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Semester 4 > case 4 - cellular biology > Flashcards

case 4 - cellular biology Flashcards

(63 cards)

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1
Q

what is atrophy

A

cell shrinking

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2
Q

how may atrophy be achieved

A

by apoptosis, reduced functional activity, loss of inervation, reduced blood supply, diminished nutrition, loss of hormonal or growth factor stimulation

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3
Q

what is hypertrophy

A

increase in size of existing cells

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4
Q

what is hypertrophy accompanied by

A

an increase in functional capacity

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5
Q

what is the change in number of cells called

A

hyperplasia or aplasia

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6
Q

what is hyperplasia

A

increased number of cells caused by an increase in cell division

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7
Q

what is aplasia

A

decreased number of cells

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8
Q

what is metaplasia

A

this is an adaptive response to evironmental stimuli

specialised cell types change their pattern of differentiation to a new mature stable cell type

this allows them to withstand stress better

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9
Q

what is dysplasia

A

the enlargement of tissue by the proliferation of abnormal cells as a developemtal disorder or an early stage in the development of cancer

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10
Q

what is anaplasia

A

loss of intracellular structural differentiation within a cell often with increased capacity for multiplication as in a malignant tumour

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11
Q

what is the steps in cancer

A

metaplasia followed by dysplasia followed by anaplasia

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12
Q

what does interphase commence with

A

G1

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13
Q

what happens in G1

A

normal cell functions and cell growth, duplication of organelles

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14
Q

what happens to the cells in G1

A

they become sensitive to growth factors and anti proliferative factors

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15
Q

what happens once the cells have entered the cell cycle

A

there is no reversal - the point at which the cell enters the cell cycle and no longer be affected by growth/anti proliferative factors

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16
Q

what is this point called

A

the restriction point

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17
Q

what is G0

A

when cells stay in G1 for a long time and possibly never divide again

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18
Q

what happens during S phase

A

synthesis phase - DNA replication

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19
Q

what happens in G2

A

chromosome begins to condense in preparation for the next mitotic division

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20
Q

what do cyclins active

A

CDKs

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21
Q

what are CDKs

A

enzymes that control the progression through the cell cycle - checkpoint control

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22
Q

what do checkpoint controls prevent

A

DNA replication or mitosis of damaged cells and either stop the cell cycle to allow for DNA repair or eliminate irreversibly damaged cells by apoptosis

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23
Q

what do CDKs promote

A

DNA replication and various aspects of the mitosis process and are required for cell cycle progression

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24
Q

what inhibits CDKs

A

CKi’s - in particular p21

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25
where is cyclin B found in high quantities
in the late G2 stage, peaking during mitosis
26
what does cyclin B associated with to activate it
CDK1
27
what does this cyclin B/CDK1 complex do
phosphorylates proteins to cause mitosis
28
what do MAP do
cause spindle formation
29
what does lamin do
usually makes a protein meshwork which the nuclear envelope sits on. upon phsophorylation, this meshwork breaks down, leading to the breakdown of the nuclear envelope
30
what does histone cause
the condensation of the chromosomes
31
what is Ras normally bound to and what state is it in
normally bound to GDP and is usually inactive
32
how does Ras activate
by binding to GTP
33
what happens once Ras is in the active form
it can initiate signalling cascades to cause: - inhibition of apoptosis - cell growth - protein synthesis
34
what type of gene is ras
it is an oncogene - its mutation causes it to remain in the active form, thus causing a significant increase in cell growth and proliferation
35
what pathway must be mutated to cause colorectal cancer
wnt pathway
36
what is the intracellular protein complex comprised of that Wnt interacts with
GSK-3B APC (tumour suppressor gene) B-catenin (oncogene)
37
what happens in the absence of Wnt
it is in the unstimulated state. GSK-3B is active, thus phosphorylating B catenin this causes the proteolytic degradation of B catenin
38
what happens when Wnt signals are present
they bind to the receptor, the intracellular protein complex becomes disrupted. the GSK-3B is switched off, thus B catenin is no longer phosphorylated
39
what does this mean
that b catenin is no longer targeted for proteolytic degradation. B catenin can now move to the nucleus, where it interacts with transcription factors changing gene expression, and so increasing cell proliferation
40
what does a mutation in the beta catenin gene cause
it to remain unphophorylated and stable, thus increasing cell proliferation
41
what stimulates ras to bind to its receptors and what does this activate
growth factors stimulate ras, which binds to its receptors, thus activating transcription factors and affecting gene expression, especially cyclin D1
42
what does cyclin D1 activate
CDK4
43
what does CDK4 phophorylate
Rb into pRb
44
what is Rb normally bound to
the E2F family of transcription factors, and inhibits them
45
what happens then when CDK4 phosphorylated Rb
pRb now causes the liberation of E2F transcription factors, thus allowing them to enter the nucleus and modulating gene expression, especially of cyclin E
46
what happens to this cyclin E
it can now bind to CDK2, thus triggering the S phase of the cell cycle
47
what type of gene is Rb
a tumour supressor gene
48
what happens if one copy is mutated
it has no effect on the liberation of E2F
49
what happens if both copies of Rb are mutated
then E2F is always liberated and the cell continuously enters the cell cycle and the S phase without the importance of checkpoint control
50
what phase do external factors not influence
S phase
51
what happens if the S phase doesnt go to plan
results in the activation of p53, which will then aim to shut down the cell cycle as a defence mechanism
52
what is p53
a transcription factor which is degraded normally, but in response to stimuli it can become active and remains non-degraded
53
what happens to the kinases and ubiquitin ligases
these ligases which would normally breakdown p53 are inhibited
54
what does the activation of p53 the result of
lack of nucleotides UV radiation Ionising radiation Oncogene signalling Hypoxia Blockage of transcription factors
55
what does cell cycle arrest occur by and what does it lead to
leads to senescence or return to proliferation and this occurs by up regulation of p21 which is a CKi
56
what does the activation of p53 cause
DNA repair Block of angiogenesis Apoptosis P53 drives expression of genes such as puma and noxa. These activate the BAX intrinsic apoptotic pathway, thus leading to programmed cell death Bcl-X is a pro-survival protein in colon cancer
57
what is the principle cell type of epithelium of the small intestine
the paneth cells
58
where are the paneth cells found
below the stem cells in the crypts
59
what is apoptosis
This is a programmed sequence of intracellular events leading to the death pf the cell without the release of products harmful to the surrounding cells intrinsic/extrinsic pathways
60
what is the proteolytic cascade
1. The cell shrinks and condenses 2. Digestion of the nuclear DNA into small DNA fragments 3. Cells cytoskeleton disassembles 4. Blebbing 5. Cell surface membrane altered to allow phagocytosis
61
what is the extrinsic pathway of apoptosis
ligand (TNF alpha or Fas) bind to a receptor on the cell surface membrane of the cell The activation of the receptor causes a DISC to bind to the internal aspect of the receptor This causes the activation of enzymes known as caspases (known as paracaspases when inactivated) Proteolytic cascade occurs
62
what is the intrinsic pathway of apoptosis
cell recognises internal damage BAX (in the cytoplasm) binds to a receptor on the mitochondria Upon binding, BAX changes shape Proteins (cytochrome C) in the intramembranous space of the mitochondria leak out into the cytoplasm Cytochrome c activates the paracaspases into caspases, leading to apoptosis
63
what is necrosis due to
trauma disease ischaemia

Semester 4 (80 decks)

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