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Biol112 > Week 4 > Flashcards

Week 4 Flashcards

1
Q

Why is correct regulation of cell division important ?

A

Development
Injury
Adaptive responses

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2
Q

What are some of the adaptive responses that cell division is important in ?

A

Cells in bone marrow respond to low O2, produce more red blood cells
Lymphocytes - division triggered in response to antigen - needs to be controlled

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3
Q

What are the 2 main ways in which cell division is regulated ?

A

External and internal signals

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4
Q

Are growth factors external or internal signals ?

A

External signals

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5
Q

What do cells require in order to divide ( external signals ) ?

A

Sustained mitogen stimulation in order to progress through G1 checkpoint

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6
Q

What wad the 1st mitogen to be discovered ?

A

PDGF

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7
Q

What is the role of PDGF?

A

It binds to receptors on skin cells when it is wounded and stimulates cell division

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8
Q

How were internal cell signals first identified ?

A

Fusing cells from different stages of the cell cycle , caused the non mitotic cell to become mitotic due to a growth factor in the cell cycle

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9
Q

What stage of teh cell cycle do cells have to be in to be stimulated by M phase cells to enter mitosis ?

A

Any stage , not unique to G2 cells

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10
Q

The promotion factor for s phase cells , only works for what phase of cells ?

A

G1 cells, not G2 cells

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11
Q

What are the 3 major checkpoints in the cell cycle ?

A

G1 checkpoint
G2 checkpoint
Metaphase checkpoint or spindle assembly checkpoint (SAC)

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12
Q

What occurs in the G1 checkpoint ?

A

Start / restriction point
Commits the cell to dna replication

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13
Q

Who discovered cyclins ?

A

Sir Tim Hunt in 1982 ?

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14
Q

What protein factor regulates the G1 checkpoint ?

A

SPF ( s phase promoting factor )

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15
Q

What receptor binds phosphorylated lysosomal proteins, directing their transfer to lysosomes?

A

Mannose- 6 phosphate receptor (M-6-P): In the cis Golgi , any proteins destined for the lysosomes are phosphorylated on their mannose residues ( glycosylated in the ER). The M-6-P receptor binds these phosphorylated mannose residues in the trans Golgi, directing the proteins to lysosomes

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16
Q

What protein polymerises to form a cage-like structure to allow endocytosis of vesicles ?

A

Clathrin

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17
Q

What stain is used for electron microscope ?

A

Heavy metals

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18
Q

Which cancer has the highest no deaths for both genders ?

A

Lung cancer

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19
Q

What type of cancer and cells it derives from has the highest rate of cancer ?

A

Carcinoma (epithelial cells )

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20
Q

What are the classifications of cancers ?

A

Carcinoma , sarcoma , myeloma , lymphoma , leukaemia , mixed classifications (germ cells/stem cells )

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21
Q

What are 2 important qualities of normal cells in culture ?

A
  1. Anchorage dependent growth - no attachment no growth
  2. Density dependent growth - stop growing when confluent (signals from other cells )
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22
Q

What are 2 qualities of cancerous cells in culture ? What are dense clumps of cells called ?

A

No anchorage dependence
No density dependence - growth not controlled by other cells , they grow on top of each other
Foci

23
Q

What is the number of doublings possible in normal cells ? Cancerous ?

A

50-60 then viability decreases
Indefinite doublings

24
Q

Why do normal cells have a shorter life expectancy ?

A

Shortening of chromosomal telomeres , cancerous cells are able to maintain telomere length - telomerase

25
Q

How does the reliance on growth factors change with cancer?

A

It decreases

26
Q

What occurs in the initiation stage of cancer ?

A

Single cell undergoes a single mutation - confers a growth advantage which causes it to lose some of its growth control

27
Q

What occurs In the clonal expansion function of cancer ?

A

Proliferation begins
Mutated cells quickly divide
Clone cluster

28
Q

What happens in the 3rd stage of cancer?

