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Medicine yr1 > FOUNDATION-CELLS > Flashcards

FOUNDATION-CELLS Flashcards

1
Q

Which phases make up interphase?

A

G0
G1
S
G2

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2
Q

What happens in G0 phase?

A

rest phase

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3
Q

what happens in G1 phase?

A

organelles duplicated

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4
Q

what happens in S phase?

A

DNA synthesis-each of 46 chromosomes is duplicated by the cell

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5
Q

what happens in G2 phase?

A

cell growth and prep for mitosis -cell double checks the duplicated chromosomes for error-makes needed repairs

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6
Q

what do checkpoints do?

A
  • points in a eukaryotic cell cycle in which it examines the internal and external conditions and determines whether to continue with the cycle
  • they can halt the cell cycles and promote apoptosis in some circumstances to protect the cell from DNA damage
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7
Q

what do defects in checkpoints lead to?

A

aneuploidy

polyploidy

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8
Q

what are examples of important checkpoints?

A

G1-commit to cell division-site of action of p53 (tumour suppressor gene)
G2-ensure DNA fidelity
spindle-ensures that chromatids are attached to tubules correctly

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9
Q

what is DNA fidelity?

A

the ability of DNA polymerase to accurately synthesise a new strand from the template strand

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10
Q

what is p53 and what does it do?

A

tumour suppressor gene-a protein that regulates cells from growing and proliferating too fast

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11
Q

what are cyclins?

A

proteins that control the progression of a cell through the cell cycle by activating CDKs

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12
Q

what are CDKs?

A
  • cyclin dependent kinases

- bind to cyclins to be activated

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13
Q

which cyclins are present at which stage in the cell cycle?

A
  • G1-S transition=cyclin D
  • S-Cyclin E
  • G2-M transition=cyclin A
  • Mitosis=cyclin B
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14
Q

what are the 4 different types of cell death?

A
  • apoptosis
  • necrosis
  • anoikis
  • autophagy
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15
Q

describe apoptosis.

A
  • programmed, controlled cell death
  • extrinsic and intrinsic
  • involves FAS/TRAIL (ligands) binding to death receptors on the cell surface + involves caspases (proteases)
  • no inflammatory response
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16
Q

describe necrosis.

A
  • cell death due to acute cellular injury
  • not regulated
  • always pathalogical eg infectious agents (bacteria/ virus/ fungi), o2 deprivation, heat, radiation
  • initiates an inflammatory response
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17
Q

describe anoikis.

A
  • controlled cell death in anchorage-dependent cells (eg epithelial cells)
  • due to loss of cell extracellular matrix interaction
  • no inflammatory response
  • loss of anoikis can contribute to cancer metastasis
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18
Q

describe autophagy.

A
  • degradation and recycling of cellular components-may or may not lead to cell death
  • involves formation of an autophagosome that encapsulates cytoplasm, malformed proteins, organelles, or pathogens and then fuses with lysosome for degradation
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19
Q

what is mitosis and its purpose?

A
  • 1 cell divides into 2 genetically identical daughter cells
  • in the various stages the cells chromosomes are copied and then distributed equally between 2 nuclei of daughter cells
  • purpose=growth and repair
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20
Q

what happens in prophase?

A
  • chromosomes condense
  • nuclear envelope disappears
  • spindles form
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21
Q

what happens in metaphase?

A
  • sister chromatids line up at equator

- spindles attach to centromere

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22
Q

what happens in anaphase?

A
  • spindles contract

- sister chromatids are pulled apart to opposite poles of cell

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23
Q

what happens in telophase?

A
  • mitotic spindle breaks down
  • nuclear envelope reforms around chromosomes
  • chromosomes begin to decondense and return to stringy form (chromatin)
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24
Q

what occurs after telophase?

A

cytokinesis-cytoplasm splits in 2 and cell divides

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25
Q

what is meiosis?

A

-1 diploid cell (2n) undergoes 2 rounds of division but only 1 round of DNA replication

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26
Q

what does meiosis result in?

A

4 haploid (n) daughter cells

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27
Q

how do the cells produced in meiosis have genetic variation?

A
  • independent assortment of chromosomes in metaphase 1

- chiasmata (recombination)-allele shuffling in prophase 1

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28
Q

what are stem cells?

A

undifferentiated cells which have the ability to specialise into cells of different lineages/potency

29
Q

what does totipotent mean?

A

can differentiate into any cell type-embryonic & extraembryonic (zygote/ blastomeres)

30
Q

what are pluripotent cells?

A

-can develop into cells of any of the 3 germ layers (inner cell mass of blastocyte that give rise to the embryonic stem cells ESCs)

31
Q

what are multipotent cells?

A

can develop into several different cell types (haematopoietic and epithelial stem cells)

32
Q

what are the types of membrane transport?

