Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

322 > Final > Flashcards

Final Flashcards

1
Q

What cells r involved in tumor recognition

A

Natural killer cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are natural killer cells

A

Circulate in blood as large lymphocytes with distinct cytotoxic granules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What cells r the first line of defence again virus

A

NKC’s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is KIR

A

Killer-cell inhibitory receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What cell expresses KIR

A

Natural killer cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is apoptosis

A

Programmed cell death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the purpose of programmed cell death

A
  1. Eliminating unwanted cell cells during development

2. Quality control

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What do apoptotic cels often lose

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How is cytochrome c used

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the inflammatory response of macrophages

A

release of cytokines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Fxn of capspases in apoptosis

A

Capspases mediate an intracellular proteolytic cascade in apoptosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What r caspases

A

Protease family w/a cysteine in their active site

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Where do caspases cleave

A

Their target proteins at specific aspartic acid residues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What begins the process of apoptosis?

A

Initiator caspaces

Have a protease domain and an adaptor binding domain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are executioners

A

Effector caspases

- cleave a wide variety of cellular proteins resulting in apoptosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

2 pathways of apoptosis in mammalian cells

A

Extrinsic and intrinsic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Extrinsic pathway of apoptosis is activated by what

A

Cell surface death receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

How is the extrinsic pathway started

A

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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Another name for fas ligand

A

death ligand

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What does Fas ligand/death ligand binding to 3 Fas molecules (death receptor) cause

A

The Fas molecules cytoplasmic domains (death domains) to trimerize

28
Q

What does trimerized Fas do

A

recruits adaptor proteins called FADD

29
Q

What does FADD stand for

A

Fas-associating-death domain containing protein

30
Q

What does FADD do

A

Recruits initiator procaspase which then activates the effector (executioner)

31
Q

What does the intrinsic pahway depend on

A

Release into cytosol of mitochondrial cytochrome c

32
Q

What happens in intrinsic pathway

A
  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
Q

What is Go

A

Resting

34
Q

What is G1

A

Gap phase before intitation of DNA synthesis

35
Q

What is S phase

A

DNA synthesis (chromosome duplication)

36
Q

G2

A

gap phase in which cel contains twice the # of chromosomes as G1 cells

37
Q

M phase =

A

mitosis - cell division

nucleus and cytoplasm

38
Q

Fxn of cell cycle

A 
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
Q

What does interphase consist of

A

G1, S, G2

40
Q

What is mitotic index

A

In a population of cells, the ratio of the # of cells undergoing mitosis (cell division) to the # of cells not undergoing mitosis

41
Q

What is M phase

A

Mitosis (nuclear division)

Cytokinesis (cytoplasmic division)

42
Q

How do we follow cell cycle progression

A

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
Q

How do u identify cell in S phase under microscope

A

Adding compound that incorporates into newly synthesized DNA

e.g. adding thymidine analog BrdU and later stain w/an antibody to BrdU

44
Q

What occurs during Go

A

Cells partially disassemble their cell cycle control system and withdraw not non dividing state

45
Q

Most cells in our body r in what phase

A

Go

46
Q

Example of cells in terminally differentiated Go where cell division rarely occurs

A

Muscle cells and most neurons

47
Q

During cell cycle once an event is initiated is it reversible

A

no

48
Q

What r the 3 transitions in cell cycle

A
  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
Q

Cell cycle control system depends on —

A

cyclically activated cyclin-dependent protein kinases

50
Q

What is cyclin

A

the primary regulator of Cdks

51
Q

How do cyclins work in cell cycle

A

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
Q

Which lvls remain constant which flucuate

A

cyclin lvls remain constant

cdk lvls fluctuate

53
Q

3 cyclins we need

A
  • G1/S
  • S cyclins
  • M cyclins
54
Q

role of G1/S

A

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
Q

role of S cyclin

A

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
Q

role of M cyclin

A

activate Cdks that stimulate entry into mitosis at the G2/M transition. M cyclins levels fall in mid-mitosis

57
Q

G1 cyclin role

A

regulate G1/S cyclins

58
Q

why isnt binding of a cyclin and its cdk not enough

A

phosphorylation and dephosphorylation as well as cyclin binding is required for Cdk activation

59
Q

Describe acitvation of cdks during M phase

A

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
Q

Two ways to suppress a cyclin-Cdk complex

A

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
Q

What are CKIs

A

Cdk inhibitory proteins

62
Q

Role of CAK (Cdk-activating kinase)

A

phosphorylates an activating site in cdks

63
Q

Wee1 kinase

A

phosphorylates inhibitory site on cdk1; primarily involved in surpressing cdk1 activity before mitosis

64
Q

Cdc 25 phosphatase

A

removes inhibitory phosphatases from cdks

65
Q

What is APC

A

anaphase promoting complex (cyclosome)

- a ubiquitin ligase

322 (1 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions