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Unit 1: LGS > Week 3 > Flashcards

Week 3 Flashcards

1
Q

Components of a nucleotide (3) and bond involved

A
  • nitrogenous base
  • sugar
  • phosphate
  • linked by phosphodiester bonds
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2
Q

Difference between nucleotides and nucleosides

A

Nucleotides include phosphates attached on nucleoside

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3
Q

Clinical significance of using RNA as template

A
  • Cell will first makes everything for RNA and then convert it to DNA structure
  • dUMP to dTMP through RR (ribonucleotide reductase)
  • used as treatment for cancer by inhibiting process of methylenation of uracil to thymine to stop proliferation of cell
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4
Q

Clinical significance of different classes of amino acids/ how is central dogma affected by mutations?

A

if mutation is made to DNA (translation/transcription) can change which AA is added to protein, if the AA added is not from similar family of original AA then will change structure of that specific protein and protein will not be able to carry out its function correctly

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5
Q

Forms of Lipid

A
  • Triglyceride: storage form of lipid
  • Cholesterol: provides fluidity to inside of cell membrane
  • Phospholipids: main component of cell membrane, ampiphilic
  • Glycolipids: lipid attached to sugar molecule, allow for cell to cell interactions
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6
Q

Monosaccharides

A

glucose, fructose, galactose, ribose, deoxyribose; can be classified in aldose or ketose

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7
Q

Diasccharide

A

has 2 mono joined by O bonds

Lactose- glucose and galactose

Fructose- glucose and fructose

Maltose- 2 glucose

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8
Q

Oligosaccharide

A

has 3-12 mono joined by O or N bonds

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9
Q

Glycosidic bond

A

O bonds: bind sugars together

N bonds: bind sugar to amine

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10
Q

Epimers

A
  • Same chemical formula,
  • Differ in where OH’s are around asymmetric carbon (glucose and galactose)
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11
Q

Enantiomers

A
  • two compounds that are mirror images but are not superimposable
  • where last OH group is at on sugar (D-right, L-left)
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12
Q

Polysaccharides

A
  • homo: made of same kind of sugar; glycogen
  • hetero: made of mult. kinds of sugar
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13
Q

List the organelles found in a typical eukaryotic cell and describe their functions (7)

A
  • Nucleus: Contains genetic information
  • Smooth ER: Synthesis of lipids, Ca storage
  • Rough ER: Where mRNA is translated and proteins are made
  • Mitochondria: Produces energy for the cell to use in day to day activities
  • Lysosome: Degrades various biochemical substances that are seen as waste and distributes them in vesicles to be released into extracellular space.
  • Cytoplasm: Holds cell shape and allows for movement of various components in cell.
  • Golgi apparatus: Where proteins are adjusted and then packaged for transport
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14
Q

plasma membrane: -made of? -function?

A
  • made of lipid bi-layer, with hydrophilic heads and hydrophobic tails.Contain different types of proteins and cholesterol which add to their fluidity and function
  • barrier of the cell and controls what goes in and out
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15
Q

Driving force for movement of water and how it functions

A

Osmosis-passive transport that flows from areas of high concentration to low concentration to achieve equilibrium.

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16
Q

Types of receptors and how they work (4)

A
  • Ligand: when activated will open/close ion channels, will make chemical into electrical signal
  • GPCR: when activated will stimulate G protein and activate signaling cascade
  • Enzyme linked: when activated will act as an enzyme or regulate an enzyme; protein kinase-phosphorylates proteins to activate/inhibit
  • Nuclear: when activated will bind with hormones to regulate specific genes
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17
Q

Effects of cholera toxin and pertussis on body

A
  • Cholera: keeps As in active form so GTP is to remain bound and which increases adenylyl cyclase – increase cAMP – increases PKA– increases pumping of electrolytes to lumen–water follows–causes diarrhea
  • Pertusis: Ai is inhibited–reduces inhibition of adenylyl cyclase–increased cAMP and PKA–increases pumping of electrolytes to lumen–water follows–causes diarrhea
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18
Q

