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BIOC 3560 Final exam questions correct answers, Exams of Advanced Education

Cheyney University of PennsylvaniaAdvanced Education

BIOC 3560 Final exam questions correct answers

Typology: Exams

2025/2026

Available from 07/02/2026

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BIOC 3560 Final exam questions correct
answers
1. Glucose is an excellent fuel
that yields kJ/mol: -2840
2. Which steps in glycolysis are exergonic under cellular conditions?:
1,3,10
3.
What is glycolysis reactants and products?: React: 1 glucose, 2
ATP, 2 NAD+
Prod: 2 pyruvate, 4 ATP, 2 NADH
4. Catabolism usually while anabolism
usually
:
converging,
diverging
5. Rate limiting
steps usually have a high ratio of to , and
a
large:
substrate to product, negative delta G
6. How do cells overcome problem of having to regulate every
single enzyme
in
a
pathway?:
They only focus on enzymes for rate limiting steps
7. Hexokinase is
by
its
product:
allosterically
inhibited
8. In muscle, hexokinase is
expressed and is inhibited by
:
I,
Glu-
cose-6P
9.
In liver, hexokinase
is
expressed and inhibited by
, causing
to HK4 in the
:
4,
Fructose-6P,
glucokinase
to
sequester
in
the
nucleus
10.
Compared to hexokinase I,
hexokinase 4 has a poor
, allowing it to be more sensitive to
changes in
:
Kd, blood sugar
11. What commits F6P to glycolysis?: PFK-1
12.
4 ways of allosteric regulation of PFK-1: ATP lowers aflnity for F6P, ADP and
pf3
pf4
pf5
pf8
pf9
pfa
pfd
pfe
pff
pf12
pf13
pf14
pf15
pf16
pf17

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BIOC 3560 Final exam questions correct

answers

  1. Glucose is an excellent fuel that yields kJ/mol: - 2840
  2. Which steps in glycolysis are exergonic under cellular conditions?: 1,3,
  3. What is glycolysis reactants and products?: React: 1 glucose, 2 ATP, 2 NAD+ Prod: 2 pyruvate, 4 ATP, 2 NADH
  4. Catabolism usually while anabolism usually : converging, diverging
  5. Rate limiting steps usually have a high ratio of to , and a large: substrate to product, negative delta G
  6. How do cells overcome problem of having to regulate every single enzyme in a pathway?: They only focus on enzymes for rate limiting steps
  7. Hexokinase is by its product: allosterically inhibited
  8. In muscle, hexokinase is expressed and is inhibited by : I, Glu-cose-6P
  9. In liver, hexokinase is expressed and inhibited by , causing to HK4 in the : 4, Fructose-6P, glucokinase to sequester in the nucleus
  10. Compared to hexokinase I, hexokinase 4 has a poor , allowing it to be more sensitive to changes in : Kd, blood sugar
  11. What commits F6P to glycolysis?: PFK- 1
  12. 4 ways of allosteric regulation of PFK-1: ATP lowers aflnity for F6P, ADP and

2 / 23 AMP relives ATP inhibition, Citrate increases inhibition by ATP, F26BP strong activator

  1. Pyruvate kinase transfers from to : Pi, PEP, ADP
  2. Pyruv ate kinase is inhibited by (4) and positively modulated by : High ATP, Acetyl-CoA, long chain FA and alanine, F16BP
  3. The liver isoform of PK is also subject to by phosphorylation- : Inactivation by PKA
  4. Describe step 1 of gluconeogenesis (pyruvate to phosphoenolpyruvate): 1. Pyruvate carboxylase converts pyruvate and ATP to oxaloacetate and ADP
  5. Malate dehydrogenase reduces OAA and NADH to L-malate and NAD+
  6. Cytosolic malate dehydrogenase oxidizes malate and NAD+ back to OAA and NADH
  7. PEP carboxykinase oxidativily decarboxylates OAA and GTP to phosphoenolpyruvate, GDP and CO
  8. Why is malate an intermediate in gluconeogenesis?: Oxaloacetate and NADH cannot pass mitochondrial membrane
  9. What happens when lactate is feedstock?: Doesn't need NADH so liver PEP produces PEP directly
  10. Step 8 of gluconeogenesis is conversion of to by - : F16BP to F6P by F1,6-bisphosphatase
  11. Step 10 of gluconeogenesis is conversion of to by : G6P to glucose by glucose-6-phosphatase
  12. Gluconeogenesis is , it costs ATP, GTP and NADH: expensive, 4, 2, 2
  13. What does gluconeogenesis allow?: Generation of glucose when glycogen stores are deplet-ed... important as brain, nervous, and RBC only rely on glucose
  14. FBPase-1 is negatively modulated by (2): F26BP and AMP
  15. F26BP acts on both and in a reciprocal

