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Final Flashcards

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1
Q

What cells r involved in tumor recognition

A

Natural killer cells

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2
Q

What are natural killer cells

A

Circulate in blood as large lymphocytes with distinct cytotoxic granules

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3
Q

How do NKC’s and B and T cells differ

A

NKC’s lack antigen specific receptors (non-specific cytotoxicity compared to B and T cells)

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4
Q

What cells r the first line of defence again virus

A

NKC’s

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5
Q

What is KIR

A

Killer-cell inhibitory receptor

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6
Q

What cell expresses KIR

A

Natural killer cell

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7
Q

What does KIR bind to

A 
MHC class I. 
The ligation of MHC class I and KIR prevents the killer cell from killing the target cell
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8
Q

Virus infected cells or tumor cells often have reduced # of MHC class I on surface… importance?

A

NKC’s will attack tumor cell, causing apoptosis

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9
Q

What is apoptosis

A

Programmed cell death

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10
Q

Diff between Necrosis and apoptosis

A
  • necrosis has release of intracellular contents and inflammation
  • apoptosis nothing escapes everything contained within vesicle and eventually phagocytosed
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11
Q

What is the purpose of programmed cell death

A
  1. Eliminating unwanted cell cells during development

2. Quality control

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12
Q

In developing vertebrate NS over half nerve cells die soon after generation, why?

A

Overproduction followed by culling ensures that target cells r contacted by nerve cells n extra nerve cells eliminated

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13
Q

Quality control of vertebrate adaptive immune system:

A
  • developing T that don’t recognize self or that recognize self with too high an affinity
  • B cells with non-productive BCR or BCR that recognizes self
  • Elimination of lymphocytes following an infection
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14
Q

How are apoptotic cells biochemically (in addition to morphologically recognizable)?

A

Phosphatidylserine flips to outer leaflet. Serves as phagocytic marker for macrophages that also blocks the inflammatory response (release of cytokines) of macrophages

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15
Q

What do apoptotic cels often lose

A

the electrical potential that normally exists across the inner membrane of their mta

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16
Q

How is cytochrome c used

A

Cytochrome c is released from intermembrane space and cytochrome c relocation is a marker

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17
Q

What is the inflammatory response of macrophages

A

release of cytokines

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18
Q

Fxn of capspases in apoptosis

A

Capspases mediate an intracellular proteolytic cascade in apoptosis

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19
Q

What r caspases

A

Protease family w/a cysteine in their active site

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20
Q

Where do caspases cleave

A

Their target proteins at specific aspartic acid residues

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21
Q

What begins the process of apoptosis?

A

Initiator caspaces

Have a protease domain and an adaptor binding domain

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22
Q

What are executioners

A

Effector caspases

- cleave a wide variety of cellular proteins resulting in apoptosis

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23
Q

2 pathways of apoptosis in mammalian cells

A

Extrinsic and intrinsic

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24
Q

Extrinsic pathway of apoptosis is activated by what

A

Cell surface death receptors

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25
How is the extrinsic pathway started
Homotrimeric Fas ligand on surface of an effector cell binds and activates the 3 Fas proteins on surface of target cell - Adaptor protein recruits specific procaspase - clustered molecules become activated n initiate a proteolytic capspase cascade leading to apoptsis
26
Another name for fas ligand
death ligand
27
What does Fas ligand/death ligand binding to 3 Fas molecules (death receptor) cause
The Fas molecules cytoplasmic domains (death domains) to trimerize
28
What does trimerized Fas do
recruits adaptor proteins called FADD
29
What does FADD stand for
Fas-associating-death domain containing protein
30
What does FADD do
Recruits initiator procaspase which then activates the effector (executioner)
31
What does the intrinsic pahway depend on
Release into cytosol of mitochondrial cytochrome c
32
What happens in intrinsic pathway
1. Apoptotic stimulus 2. Release of cyt c 3. Activation of Apaf1 by cyt c and hydrolysis of bound dATP to dADP 4. Assembly of apoptosome triggered by release of dADP in exchange for dATP or ATP 5. Recruitment n activation of procapspase 9 6. Caspase 9 cleaves and thereby activates executioner procaspases 7. Caspase casacde leading to apoptosis
33
What is Go
Resting
34
What is G1
Gap phase before intitation of DNA synthesis
35
What is S phase
DNA synthesis (chromosome duplication)
36
G2
gap phase in which cel contains twice the # of chromosomes as G1 cells
37
M phase =
mitosis - cell division | nucleus and cytoplasm
38
Fxn of cell cycle
``` Duplicate all DNA in a cell's chromosome (S) and then precisely segregate the copies into 2 daughter cells (M) Gap phases (G1 and G2) allows time for cells 2 double their their mass of proteins n organelles n monitor fiedlity of other processes ```
39
What does interphase consist of
G1, S, G2
40
What is mitotic index
In a population of cells, the ratio of the # of cells undergoing mitosis (cell division) to the # of cells not undergoing mitosis
41
What is M phase
Mitosis (nuclear division) | Cytokinesis (cytoplasmic division)
42
How do we follow cell cycle progression
W/a microscope or fluorescent labelling | looking (flat r in G0, bulbous = about to divide, begin to lift off plate begin to enter cell cycle)
43
How do u identify cell in S phase under microscope
Adding compound that incorporates into newly synthesized DNA | e.g. adding thymidine analog BrdU and later stain w/an antibody to BrdU
44
What occurs during Go
Cells partially disassemble their cell cycle control system and withdraw not non dividing state
45
Most cells in our body r in what phase
Go
46
Example of cells in terminally differentiated Go where cell division rarely occurs
Muscle cells and most neurons
47
During cell cycle once an event is initiated is it reversible
no
48
What r the 3 transitions in cell cycle
1. Start transition - Late G1 - Cell commits to cell cycle entry and chromosome duplication 2. G2/M transition (in G2 before M) 3. Metaphase-to-anaphase checkpoint - chromatid separation is triggered leading 2 completion of mitosis and cytokinesis
49
Cell cycle control system depends on ---
cyclically activated cyclin-dependent protein kinases
50
What is cyclin
the primary regulator of Cdks
51
How do cyclins work in cell cycle
Undergo a cycle of synthesis and degradation during cell cycle - a cdk must b tightly bound to cyclin in order to b activated - lvls of cdk r consant thruout cell cycle - changes in cyclin lvls result in assembly n activitation of cyclin-cdk complexes
52
Which lvls remain constant which flucuate
cyclin lvls remain constant | cdk lvls fluctuate
53
3 cyclins we need
- G1/S - S cyclins - M cyclins
54
role of G1/S
activate Cdks late in G1 and thereby help trigger progression through start resulting in a commitment to cell cycle entry. Their levels fall in S-phase
55
role of S cyclin
bind Cdks soon after progression through start and help stimulate chromosome duplication. S-level cyclins remain elevated until mitosis and contribute to the control of early mitotic events
56
role of M cyclin
activate Cdks that stimulate entry into mitosis at the G2/M transition. M cyclins levels fall in mid-mitosis
57
G1 cyclin role
regulate G1/S cyclins
58
why isnt binding of a cyclin and its cdk not enough
phosphorylation and dephosphorylation as well as cyclin binding is required for Cdk activation
59
Describe acitvation of cdks during M phase
In M-phase the cyclin is cyclin B and the Cdk partner is Cdk1 Wee-1: the inhibiting kinases that phosphorylate a Cdk1 on two sites CAK; cyclin activating kinase phosphorylates another site on a Cdk1 At this stage, the cyclin-Cdk complex is inactive and accumulating in the cell (for simplicity we’ll call it the M-Cdk complex) When the right signal is release, Cdc 25 phosphatase will dephosporylate the two inhibitory sites and the complex is now active
60
Two ways to suppress a cyclin-Cdk complex
Inhibitory phosphoryation: In this example Wee1 kinase phosphorylates the active Cdk thereby inhibiting it Cdc25 phosphatase dephosphorylates the site that Wee1 phosphorylated and thereby reactives Cdk Cdk inhibitory proteins (CKIs): CKI binding alters the structure of the cyclin-Cdk complex thereby inactivating it In this example p27, the CKI, binds to both the cyclin and the Cdk distorting the active site, as well as inserting into the ATP binding site further inhibiting enzyme activity
61
What are CKIs
Cdk inhibitory proteins
62
Role of CAK (Cdk-activating kinase)
phosphorylates an activating site in cdks
63
Wee1 kinase
phosphorylates inhibitory site on cdk1; primarily involved in surpressing cdk1 activity before mitosis
64
Cdc 25 phosphatase
removes inhibitory phosphatases from cdks
65
What is APC
anaphase promoting complex (cyclosome) | - a ubiquitin ligase

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