Pharmacodynamics

A

actions of the drug on the body

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19
Q

Compare: competitive inhibitor, allosteric inhibitor, and allosteric activator

A
  • Competitive inhibitor: Competes with agonist to bind receptor; can be overcome with increase in agonist
  • Allosteric inhibitor: Binds to allosteric receptor on enzyme, changing confirmation of enzyme and preventing agonist from binding
  • Allosteric activator: Binds to allosteric receptor on enzyme, changing confirmation of enzyme and allowing agonist to bind
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20
Q

trastuzumab (Herceptin), cetuximab (Erbitux), and bevacizumab (Avastin)

A

monoclonal antibodies

  • Trastuzumab (Herceptin): breast cancer- Inhibits protooncogene Her2 to stop proliferation in cells that over express Her2
  • Cetuximab (Erbitux): metastatic colorectal cancer and cancers of the head and neck; allosteric inhibitor on EGFR which prevents EGF from binding
  • Bevacizumab (Avastin): metastatic colorectal cancer and cancers of the head and neck; binds to VEGF (ligand) preventing from binding to VEGF receptor
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21
Q

sildenafil (Viagra), tadalafil (Cialis), and vardenafil (Levitra)

A

Inhibit cGMP–prolong the vasodilatory effects of NO to treat erectile dysfunction and pulmonary arterial hypertension

22
Q

Relate the classification of alleles as “dominant” or “recessive” to the function of their protein products

A
  • dominant alleles can cause harm to cell by manipulating the protein because they are always expressed.
  • recessive alleles do NOT always cause harm cause they can only be expressed and change the protein if both alleles are expressed
23
Q

phases of the cell cycle and their regulation

A
  • G0: Quiescent cells not actively proliferating
  • G1: Presynthetic growth
  • G1-S: ensures integrity of DNA before cell expends a lot of its energy replicating it.
  • S phase: DNA replication -

G2: Premitotic growth

  • G2-M: ensures there has been accurate DNA replication before cell divides into 2
  • Mitosis: Cell splitting
24
Q

CDK inhibitors and what occurs with damage

A
  • Ensure that cell cycle checkpoint is met by modulating CDK-cyclin activity
  • Defective CDKI leads to cells with damaged DNA to proliferate which can develop malignant tumors.
25
Q

List hallmarks of Cancer

A

1: Ability to change genetics 2: Resists self destructive nature 3: Increases proliferation through receptors 4: Mutate growth suppressors: 5: Replicative immortality: 6: Angiogenesis: 7: Metastasis: 8: Reprogramming energy metabolism: 9: Tumor Promoting inflammation: 10: Evading Immune Destruction:

26
Q

Ability to change genetics

A

Can stop DNA repair mechanisms

27
Q

Resists self destructive nature

A

Immune to autophagy (cells contents degraded by lysosomes within the cell) by becoming dormant and then reversing back into normal state of action.

28
Q

Increases proliferation through receptors

A

Increase tyrosine kinase gene expression so that more sensitive to growth factor, can also sometimes turn tyrosine kinase on without stimulation allowing for proliferation

29
Q

Mutate growth suppressors

A

Contain mutations on inhibitory proteins that would stop cell proliferation due to mutations in DNA

30
Q

Replicative Immortality

A

Over expression of telomerase– continues to add nucelotides to telomeres. Since the telomeres are never shortened the cell is never signaled to stop replicating as it would in normal cells.

31
Q

Angiogenesis

A

Induce angiogensis allowing for continual nutrition

32
Q

Metastasis

A

Infiltrate nearby tissues and blood/lymph vessels

33
Q

Reprogramming energy metabolism

A

Uses anaerobic energy production which produces substantially less energy but allows for production of nucleosides and AA from byproducts of glycolysis

34
Q

Tumor promoting inflammation

A

Neutrophils release growth factor when they self destruct which allows for increased proliferation of cell. Also use release of reactive oxygen species from self destruction to increase genetic mutations in cancer cell.