4 / 23

  1. The non-oxidative phase regenerates from : G6P from R5P
  2. In the pentose phosphate pathway, G6P dehydrogenase is stimulated by and inhibited by : NADP+ and NADPH
  3. Deficiency of helps protect against malaria by allowing production of : G6PD, free radicals
  4. Glycogen is linked a( --> ) with a --> linkage every 12 to units: 1-- >4, 1-->6 every 12 to 14 units
  5. Glucose residues removed from glycogen by : glycogen phospho-rylase
  6. Where is phosphate attached to glucose?: C
  7. Phosphorylase cannot break: a(1-->6) linkages
  8. G lycogen phosphorylase works on non-reducing ends until it reaches residues before : four, a(1-->6)
  9. What does the debranching enzyme do and form?: Transfers 3 of 4 glucose residues to non reducing end then cleaves a(1-->6) bond, forming glucose
  10. What converts G1P to G6P?: Phosphoglucomutase
  11. G6P is sequesterd in lumen where is removed: ER, phosphate
  12. of glycogen requires more enzymes than : synthesis, degradation
  13. In glycogen synthesis, G6P is converted to via. then added onto G1P via .: G1P via phosphoglucomutase, UDP via UDP-glucose pyrophospho-rylase
  14. What starts a new glycogen chain?: Glycogenin
  15. Glycogen

5 / 23 phosphorylase is activated by and inactivated by : kinase, phosphatase

  1. Regulators of glycogen phosphorylase a: -Glucagon/epinephrine/calcium/AMP activate -Insulin inhibits -Glucose binding/concentration inhibits
  2. What is significance of phosphoprotein phosphatase 1?: Can remove phosphoryl groups from all three enzymes phosphorylated from glucagon and EPE
  3. Myocytes lack. Muscles lack enzymes for and . Muscle pyruvate is phosphorylated by .: glucagon receptors, gluconeogenesis and glucose export, not phosphorylated by PKA
  4. Females should be % fat and males %: 25, 15
  5. T/F: Margerine is healthier than fat: No
  6. FA oxidation route: binds receptor and signal sent in form of which activates which phosphorylates and. re- leases CGI which activates. Triaglycerols broken down by. Fatty acids released and bind to. Transporter takes up and is oxidized to form and CO2: Hormone, cAMP, PKA, perilippin and HSL, perilippin, ATGL, HSL, albumin, FA, ATP
  7. Describe carnitine shuttle (3): FA group transferred to carnitine via CAT1, FA- carnitine enters mito via transporter, FA regenerated inside mito via CAT
  8. What is first metabolite of FA synthesis? What does it inhibit?: Malonyl-CoA inhibits CAT
  9. What is aerobic metabolism driven by?: Oxygen's desire to bind electrons more than anything else (except F gas)
  10. What happens before beta oxidation?: Fatty acid + ATP + CoA --> Acyl-CoA
    • AMP + PPi
  11. First step of beta oxidation: Process:

7 / 23

  1. FA synthesis step 2: Reduction of B-ketobutyryl ACP to B-hydroxybutyryl-ACP and NADPH via B-ketoa-cyl-ACP-reductase
  2. FA synthesis step 3: Dehydration of B-hydroxybutyryl-ACP to form trans C=C and water via B-hydroxya-cyl-ACP-dehydratase (forming trans-2-butenoyl-ACP)
  3. FA synthesis step 4: C=C of trans-2-butenoyl-ACP reduced by NADPH to form saturated acyl group via Enoyl-ACP-reductase
  4. Beginning of second round occurs when is recharged by : ACP, MAT
  5. The fatty acid synthase molecule in humans is polypeptide and is product of : single, evolution
  6. The end product of FA synthesis is which is the product of cycles: palmitate, 7
  7. What do fatty acyl-CoA desaturases do?: Introduce double bond
  8. 3 methods of regulation and method: Rapid - cellular regulation Slow - hormonal regulation Gradual - gene expression
  9. Example of rapid regulation (citrate): Excess citrate in mito signals excess energy and is exported to cyto and allosterically acitvates ACC to begin fatty synthesis
  10. Example of slow regulation (glucagon): Glucagon signals low energy and stimulates PKA to inactivate ACC
  11. Example of adaptive regulation: High fat diet triggers B-oxidation enzyme synthesis
  12. What inhibits B-hydroxyacyl-CoA dehydrogenase and TCA?: High [NADH]/[NAD+]
  13. What inhibits thiolase?: Acetyl-CoA
  14. Insulin citrate lyase by Citrate ACC Palmitoyl-CoA ACC: activates, phosphorylation, activates, inhibits
  15. How does sugar become fat?: Enters glycolysis and becomes pyruvate, shuttled to mito and converted to OAA then citrate... citrate shuttled out and converted back to OAA and

8 / 23 acetyl-CoA... Acetyl-CoA starts fatty acid synthesis

  1. OAA to malate electrons, and malate to OAA electrons: re-duces, regenerates
  2. Glycerol-3P can be formed from glycerol via and then into triacylglyc-erol via 3 reactions: glycerol kinase, acyltransferase
  3. How does gluconeogenesis lead to ketone bodies?: Uses OAA... prevents TCA cycle so acetyl-CoA is recycled to form ketone bodies
  4. First committed step of cholesterol synthesis is formation of: HMG-CoA
  5. Acetoacetate is "fat" and is converted to which is exhaled: soluble, acetone
  6. Why can't the liver use ketone bodies?: Lacks transferase
  7. Ketone bodies in periphery are converted back to : acetyl-CoA
  8. T/F: Myocytes change which enzymes they express to match nutrients in diet: True
  9. 4 routes and function of G6P in liver: Dephosphorylated to glucose (replenish blood glucose), glycogen synthesis, enter glycolysis, enter pentose-PO4 pathway to make NADPH and nucleotides
  10. 4 routes of fatty acids in liver: Membranes/repair, oxidative fuel, can synthesize TAG, excess acetyl-CoA to make ketones/cholesterol/bile acids etc
  11. Describe Well-Fed state: Insulin stimulates storage of blood glucose, GLUT transporters increase uptake, increase glycolysis leads to increased pyruvate into TCA leading to more FA synthesis
  12. Describe Active state (EPI): Signals impending activity, activates glycogen phosphorylase, stimu-lates glycolysis for fast muscle energy, stimulates mobilization of adipose
  13. Describe Active state (Glucagon): Increase blood sugar In liver: increase glycogen phosphorylase, decreases glycolysis and glycogen synthase, increase GNG and ketogen-esis In fat: increases release of fatty acids
  14. Describe stressed state (cortisol): Signals hypoglycemic

10 / 23 phospho-diester

  1. In sphingolipids, the backbone is , the head group is_____, and 1 fatty acid is in an link: sphingosine, choline, amide
  2. Glycolipids have a backbone of , a head group, and 1 fatty acid in an link: spingosine, carb, amide
  3. Cholesterol shape and structure: -Flat, planar fused rings that are rigid and hydrophobic -Alkyl side chain with OH is flexible
  4. Which fatty acid is usually saturated?: C
  5. Phosphate has a pKa so the head group is usually or : -1 or 0
  6. What are two most abundant glycerophospholipids?: Phosphatidylethaolamine and phosphatidylcholine
  7. Sphingolipids are similar in shape to : glycerolipids
  8. Glycosphingolipids have role in what system?: ABO blood type
  9. Monolayers occur at interface... air interacts with: air-water, acyl chains
  10. Micelles have acyl tail with shape: 1, wedge
  11. Bilayers are and are thick: stable, 30A
  12. What can be used to carry anti-cancer drugs?: Liposomes
  13. Transporters and channels use what % of total energy?: 30
  14. Peripheral proteins interact with of membrane lipids: polar head
  15. Integral membrane proteins can be anchored or : lipid, trans-membrane
  16. Trans-membrane proteins are usually and are with amino acids: a-helical, hydrophobic

