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FS YEAR 2 > NORMAL CELL REVISION > Flashcards

NORMAL CELL REVISION Flashcards

1
Q

What are examples of signalling molecules?

A
  • growth factors
  • hormones
  • cytokines
  • neurotransmitters
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2
Q

What are growth factors

A

signalling molecules that after binding to growth factor receptors signal cells to grow and proliferate

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3
Q

What are the 3 steps of signalling?

A
  1. reception
  2. transduction
    - single-transduction pathway
  3. response
    - activation of cellular responses
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4
Q

What are protein kinases?

A

Enzymes that transfer phosphate groups to substrates that contain serine, threonine or tyrosine residues
Protein kinases can be tyrosine kinase (e.g. EGFR, VEGFR) or serine/threonine kinase (e.g. CDK)
Kinases can be cell-surface receptor kinases (e.g. EGFR) or intracellular receptor kinases (e.g. JAK)

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5
Q

What are tyrosine kinases and what do they do?

A

They selectively phosphorylate tyrosine residues in proteins
Phosphorylate: transfer a phosphate group from ATP to tyrosine residues
This activates inactive cells (“on-off switch”)
Receptor tyrosine kinases are activated by ligand binding to extracellular domain
Binding of growth factor switches tyrosine kinase ‘on’–> signals cell to divide

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6
Q

What is the DNA structure

A

Double helix of 2 complementary strands
Composed of nucleotides:
Sugar (deoxyribose)
Phosphate group
Nitrogenous bases (Adenine, Thymine, Guanine, Cytosine)
Pyrimidines: Cytosine & Thymine
Purines: Adenine & Guanine
Hydrogen bonds between bases on opposite strands
G-C base pairs have 3 hydrogen bonds
A-T base pairs have 2 hydrogen bonds

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7
Q

What does topoisomerase do?

A

unwind & rewind DNA strands to prevent DNA getting tangled (supercoiling)

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8
Q

What does telomerase do?

A

adds telomeres (protective end caps of chromosomes) at DNA 3’ ends
Without telomeres, the chromosomes will be prone to genomic instability & degradation
Cancer can upregulate telomerase, giving the cancerous cells a survival advantage

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9
Q

What do telomeres do?

A

(TTAGGG repeats) protects DNA from progressive degradation
Are repeated hundreds or thousands of times
Steady shortening of telomeres with each replication in somatic cells has a role in senescence (state of permanent cell cycle arrest)

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10
Q

What is the G1?

A

growth phase: increase in size, cellular contents duplicated

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11
Q

S phase?

A

DNA replication

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12
Q

G2 phase?

A

more growth, organelles & proteins developed (preparation for cell division)

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13
Q

M phase?

A

mitotic phase: mitotic divison and cytokinesis -> 2 daughter cells

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14
Q

what is the G0 phase?

A

resting phase - growth arrest (quiescence or senescence)

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15
Q

What are the cell cycle regulators

A

Positive & negative regulatory events (phosphorylation/dephosphorylation) involve:
Protein kinases
Protein phosphatases (remove phosphate groups)
Cyclins
Cyclin-dependent kinases (CDKs)
Cyclin-dependent kinase inhibitors (CDKIs)

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16
Q

What do cyclins do?

A

activate cyclin dependent kinases (CDK)
without cyclins, CDK’s have no activity

17
Q

What do CDK’s do

A

-phosphorylate (to activate or inactivate) proteins on serine or threonine residues
-CDKI’s inhibit the activity of CDK/cyclin complexes

18
Q

What is the purpose of cell cycle checkpoints?

A

Progression through each phase is monitored by cell cycle checkpoints
Unreplicated, mutated or damaged DNA blocks progression of cell cycle at checkpoints
Cell cycle can progress unchecked–> further mutations–> cancer
- G1 checkpoint - cell growth checkpoint
- S checkpoint - DNA synthesis checkpoint
- M checkpoint - mitosis checkpoint

19
Q

What are the steps of mitosis and what is mitosis

A

2 identical daughter cells are generated
1, prophase
2. prometaphase
3. metaphase
4. anaphase
5. telophase &cytokinesis

20
Q

Explain the steps of prophase

A
  1. Prophase: sister chromatids condense, mitotic spindle begins to form, centromeres more to opposite poles of cell
21
Q

What are the steps of pro metaphase?

A

the nuclear membrane breaks down, spindles fibres attach to centromeres of sister chromatids at the kinetochore

22
Q

What is metaphase

A

spindle fibres align chromosomes along the equator

23
Q

What is anaphase

A

sister chromatids separate
- spindle fibers pull chromosomes toward oposite poles
- chromosomes segregate at opposite poles

24
Q

What is telophase & cytokinesis

A

mitotic spindle breaks down
- new nucleus forms around chromosomes at each pole
- cleavage furrow forms
- cytokinesis occurs, pinching cell of into two new daughter cells

25
Q

Aerobic respiration?

A

glycolysis :
- cytoplasm, glucose into 2 pyruvate, generates net of 2 ATP

mitochondria
- pyruvate undergoes oxidative phosphrylation& will produce approx. 32 ATP molecules, in addition to the 2 molecules produced by glycolysis

aerobic metabolism:
Acetyl-CoA feeds into TCA cycle & then oxidative phosphorylation
Produces approx. 34 molecules of ATP, plus CO2 & H2O waste
Needs O2

26
Q

Anaerobic conditions?

A
  • glycolysis
  • Lactate fermentation
    2 ATP molecules that were produced previously from glycolysis
    Oxidative phosphorylation produces lots of energy

When no oxygen present, pyruvate fermented to lactate
Lactate is transported to liver for gluconeogenesis
No extra ATP

27
Q

What are the example forms of programmed cell death

A

Apoptosis (type I)
autophagy (type II)

28
Q

What is necrosis

A

non-physiological process due to infection or injury

29
Q

What are the steps of apoptosis

A
  1. Cytoplasmic shrinkage
  2. Chromatin condensation
  3. Nuclear fragmentation
  4. Plasma membrane blebbing & formation of vesicles (apoptotic bodies)
  5. Apoptotic bodies taken up by phagocytic cells & degraded in lysosomes

Doesn’t cause inflammation

30
Q

What are the two major pathways of apoptosis

A

Intrinsic (or mitochondrial): due to internal stress signals (DNA damage, oxidative stress)
Extrinsic: due to extracellular cues detected by death receptors

Apoptotic machinery is composed of upstream regulators & downstream initiators & effectors (caspases: intracellular proteases)

31
Q

What are the steps of extrinsic apoptosis?

A
  1. Extracellular death-inducing signals received by death receptors (FAS & TRAIL-R)
  2. Caspase-8 (or 10) is activated
  3. Effector caspases (caspase 3) are activated & execute the death programme
32
Q

What are the steps of intrinsic apoptosis

A
  1. BH3-only molecules sense intracellular signals
  2. Proapoptotic proteins (Bax, Bak) permeabilise mitochondria membranes to allow cytochrome C release
  3. Cytochrome C release activates caspase-9
  4. SMAC is also released
  5. Effector caspases (caspase-3) are activated & execute the death programme
33
Q

What are the steps of inhibitory signalling of apoptosis

A
  1. Antiapoptotic Bcl-2 proteins (Bcl-2, Bcl-XL) block cytochrome C release from mitochondria
  2. Inhibitors of apoptosis (IAP) proteins inhibit effector caspases
  3. SMAC inhibits IAPs allowing apoptosis to happen
34
Q

What is autophagy?

A

cells eat themselves up and recycle products

35
Q

How does autophagy-microphological changes occur?

A

-Extensive cytoplasmic vacuolization
-Intracellular vesicles (autophagosomes) envelope organelles
-Fuse with lysosomes
-Lysosomal degradation

Enables break down of cellular organelles (ribosomes, mitochondria)–> recycled products used for biosynthesis & energy metabolism

36
Q

What are the steps of necrosis

A

Cell digestion due to infection or injury
Cell swelling
Membrane disruption
Disposal of cell corpses without phagocytic & lysosomal involvement
Inflammatory response

FS YEAR 2 (10 decks)

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