35
Q

Evading Immune Destruction

A

Shed surface antigens into the circulatory system and recruit inflammatory cells to defend against lymphocytes

36
Q

Describe the function of the tumor suppressor gene products

A

Genes create proteins that control the cell check points and ensure that the cell and DNA meet requirements to progress into next stage of proliferation.

37
Q

Describe what is meant by “aerobic glycolysis” and the “Warburg effect”

A

Aerobic glycolysis: anaerobically break down glucose even in the presence of oxygen, what cancer cells utilize

38
Q

Differentiate amongst compassion, empathy, mercy, and pity.

A
  • Compassion: focuses on the other persons suffering and trying to realize what it must feel to be in their place. Understand leniency must be shown to patient as an equal.
  • Empathy: broader than compassion and can be used to picture the emotions, actions, or the way one might speak
  • Mercy: realizes there needs to be leniency shown due to a patients predicaments but leniency is shown from someone in power to a subordinate -Pity: trying to feel what it is like for that person to suffer due to the conditions they are currently in but involves one person lowering themselves to the level of another and thus makes it seem that the person showing pity is superior to the one receiving it.
39
Q

types of cell signaling

A
  • Contact dependent: membrane bound signal molecule
  • Paracrine: hormone sent out locally
  • Autocrine: hormone sent to self
  • Synaptic: neurotransmitter releases into synaptic cleft to work on specific target cell
  • Endocrine: hormones released into blood for systemic effect
40
Q

Types of target proteins

A
  • transport: alter ion transport
  • metabolic enzyme: alter metabolism
  • gene regulatory protein: alter gene expression
  • cytoskeletal protein: alter cell shape/movement
  • cell cycle protein: alter cell growth/ division
41
Q

what does each curve represent?

A

full agonist: High affinity for active state

partial agonist: Less affinity for active state

inverse agonist:High affinity for inactive state and forces rxn to produce opposite effect than usual

42
Q

efficacy

A

drug that has highest output

43
Q

potency

A

-dose at 50% of output

44
Q

Insulin pathway

A

1: insulin receptor
2: IRS protein
3: PI3K
4: PIP2
5: PIP3
6: AKT–leads to insertion of glut 4 in membrane to bring in extracellular glucose and phosphorylates GSK-3 to inactivate form which allows for glycogen synthase to be activated

AND

  1. Insulin receptor
  2. IRS protein
  3. GRB binds to IRS protein
  4. SOS binds to complex
  5. Complex activates Ras
  6. Ras-MapKKK-MapKK-MapK
45
Q

AKT effects

A

Glut 4 to membrane: allows glucose to enter cells

GKT3: inactivated–which allows for glycogen synthesis

46
Q

Draw out MAPK pathway

A

ligand binds receptor tyrosine kinase–GRB2 attaches to SOS–Ras-GEF attaches to GRB2 activated RTK complex– whole complex will send singnal which activates Ras by phosphorylating GDP to GTP–Ras signals Raf (MapKKK)– Raf signals Mek (MapKK)–Raf signals Erk (Mapk)

47
Q

Non-Polar

A

Glycine (GLY,G)

Leucine (LEU, L)

Proline (PRO,P)

Methionine (MET,M)

Pheylalanine (Phe, F)

Isoleucine (ILE,I)

Valine (VAL,V)

48
Q

Basic AA

A

Lysine (Lys, K)

Arginine (Arg, R)

Histidine (His, H)

49
Q

Polar AA

A

Glutamine (Gln,Q)

Tyrosine (Tyr,Y)

Serine (Ser, S)

Threonine (Thr,T)

Cysteine (Cys,C)

Asparagine (Asn, N)

Tryptophan (Trp,W)

50
Q

Acidic AA

A

Aspartic acid (Asp, D)

Glutamic acid (Glu, E)

51
Q

PKU

A
  • build up of phenylalanine due to phenylalanine hydroxylase not working and not converting to tyrosine
  • will treat with low phenylalanine diet and tyrosine supplement

Unit 1: LGS (9 decks)

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