11 / 23

  1. Peripheral proteins removed by change or and integral are removed by or : pH or chelator, phospholipase or detergent
  2. What are annular lipids?: Lipids which preferentially stick to surface of membrane proteins... this causes them to become immobiilized
  3. What does hydropathy plot show? Above 0 means what?: Hydrophobicity of membrane, hydrophobic
  4. What is unique about glycophorin A?: Has sugars on protein which keeps RBC from sticking to capillaries
  5. What does bacteriorhodopsin do?: Captures light to pump H+
  6. and go on extracellular side because they are and extra-cellular is : Asp, Glu, negative, positive
  7. and go on cytosolic side: Arg and Lys
  8. Which amino acids go at interface between hydrophobic/philic: Trp and Tyr
  9. N-linked carbohydrate chains have side chain and : Asn, N-acetylglucosamine
  10. O-linked carbohydrate chains have a or side chain and - : Ser or Thr, N-acetylgalatcoseamine
  11. Sugar groups of glycoproteins/glycolipids generally face and con-tribute to cell : out, recognition
  12. In the membrane movement is quicker than movement: lateral, across
  13. Gel phase is in state and FA align : para-crystalline, linearly
  14. Fluid state has motion and acyl chains have structure: thermal, little
  15. T/F: Plant fats that go cis to trans are worse than animal fats:

13 / 23 and do not have pore through membrane: selective, continuous

  1. GLUT in erythrocytes, liver, and muscle: GLUT1, GLUT2 and GLUT
  2. Transporter operation: Substrate binds one side, conformational change takes place, site opens on other side and substrate is released
  3. Active transporters are powered by and generate across membranes: ATP hydrolysis, ion gradients
  4. What is also pumped out in Na/K pumping?: Water
  5. Describe Uniport, symport, and antiport: Uniport transfers one molecule one way, symport has two molecules in same direction, antiport transfers two molecules in ditterent directions
  6. Na concentration outside vs inside: 150mM vs 10mM
  7. Cl concentration outside vs inside: 110mM vs 5mM
  8. Potassium concentration outside vs inside: 5mM vs 140mM
  9. Ca concentration outside vs inside: 5mM vs 1uM
  10. Na/K-ATPase is a that pumps Na out and K in, powered by: tetramer, 3, 2, ATP hydrolysis

14 / 23

  1. Transport cycle of Na/K-ATPase: Binds 3 Na+ from inside cell, transporter phosphorylated on cytosolic side (Asp) which induces conformational change, 3Na released and 2K bind, transporter de-phosphorylated and K released
  2. Ion gradients can power : transport
  3. Na is carried with in intestinal cells, and in the brain: glucose, amino acids
  4. Ion channels vs. transporters (speed, saturation, gated): Channels faster Transporters saturated Channels gated
  5. Ion channels the of membrane to ions: define the permeability
  6. Channels can be or gated: ligand, voltage
  7. What depolarizes the cell? Repolarizes?: Na influx, K efflux
  8. Voltage gated K+ channels are tetramers with each subunit containing transmembrane helices and a helix: 2, shorter
  9. Outer helices interacts with while inner contribute to - : bilayer, inner pore
  10. Selectivity of K+ channel: 10,000 fold over Na+
  11. K+ channel signal helix has 4 or repelled by outside: Arg or Lys
  12. What happens when outside becomes negative?: Helices shift up and open channel
  13. Selectivity of K+ channels comes from interaction with : oxygen molecules
  14. Consensus sequence of K+ gated channels: Gly-Tyr-Gly-Val-Thr
  15. Voltage gated Na+ channels have domains with helices each: 4, 6
  16. Which helices form central channel?: S5 and S

16 / 23

  1. Bacterial cells receive input from proteins that act as recep-tors, for example (2): membrane, information, chemotaxis, macrophage travelling towards bacterium
  2. In multicellular organisms signals represent information that is detected by receptors: specific
  3. Signals are converted to a response which always involves a process, called: cellular, chemical, signal transduction
  4. What is additional specificity in multi-cellular organisms?: Some receptors only present in certain cell types
  5. Three factors which account for extraordinary sensitivity to signal trans-ducers:: High aflnity of receptors for signal molecule (Kd = 10^-10M) Co-operativity of ligand receptor Amplification of signal by enzyme cascade
  6. Amplification occurs when enzymes activate other enzymes in which af-fected molecules increases : geometrically
  7. Dese nsitization is then a receptor activation triggers a circuit that: feedback, shuts ott receptor or removes it from surface
  8. Integration is when two signals have effects on a metabolic char-acteristic... resulting outcome results from input of : opposite, both
  9. Explain G-protein coupled receptors: External ligand binds receptor and activates GTP-bind-ing proteins which regulates enzyme that generates intracellular messenger (adrenaline, fast)
  10. Explain tyrosine kinase receptors: Ligand binding activates tyrosine kinase activity by auto-phosphorylation (insulin, timely)
  11. Explain guanylyl receptor: Ligand binds extracellular domain and stimulates formation of cyclic GMP

17 / 23

  1. Explain nuclear receptor: Dittuses into cytoplasm and binds receptors on nucleus to alter transcrip-tion of genes
  2. Explain gated ion channel: Open/close in response to concentration of signal ligand or membrane potential
  3. carries electrical signal down axon, carries signal to next cell: Action potential, neurotransmitter
  4. All of these trigger opening of cation channels (4): Ach, GABA, serotonin, glutamate

19 / 23 and SH

  1. The SH domains of other signalling proteins bind on IRS-1: P- Tyr
  2. How does diabetes interfere with this process?: Stimulates P-serine on IRS to interfere with P-Tyr
  3. Phosphorylated .............................bound by domain of Grb- 2 .............................. binds Sos via SH3 domain... Grb-2 bound Sos activates which is a .... bound Ras then activates : IRS-1, SH2, Grb-2, Ras, G-protein, GTP, protein kinase cascade

20 / 23

  1. How do G-proteins regulated GTP binding?: They are GTPases so hydrolyze GTP after certain time
  2. Inhibitors of G-proteins are activating proteins: GTPase
  3. Raf-1 phosphorylates on two residues activating it... This then phosphorylates on a and ... This then moves into the and phosphorylates factors ( ) These then stimulate transcrip-tion and translation of enzymes like (3): MEK, serine, ERK, thr, tyr, nucleus, nuclear transcription (Elk1), HK, ACC, and FAS
  4. Besides changing transcription, protein-protein interactions and phospho-rylation culminate in activation or inactivation of already present: en-zymes
  5. This starts with which binds to domain of , activating it. This phosphorylates to. This binds which phosphorylates and activates/inactivates downstream targets: P-IRS1, SH2, PI-3K, PIP2, PIP3, PKB
  6. Thus insulin has 3 major effects: 1. PKB phosphorylates GSK3 inactivating it and thus indirectly upregulating glycogen synthase
  7. PKB stimulates movement of GLUT4 towards plasma membrane, increasing glucose uptake
  8. Modulates insulin-responsive transcription factors
  9. Most common type of receptor? 3 examples: G-protein couple receptors, glucagon, histamines, epinephrine
  10. How many smell receptors? Most are?: 350, vestigial
  11. GPCR signalling consists of 3 components: 1. Plasma membrane receptor with 7 TM spans
  12. Heterotrimeric guanosine nucleotide binding protein (G-protein)
  13. Intracellular enzyme that generates 2nd messenger