A
  • endocytosis
  • exocytosis
  • pinocytosis
  • phagocytosis
33
Q

describe endocytosis

A
  • brings substances into cell
  • membrane forms a vesicle around cell
  • uses atp
34
Q

describe exocytosis

A
  • expels vesicles from cell

- cytoplasmic secretory vesicles fuse with cellular membrane-release contents into extracellular space

35
Q

describe pinocytosis.

A

-process by which liquid droplets are ingested by living cells

36
Q

describe phagocytosis.

A

uptake of solid particles by a cell

37
Q

what is simple diffusion?

A
  • movement of non-polar compounds only
  • down concentration gradient
  • passive
38
Q

what is facilitated diffusion?

A
  • diffusion down electrochemical gradient

- with help from channel/carrier proteins

39
Q

what is primary active transport?

A
  • diffusion against electrochemical gradient

- driven by ATP

40
Q

what is secondary active transport?

A
  • diffusion against electrochemical gradient

- driven by ion moving down its gradient

41
Q

how does transport occur by ion channels?

A

down electrochemical gradient

may be gated by a ligand or ion

42
Q

how does ionophore-mediated ion transport?

A

down electrochemical gradient

43
Q

what are the different types of cell junctions?

A
  • tight junctions
  • gap junctions
  • adherens junctions
44
Q

describe gap junctions.

A
  • allow movement of substances between cells
  • formed by 6 connexin proteins (in membrane of each cell)
  • 2 connexins aligned together forms a channel between 2 cells
  • passage for excitatory signals eg muscle and cardiac cells
45
Q

describe tight junctions.

A
  • stops movement of substances between cells

- contains interlocking junctional proteins which join adjacent cells

46
Q

what do adherens junctions do?

A

maintain cell position

47
Q

what are the 3 types of transporter proteins?

A
  • uniporter- single substance moves in a single direction
  • symporter- 2 substances move in the same direction
  • antiporter- 2 substances move in opposite direction
48
Q

what are 2 types of receptors?

A
  • tyrosine kinase receptors

- G-protein coupled receptors (super family)

49
Q

what is a kinase?

A

an enzyme which phosphorylates molecules

50
Q

what are tyrosine kinase receptors formed by?

A

amino acid tyrosine

51
Q

how do tyrosine receptors work?

A
  • when ligands bind to receptors the tyrosine polypeptide join together to form a dimer (the ligand activates the tyrosine regions to phosphorlyate each other)
  • relay proteins bind to the complex and initiate its own cellular response eg insulin
  • it acts as a ligand and the cellular response will lead to GLUT 4 channels being taken to the cell surface membrane to allow movement of glucose into cells
52
Q

which GPCR receptors are targets of many catecholamines (adrenaline/ noradrenaline)?

A

adrenergic receptors

53
Q

what do molecules do to GPCR receptors?

A

molecules bind to these receptors and activate an internal signal transduction pathway to eventually create a cellular response

54
Q

what does the structure of GPCR consist of?

A
  • 7 alpha helices joined by 3 intracellular and extracellular loops
  • arranged in barrel like structure
55
Q

what does a G protein itself consist of?

A
  • an alpha, beta and gamma subunit

- GDP (guanosine diphosphate) when inactive

56
Q

what does GDP turn into when activated?

A

GTP

57
Q

how are G proteins activated?

A
  • extracellular ligan binds to receptor
  • creates conformational change in tertiary structure of receptor-causes interaction between receptor and G protein
  • GDP is substituted by GTP
58
Q

what happens after GDP is substituted by GTP?

A
  • G-protein dissociates
  • the alpha-GTP complex can bind with and activate effector enzymes eg ADENYL CYCLASE/ phospholipase C
  • beta-gamma complex mainly binds with and activates ion channels and kinases
  • the activated alpha-subunits stimulates adenyl-cylclase to convert ATP to cAMP (secondary messenger)
59
Q

what does secondary messenger cAMP activate?

A

-protein kinase A

60
Q

what does protein kinase A do?

A

phosphorylates enzymes and proteins (activating them)

eg in sympathetic response-pkA stimulates many glycogen -degrading enzymes in the liver tissue

61
Q

what do protein molecules -arrestins do?

A

can bind to G protein receptors and prevent it from binding in G proteins

62
Q

what is polyploidy?

A

possessing more than 2 complete sets of chromosomes

63
Q

what is aneuploidy?

A

possessing an abnormal number of chromosomes (eg missing one or having one extra-trisomy)

64
Q

how do CDKs become activated?

A

-cyclins bind to CDKs and are phosphorlyated for them to be activated

65
Q

what is extrinsic apoptosis triggered by?

A
  • apoptosis triggered by signals from outside the cell

- FAS/ TRAIL ligands binding to death receptors

66
Q

what is intrinsic apoptosis triggered by?

A

apoptosis triggered by stress or damage to cell

67
Q

which cell death type causes an inflammatory response?

A

necrosis

occasionally autophagy

68
Q

which cell deaths are controlled?

A

apoptosis
anoikis
autophagy

Medicine yr1 (55 decks)

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