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Physiology Exam 4 > LC 41 > Flashcards

LC 41 Flashcards

1
Q

Apoptosis

A

programmed cell death, series of instruction cell goes through to catalytically fragment DNA, then cytoplasm blebs off

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2
Q

initiator caspases

A
  • type of protease (cleaves proteins)
  • specifically associated with apoptosis
  • caspase 8 and 9 –> one for inside of cell and one for outside of cell
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3
Q

effector caspases

A
  • cleaved by initiator caspases
  • caspase 3,6,7
  • start activating proteins to chop up DNA
  • leads to cell packaging and blebbing
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4
Q

caspase 8

A

Protease and initiator caspase

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5
Q

caspase 9

A

Protease and initiator caspase

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6
Q

Bax

A

Degeneration. Internal apoptosis from internal factors recognizing somethings not right in the cell. Opens membrane pores in mitochondira - Ca and Cyt-C are released into cytoplasm. Cyt-C joins to Apaf-1 to form a huge apoptomsome complex. This activates Casp 9 from proCasp9 which activates caspase 3,6,7 and apoptosis ensues

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7
Q

Bcl-2

A

Proliferation. Internal pathway that is in “tug of war” with Bax. Closes membrane pores in mitochondira. Increased transcription of Bcl-2 by trophic survival factors.

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8
Q

cytochrome C

A

involved in ETC in mitochondira.

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9
Q

p53

A

Transcription factor of Bax for internal pathway. Activated with DNA damage and inhibited CDK. Involved in stimulating Bax concentration so the cell is pushed towards apoptosis

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10
Q

Fas

A

Involved in external pathway. Single membrane receptor that interacts with Fas ligand. When Fas is bound by FasL is trimerizes and bring three Fas-FasL complexes togther which then recruit 3 FADD. FADD is now an active protease that cleave proCasp8 to Casp8 (initiator caspase). Casp8 activates Caspase 3,6,7 which causes apoptosis

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11
Q

FasL

A

Involved in external pathway. Is the external ligand that binds to Fas

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12
Q

FADD

A

Fas associated death domain. Recruited by Fas-FasL complex

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13
Q

Four things apoptosis is important for

A

1) Development
2) Surveillance
3) Maintenance
4) Regulation

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14
Q

Necrosis

A

Uncontrolled cell death that is the result of acute stress. The cell ruptures and spills into the ECM and causes inflammation

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15
Q

What has the potential to throw of the balance between mitosis and apoptosis?

A

disease

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16
Q

Neoplasia

A

mitosis outweighs apoptosis. Ex. Cancer

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17
Q

homeostasis

A

mitosis is balanced with apoptosis

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18
Q

Degenration

A

apoptosis outweighs mitosis. Ex. parkinson’s

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19
Q

Examples of triggers

A

embryology, removal of survival factors, DNA damage, Ca 2+ release (means cell has lost integrity)

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20
Q

How many apoptosis pathways are focused on?

A

two - an internal and an external pathway

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21
Q

Trophic factor

A

survival factors that tell the cell everything is going well. This is an external factor

22
Q

True or false - Fas/FasL pathway is self regulated

A

false, this pathway occurs when the cell does not self regulate and doesn’t realize it needs to go into apoptosis. This pathway chaperones the cell to apoptosis

23
Q

CD 8+ lymphocyte and FasL

A

T-cell expresses FasL to bind cells that are abnormal to cause apoptosis

24
Q

During clonal expansion (during and infection) T-cells express _____ but not not ______ until they are old and have completed their jobs

A

FasL, Fas-FADD complex. This helps to bring T-cell back down to normal levels after an infection

25
Q

Oncogenes and cancer

A

colorectal cancers often APC, Ra, and p53 mutated

26
Q

oncogene

A

mutated/overexpressed genes which can cause cancer

27
Q

Protooncogene

A

a normal gene involved in apoptosis or cell cycle which mis-regulation or mutation could turn into an oncogene. turn on cell cycle, turn off apoptosis

28
Q

Tumor-suppressor gene

A

genes involved in damage surveillance and negative cell cycle regulation. Turn off cell cycle, turn on apoptosis

29
Q

Tumor Anti-Immunity

A

Tumor cells have mutated so they can produce FasL so they can target your cytotoxic t-cells that would usually destroy them

30
Q

Oncogene

A

mutated/overexpressed genes which can cause cancer. Gene is activity causing cancer

31
Q

Protooncogene

A

a normal gene (many in our system) involved in apoptosis or cell cycle. Mis-regulation or mutation could turn into an oncogene. turn on cell cycle, turn off apoptosis

32
Q

What is the difference between protooncogene and tumor suppressor gene?

A

Protooncogene tends to turn on cell cycle - mutation leads to cancer. Tumor suppressor gene regulates through apoptosis - mutation turns it off so there is no regulation

33
Q

Ras pathway with protooncogene

A

Ras is mutated so it cannot hydrolyze GTP - now Ras is always on. This leads to uncontrolled cell division and production of G1 cyclin, E2F, G1-CDK so it is pushed through G1/S checkpoint

34
Q

What is Ras off switch

A

monomeric GTPase - hydrolyses GTP over time to inactivate itself

35
Q

AKT pathway with protooncogene

A

Purpose of pathway - inhibit apoptosis through Bcl-2 production and inhibit cell cycle arrest. When mutated Akt can’t turn off so there is no cell death, apoptosis goes way down and now we have cancer

36
Q

Examples of protooncogenes

A

Akt and Ras - many others these are just ones we discuss

37
Q

p53 as a tumor suppressor gene

A

When its turned off (unable to be phosphorylated) it doesn’t increase Bax, p21 is not stimulated so now it causes cancer because there is unregulated growth.

38
Q

p53

A

involved in cell damage surveillance

  • increases Bax
  • Turns off cell cycle
  • push towards apoptosis
39
Q

APC as a tumor suppressor gene

A

APC does not phosphorylate Beta-catenin (so it can be marked for degradation) so it builds up in the cells and translocates to the nucleus where it is a translation factor for cyclin D that pushes the cell through the G1/S checkpoint.

40
Q

Beta-catenin side effect of APC tumor suppressor gene pathway

A

disrupts cell-cell adhesion so it losses connection to neighbors. Now it breaks away and can travel through the body

41
Q

Two examples of tumor suppressor genes

A

APC and p53

42
Q

Viral oncogene - vRAS (viral rat sarcoma virus)

A

vRAS is independent of EGF signaling pathway

43
Q

Viral oncogene

A

an oncogene delivered by a virus for the purpose of causing tumorigenesis

44
Q

Can mutated protooncogenes be viral oncogenes?

A

yes, viral RAS cannot be turned off similarly to mutated proooncogenes

45
Q

Can mutated tumor suppressor genes be viral oncogenes?

A

No, a tumor suppressor gene doesn’t do anything when mutated whereas a viral gene is implanted to run a cancerous system independent of the cell’s system

46
Q

Viral oncogenes and HPV

A

1) E6 protein (causes ubiquitination of p53 leading to degradation of p53
2) this means the cell loses damage control
3) E7 protein binds Rb protein so that it cannot inhibit E2F
3) E2F pushes the cell forward into the cell cycle
4) Loss of p53 and always active E2F causes tumorigenesis

47
Q

Does HPV guarantee the affect person will get cancer?

A

No but it does push them that way

48
Q

Approximately how many crucial mutations does it take to to create a tumor/cancerous growth?

A

3-5

49
Q

Oncogenes and colon cancer - stages

A

1) Normal epithelium –> APC mutation
2) relatively normal –> Ras mutation
3) proliferating adenoma –> p53 mutation
4) carcinoma and metastasis

50
Q

What are the three common mutations that push towards the development of colon cancer

A

1) APC mutation
2) Ras mutation
3) p53 mutation

Physiology Exam 4 (8 decks)

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