport (Rab-GTPase, tethering protein)
• Fusion with target membrane (V-snare and T-snare)

PROTEINS OF VESICULAR BUDDING AND FUSION

• Cargo receptors – select and concentrate molecules to be transported in vesicle
• Adaptor proteins – bind cargo receptor and coat proteins
• Coat proteins – form protein scaffold around vesicle that facilitate facilitate vesicular budding
• Dynamin – GTPase involved in vesicular fission
• RabGTPase – associates with vesicle after coat has dissociated. Facilitates transport of vesicle to appropriate target membrane. Locks vesicle to target membrane by attaching tethering proteins
• Tethering proteins – anchored in target membrane, attach rabGTPase. Move vesicle close to target membrane for vesicular fusion.
• V-snares(vesicular) and T-snares(target membrane) – Play role in vesicular fusion

COAT PROTEINS DIRECT VESICLE TRANSPORT

• Clathrin +adaptin 1: Golgi → Lysosome
• Clathrin + adaptin 2: Plasma membrane → Endosomes (endocytosis)
• COP 1: Cis golgi → ER AND Later cisternae → Earlier ones (retrograde transport)
• COP II: ER → Cis golgi