Brainscape's Knowledge GenomeTM

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


See full index

Pathology > 6.11 Transforming cells > Flashcards

6.11 Transforming cells Flashcards

1
Q

acute vs weak transforming viruses

A

acute transforming viruses transform cells quickly at low dose

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

transforming viruses are

A

retroviruses

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

why do acute transforming viruses transform cells better?

A

they have src region in thir DNA like in ATV –first proposed oncogene

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

src

A

rous sarcoma virus - rats

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

ras

A

harvey sarcoma virus

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

myc

A

maloney sarcoma virus - mice

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

sis

A

simian sarcoma virus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

fes

A

feline sarcoma virus

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

viral oncogenes were found in malignant and normal cells bc

A

transforming retroviruses evolved by picking up mammalian genes and incorporating them into their genome – picking up a gene that makes the cell immortal makes the virus immortal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

human dna fed to mice cells use Ca salt showed

A

loss of contact in hibition and tumor growth, with greater efficiency each time experiment was repeated with tumor DNA

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

conclusion of contact inhibition mouse cell experiment

A

the v-ras gene caused the tumor but there was no virus! This means that the gene was simply a mutated mammalian gene, differing on the 12th AA from glycine to valine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

ras is a

A

signal transduction protein - it is a GTP dependent protein, active when bound to GTP, has intrinsic GTPase activity, inactive when bound to GDP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

ras is involved in

A

many function including cell replication

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Ras is held to the membrane by

A

a farnesy membrane anchor and is linked to a growth factor receptor by a bridging protein

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

activated ras binds

A

Raf-1, GAP, and activates the Map kinase path, that activates transcription, that activates the myc gene, leading to cell cycle progression

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

the G to V mutation in v-ras causes

A

reduces the GTPase activity so ras is locked in the “on” position –>abnormally active signalling for growth

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

why was ras the first oncogene discovered by random transfecting of DNA?

A

Ras is the most common activated oncogene encountered in human tumors. Not the most common gene affected, that’s p53

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

what is a good drug target against v-rase

A

the farnesyl membrane anchor – farnesyl transferase inhibitors might take away the capacity for ras to bind the membrane so it won’t be able to effectively transduce the signal

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

NF-1 tumor suppressor gene

A

GAP protein that binds to ras before map kinase path activation

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

Molecular basis of cancer

A

oncogenes, tumor suppressor genes, apoptosis genes, DNA repair genes

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

Oncogenes

A

growth factors, growth factor receptors, signal transduction proteins, nuclear regulatory proteins, cell cycle regulators

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

Growth factors

A

sis, hst-1, int-2

23
Q

GF sis

A

PDGF overexpression

24
Q

GF hst-1

A

FGF overexpression

25
Q

GF int-2

A

FGF amplification

26
Q

Growth factor receptors

A

erb-B1-3, fms

27
Q

GF-rec erb-B1-3

A

EGF Truncation

28
Q

GF-rec fms

A

CSF-1 point mutation

29
Q

Signal transduction protein

A

ras, abl

30
Q

ST ras

A

GTP-protein point mutation

31
Q

ST abl

A

tyrosine kinase translocation

32
Q

nuclear regulatory protein

A

myc, L-myc, N-myc, fos, jun

33
Q

NucReg myc and APC casset

A

transcription, changed by translocation/amplification

34
Q

cell cycle regulation

A

Cyclin D, CDK4

35
Q

CellCycle Cyclin D

A

Cyclin, translocation/amplification

36
Q

CellCycle CDK4

A

CD kinase, amplification/point muation

37
Q

how CDK and Cyclins work together

A

CDK is always present, cyclin is synthesized to activate CDK

38
Q

major cyclins in G1-S

A

D and E

39
Q

major CDK in G1 to S

A

2, 4, 6

40
Q

inhibitors of CDK 4 and 6

A

p21, 27, 57, 26-19

41
Q

action of activated CDK 2, 4, 6

A

phosphorylates Rb which releases E2F family of transcription factors, allowing cell to proceed from G1 to S

42
Q

Cyclin D binds

A

CDK 4/6 for G1 to S passage

43
Q

Cyclin E binds

A

CDK 2 for G1 to S passage

44
Q

Cyclin A binds

A

CDK 2/1 for S to G2 passage

45
Q

Cyclin B finds

A

CDK 1 for passage from G2 to M

46
Q

CDK4 inhibitors

A

p 15, 16, 18, 19

47
Q

CDK 6,2,1 inhibitors

A

p 21, 27, 57

48
Q

CIP/KIP family CDK inhibitors

A

p27, p16

49
Q

p21 is induced by

A

p53

50
Q

p27 is induced by

A

TGFbeta and other suppressors

51
Q

INK4/ARF family CDP inhibitors

A

p16, p14

52
Q

p16 inhibits by

A

binding cylinD-CDK4 promoting Rb inhibition

53
Q

p14 inhibits by

A

increasing p53 by inhibiting MDM2

54
Q

p53

A

tumor suppressor, causes cell cycle arrest and apoptosis by inducing p21 and BAX; inhibited by MDM2

Pathology (26 decks)

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