cell and molecular biology exam 4

0.0(0)
learnLearn
examPractice Test
spaced repetitionSpaced Repetition
heart puzzleMatch
flashcardsFlashcards
Card Sorting

1/72

encourage image

There's no tags or description

Looks like no tags are added yet.

Study Analytics
Name
Mastery
Learn
Test
Matching
Spaced

No study sessions yet.

73 Terms

1
New cards

definition of signal transduction

one type of signal is converted into another one

2
New cards

categories of signal transduction

paracine

endocrine

neuronal

autocrine

3
New cards

paracine

goes a short distance and effects multiple cells in vicinity

  • ex. pacemaker cell

4
New cards

endocrine

travels over larger distances, travels in bloodstream to target cell

  • ex. hormones

5
New cards

neuronal

hybrid type

stimulates neuron that causes release of neurotransmitter over a short space called the synapse

6
New cards

autocrine

cell “self-targets” signal, will go back to cell it was released from

7
New cards

extracellular cells act rapidly when

altering an existing protein

ex. contracting muscles

8
New cards

extracellular signals act slowly when

you have to make a new protein (proteins synthesis)

  • size and type of protein can dictate how long it takes

ex. building muscle

9
New cards

cell surface receptors use

cell surface receptor proteins that sends message to intracellular signaling molecule

10
New cards

cell surface receptor signals can’t

cross the membrane

11
New cards

intracellular receptors receive

small hydrophobic signal molecules that are able to cross the membrane to the intracellular receptor (ex. hormones)

12
New cards

major types of cell surface receptors

ion channel-coupled receptors

G-protein coupled receptors (GPCR)

enzyme-coupled receptors

13
New cards

ion channel-coupled receptors

signal molecule attaches to channel to open channel and let selected ions through

once ions pass into cytosol, they can become 2nd messengers

14
New cards

G-protein coupled receptors (GPCR)

once receptor receives signal, it recruits and activates G protein

G protein recruits and activates the enzyme (which can be a 2nd messenger)

15
New cards

enzyme-coupled receptors

signal molecules bind to 2 receptors at the same time that have enzyme activity (enzyme built in)

16
New cards

2nd messengers help

amplify and spread the intracellular signal

17
New cards

common 2nd messengers

cyclic AMP (most common)

cyclic GMP

inositol triphosphate

Diacylglycerol (DAG)

calcium

18
New cards

two common 2nd messenger systems

phosphorylation & G-protein

19
New cards

protein phosphorylation

kinase cascade

scaffold helps bring kinases closer together so they can phosphorylate

20
New cards

protein kinase means

on

21
New cards

protein phosphatase means

off (removes phosphate)

22
New cards

with G-protein, GTP binding means

on

23
New cards

with G-protein, GDP hydrolysis means

off (breakdown of GTP to GDP)

24
New cards

stages of cell cycle

  1. G1 phase

  2. S phase

  3. G2 phase

  4. M phase

25
New cards

G1 and G2 phase

growth

26
New cards

S phase

synthesis/duplicate DNA

27
New cards

M phase

mitosis/cell divides

28
New cards

interphase is considered

G1, S, and G2 phase

29
New cards

CDKs

cyclin dependent kinases

30
New cards

CDK only work when

kinases are bonded to cyclin protein

31
New cards

in order to get through a CDK

you must have the right amount of cyclin to turn on kinase

32
New cards

degrading cyclin

turns off

33
New cards

S-CDK (S cyclin)

between G1 and S

34
New cards

M CDK (M cyclin)

between G2 and M

35
New cards

G1/S checkpoint

checks to make sure no DNA is damaged

36
New cards

G2/M checkpoint

checks to make sure complete replication of DNA has occurred and no new mutations

37
New cards

cancer has occurred in

man and other animals throughout recorded history

38
New cards

“karkinos” (Hippocrates) means

crabs

39
New cards

cancer can arise because of

genomic instability (damage to DNA)

40
New cards

examples of genomic instability

radiation

chemicals

loss of repair mechanisms

some viruses

41
New cards

to create a cancer cell you need

a series of mutations

42
New cards

alterations in multiple pathways are needed to

transform a normal cell to cancer cell

43
New cards

what alterations are needed to transform a normal cell to cancer cell

cell proliferation

DNA damage response

cell growth

44
New cards

cancer cells have mutations that turn on BLANK and BLANK signaling pathways all of the time

survival and growth

45
New cards

cancer cells disable BLANK, which causes the cell to grow out of control

death signaling pathways (apoptosis)

46
New cards

proto-oncogene is the

normal form of the gene

47
New cards

oncogene is the

mutation form, which is a dominant mutation that causes excessive cell survival, proliferation, or both

48
New cards

Ras gene (proto-oncogene)

mutation in this gene causes the Ras protein to always be active, promoting cell proliferation

49
New cards

tumor repressor gene is the

normal gene

50
New cards

for mutations in tumor suppressor genes

both copies must be mutated (recessive)

51
New cards

Retinoblastoma (Rb) controls the activity of

E2F transcription factors

52
New cards

E2F factors are needed for

S-phase genes

53
New cards

active G1 CDKs phosphorylate Rb which will

inactive it while it attaches to the E2F protein, causing it to release the E2F protein, allowing S-phase to progress

54
New cards

BLANK or BLANK can inactive Rb

mutations or viral proteins (ex. human papillomavirus)

55
New cards

Rb mutation can lead to

eye tumors in young children

56
New cards

inactivation of both copies of p53 allows

cancer cells to continue to survive and divide, even in the presence of damaged DNA

57
New cards

apoptosis =

programmed cell death

58
New cards

cell have apoptosis to

make sure cells with abnormal DNA, cell cycle division, or other messed up critical pathways are killed to protect the organism

59
New cards

genome alteration in proto-oncogene

mutation in coding sequence

gene amplification

chromosome rearrangement

60
New cards

mutation in coding sequence of proto-ocnogene normal result

hyperactive protein made in normal amounts

61
New cards

gene amplification in proto-ocnogene normal result

normal protein overproduced

62
New cards

Chromosome rearrangement in proto-oncogene normal result

nearby regulatory DNA sequence causes normal protein to be overproduced

63
New cards

Chromosome rearrangement in proto-oncogene abnormal result

fusion to actively transcribe gene produces hyperactive fusion protein

64
New cards

tyrosine kinase receptor is a type of

hyperactive receptor fusion that can lead to cancer

65
New cards

BLANK, BLANK, BLANK can lead to cancer hyperactive receptor that is ON ALL THE TIME

point mutation

fusion of receptor intracellular domain with 2nd messenger

overproduction of receptor

66
New cards

PDGF acts through

receptor tyrosine kinase (IDK)

67
New cards

TEL-PDGFR-beta is an example of

oncogene-fusion

68
New cards

the helix-lopp-helix domain of TEL transcription factor fused to BLANK causing dimerized receptor

PDGF receptor beta

69
New cards

the TEL-PDGFR-beta causes

chronic Myelomonocytic Leukemia (CMML) (white blood cell cancer)

70
New cards

first parentheses in translocation gives

chromosomes involved

71
New cards

second parentheses gives

precise location

72
New cards

q =

long arm

73
New cards

p =

short arm