Brainscape's Knowledge GenomeTM

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


See full index

Block 2: Fundamentals of Medicine > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

microtubules

A

tubulin dimers of alpha and beta tubulin –> 13 protofilaments

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

tubulin is a

A

GTPase

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

+/- end of microtubules

A

+ end: high exchange rate of alpha and beta tubulin - end: static end

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

functions of Microtubules

A

mitotic spindle, organelle transport, cell shape

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

dynamic instability in microtubules

A

catastrophe = shrink, rescue = grow

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

microtubule associated motor proteins

A
  1. dyenin (- end directed) 2. kinesin (+ end directed)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

centrosome

A

MT ognizing center/site of nucleation (genesis of cytoskeletal polymer) - uses gamma tubulin

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

basal body

A

MT organizing center for cilia and flagella

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

axonemone

A

9+2 microtubule structure of cilia and flagella *dyenin drives axenemal activity

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

immotile cilia syndrome

A

defect in anexome structure –> obtrusive lung disease, male sterility

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

kartagene’s syndrome

A

situs inversus and immotile cilia cyndrome

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

lissencephaly

A

mutations in microtubule proteins HS1 and doublecortin

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

Charcot-Marie-Tooth

A

kinesin mutation

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

microfilaments

A

nonhollow polymers of actin with ATPase activity

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

ends of microfilaments are called

A

barbed end (+) and pointed end (-) **myosin moves towards the + end

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

hereditary spherocytosis

A

RBC forms spherocyte because weak binding of spectrin to band 4

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

epidermis bullose simplex

A

intermediate filament disorder - keratin mutation in basal skin cell layer, results in very sensitive skin that easily is torn

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

progeria (hutchinson gilford syndrome)

A

intermediate filament disorder - “fast again” mutation in nuclear lamin protein autosomal dominant

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

Most cells in our bodies are in what phase?

A

G0

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

CDKs control cell cycle progression by activating

A

cyclins

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

p54

A

induces cell cycle arrest by inhibiting CDKs - can also trigger apoptosis

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

terminally differentiated cells

A

have permanently exited the cell cycle (so differentiated that they can’t re-enter)

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

totipotent

A

cells from the fertilized egg/morula; can become any cell type

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

pluripotent

A

cells from the blastula –> can be ecotoderm, mesoderm, and endoderm

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

multipotent

A

ex. progenitor hematopoetic cells

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

unipotent

A

cells that give rise to a particular cell type

27
Q

VEGF

A

for endothelial cell proliferation

28
Q

stem cell renewal

A

required to replace differentiated cells

29
Q

forms of senesence:

A
  1. stress induced senescence 2. telomere shortening-induced senescence (replicative) 3. oncogene-induced senescence
30
Q

telomere shortening induces

A

p53 and pRb pathway leading to growth arrest and senescence –> facilitate tumor progression

31
Q

werner syndrom

A

rare autosomal recessive premature aging single gene WRN (DNA helicase RecQ protein)

32
Q

paracrine signaling

A

acts locally

33
Q

autocrine signaling

A

cell makes a peptide and is activated by it (inflammation)

34
Q

scaffold proteins

A

bring specific proteins together in proximity. they are non-catalytic proteins

35
Q

tyrosine kinases

A

associated with activated growth factor receptors; are rapid and transient

36
Q

ser/thr kinases

A

longer lasting phosphorylation

37
Q

phosphorylation is currency of growth factor signaling because it…

A

is rapid, reversible, and linked to signaling cascade

38
Q

second messengers

A

soluble, low MW regulators of signaling proteins; rapid signal amplification

39
Q

steps of signal transduction

A
  1. receptor-ligand binding 2. G protein activation 3. MAPK cascade 4. TF actvation
40
Q

3 main families of cell surface receptors

A
  1. ion channel 2. G protein linked 3. enzyme linked
41
Q

GEF (guanine nucleotide exchange factor)

A

facilitates dissoication of GDP from G protein (alpha subunit)

42
Q

GAP (GTpase activating protein)

A

stimulates GTP hydrolysis for inactive form of GDP bound to G protein

43
Q

adenylyl cyclase

A

large transmembrane protein regulated by G proteins and Ca2+; coupled to Gs; stimulates cAMP which modifies gene expression

44
Q

receptor desensitization

A

GRKs (G protein linked receptor kinases) phosphorylate a receptor; arrestin binds and desensitizes via: 1. inactivates receotir through uncoupling 2. acts as adaptor protein to couple receptor to clathrin coated pits for sequestration/degradation of receptor

45
Q

cholera

A

toxin gives ADP ribose to alpha subunit of Gs so it can’t hydrolyze GTP –> acitve state –> Cl and water efflux into gut –> diarrhea

46
Q

steps in enzyme linked receptors

A
  1. receptor dimerization 2. autophosphorylation 3. phosphorylation if cytoplasmic signaling proteins
47
Q

Ras

A

monomeric GTPase - mutations in it cause cancer

48
Q

MAPK

A

ser/thr kinases; usually at end of cascade

49
Q

PKC steps

A
  1. ligand receptor binding via G protein 2. PLC cleaves PIP2 to IP3 and DAG 3. IP3 binds to receptors on the ER and Ca2+ released into cytoplasm 4. DAG is precursor in arachidonic acid generation, and in direct binding/activation of PKC
50
Q

NFKB

A

latent gene regulatory proteins that regulate inflammatory repsonses

  • heterodimer of 2 related protiens
  • inactive when bound to I-KB
51
Q

I-KB

A

Binds/sequesters NFKB. When stimulated, releases NF-KB so that it can translocate to the nucleus to stimulate transcription of certain genes

52
Q

functions of apoptosis

A
  1. sculpting/morphogenesis
  2. deleting unecessary structures
  3. control cell numbers
  4. eliminate bad cells
53
Q

caspase

A

cysteine protease

54
Q

initiator caspase

A

begins the apoptotic process (caspase 8 or 9)

55
Q

effector caspase

A

activated by upstream caspase (3, 6 or 7)

56
Q

cytochrome c

A
  • in intrinsic apoptototic pathway
  • released from mitochondria into cytosol
  • causes Apaf 1 to oligomerize into apoptosome
  • apaf recruits caspase 9
57
Q

CAD (caspase dependent deoxyribonucleosomes)

A

inactivated by ICAD (inhibitor); caspase 3 inactivates ICAD so that CAD can cut up the chromosomal DNA between nucleosomes

58
Q

FLIP

A

dimerizes with caspase 8 in the DISC (death inducing signaling complex) preventing apoptosis

59
Q

Bcl-2

A

regulates intrinsic pathway of apotosis by controlling cytochrome c relase; involved in both pro and anti apoptosis

60
Q

guardians

A

prosurvival - bind and inhibit effectors

61
Q

sensors

A

proapoptosis - inhibit guardians; can’t kill without effectors; response to environmental cues

62
Q

effectors

A

proapoptosis; perturb mito intracellular membranes. need to be primed/activated

63
Q

bax and bak

A

respond to cytotoxic signals; confirmational change causes membrane to release apoptotic mediators

64
Q
A

Block 2: Fundamentals of Medicine (11 decks)

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