A

Primary tumour - surgery possible

29
Q

What happens in the 4th stage of cancer ?

A

Secondary mutation - new phenotype with a selective advantage

30
Q

What happens in the 5th stage of cancer?

A

Malignant cancer
- becomes invasive , proteases produced to breakdown the ECM holding cells in place

31
Q

6th stage of cancer ?

A

Invasion of lymph and or blood vessels
1st few stages of metastasis - can break off tumour and enter vessels

32
Q

Stage 7 of cancer ?

A

Cell from tumour entered a vessel

33
Q

What are the ways in which proto-oncogenes can become oncogenes?

A

Translocation - gene moved to a new locus - New promoter means gene transcribed more efficiently - more protein
Gene replicated - more total protein
Mutation in existing promoter - more efficient transcription
Change to protein itself - more growth promoting

34
Q

How was the Ras oncogene discovered ?
What happens due to Ras oncogene ?

A

A bladder tumour was used to transform mouse 3T3 cells
Only a single nucleotide change between the oncogene and proto-oncogene in protein G12V causes it to become permanently active , excessive cyclin production

35
Q

What occurs in the G 2 checkpoint ?

A

Cell makes decision whether or not to enter mitosis

36
Q

What is the combination of cyclin and cdk referred to as ?

A

Promoting factor

37
Q

What is the m phase promoting factor ?

A

MPF composed of Cdk1 and cyclin B

38
Q

Cdk is the internal regulator for G1 and G2 checkpoints , what is the checkpoint for M checkpoint?

A

Anaphase promoting complex (APC)

39
Q

What happens when Ras becomes mutated?

A

Permanent stimulation of signalling cascade

40
Q

Are tumour suppressor dominant or recessive ?

A

Recessive

41
Q

What is the name of a retinal tumour ? What are the 2 forms ?

A

Retinoblastoma
Familial - 10% young children in both eyes
Sporadic - 90% - later in life - usually only one eye affected

42
Q

If retinoblastoma Is recessive why is it often teh case 50% if kids get it from heterozygous parents ?

A

Somatic mutation
If one chromosome has teh mutation likely the other will also become mutated

43
Q

What does the retinoblastoma protein inhibit ?

A

G1- S transition

44
Q

What is the role of p53 ?

A

To protect the cell against damaged DNA

45
Q

What does inactivation of pRb by mutation lead to ?

A

loss of G1 checkpoint and uncontrolled cell division.

46
Q

What is the permanently non-replicating state called ?

A

Senescence

47
Q

How does p53 respond to damage ?

A

DNA damaged in nucleus
Signal is passed to p53 via a cascade of protein kinases each phosphorylating and activating each other
Activated p53 is a transcription factor
Triggers expression of proteins which inhibit cell cycle

48
Q

What are the functions of p53?

A

Cell cycle checkpoint in G1
Cell cycle checkpoint in G2
Upregulation of DNA damage repair enzymes

49
Q

In what ways doe sp53 alter gene expression ?

A

CDK inhibitor protein p21 is upreguakted by p53
DNA repair proteins are transcriptionally regulated by p53
Genes involved in apoptosis activated

50
Q

What family of proteins activates apoptosis ?

A

Caspases

51
Q

What induces intrinsic apoptosis ? Extrinsic ?

A

Factors within the cell
Activation of the FAS death receptor

52
Q

How is intrinsic apoptosis regulated by p53?

A

Induced Bid expression
Activated Bid induces Bax to form a pore in the mitochondrial membrane
Release of cytochrome c activates caspases present in cytoplasm leading to apoptosis

53
Q

How does p53 regulate extrinsic apoptosis ?

A

Activation of p53 induces expression of Death receptors.
Death receptors are activated by cells expressing Fas ligand e.g. Lymphocytes
Fas ligand binding activates the Fas death receptor and recruits the Fas associated death domain (FADD)
Formation of the DISC, activates caspases that regulate cellular disintegration - apoptosis

Biol112 (4 decks)

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