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Block 2: Fundamentals of Medicine > Exam 2 > Flashcards

Exam 2 Flashcards

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1
Q

microtubules

A

tubulin dimers of alpha and beta tubulin –> 13 protofilaments

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2
Q

tubulin is a

A

GTPase

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3
Q

+/- end of microtubules

A

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

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4
Q

functions of Microtubules

A

mitotic spindle, organelle transport, cell shape

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5
Q

dynamic instability in microtubules

A

catastrophe = shrink, rescue = grow

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6
Q

microtubule associated motor proteins

A
  1. dyenin (- end directed) 2. kinesin (+ end directed)
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7
Q

centrosome

A

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

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8
Q

basal body

A

MT organizing center for cilia and flagella

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9
Q

axonemone

A

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

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10
Q

immotile cilia syndrome

A

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

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11
Q

kartagene’s syndrome

A

situs inversus and immotile cilia cyndrome

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12
Q

lissencephaly

A

mutations in microtubule proteins HS1 and doublecortin

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13
Q

Charcot-Marie-Tooth

A

kinesin mutation

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14
Q

microfilaments

A

nonhollow polymers of actin with ATPase activity

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15
Q

ends of microfilaments are called

A

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

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16
Q

hereditary spherocytosis

A

RBC forms spherocyte because weak binding of spectrin to band 4

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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

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18
Q

progeria (hutchinson gilford syndrome)

A

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

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19
Q

Most cells in our bodies are in what phase?

A

G0

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20
Q

CDKs control cell cycle progression by activating

A

cyclins

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21
Q

p54

A

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

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22
Q

terminally differentiated cells

A

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

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23
Q

totipotent

A

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

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24
Q

pluripotent

A

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

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25
multipotent
ex. progenitor hematopoetic cells
26
unipotent
cells that give rise to a particular cell type
27
VEGF
for endothelial cell proliferation
28
stem cell renewal
required to replace differentiated cells
29
forms of senesence:
1. stress induced senescence 2. telomere shortening-induced senescence (replicative) 3. oncogene-induced senescence
30
telomere shortening induces
p53 and pRb pathway leading to growth arrest and senescence --\> facilitate tumor progression
31
werner syndrom
rare autosomal recessive premature aging single gene WRN (DNA helicase RecQ protein)
32
paracrine signaling
acts locally
33
autocrine signaling
cell makes a peptide and is activated by it (inflammation)
34
scaffold proteins
bring specific proteins together in proximity. they are non-catalytic proteins
35
tyrosine kinases
associated with activated growth factor receptors; are rapid and transient
36
ser/thr kinases
longer lasting phosphorylation
37
phosphorylation is currency of growth factor signaling because it...
is rapid, reversible, and linked to signaling cascade
38
second messengers
soluble, low MW regulators of signaling proteins; rapid signal amplification
39
steps of signal transduction
1. receptor-ligand binding 2. G protein activation 3. MAPK cascade 4. TF actvation
40
3 main families of cell surface receptors
1. ion channel 2. G protein linked 3. enzyme linked
41
GEF (guanine nucleotide exchange factor)
facilitates dissoication of GDP from G protein (alpha subunit)
42
GAP (GTpase activating protein)
stimulates GTP hydrolysis for inactive form of GDP bound to G protein
43
adenylyl cyclase
large transmembrane protein regulated by G proteins and Ca2+; coupled to Gs; stimulates cAMP which modifies gene expression
44
receptor desensitization
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
cholera
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
steps in enzyme linked receptors
1. receptor dimerization 2. autophosphorylation 3. phosphorylation if cytoplasmic signaling proteins
47
Ras
monomeric GTPase - mutations in it cause cancer
48
MAPK
ser/thr kinases; usually at end of cascade
49
PKC steps
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
NFKB
latent gene regulatory proteins that regulate inflammatory repsonses * heterodimer of 2 related protiens * inactive when bound to I-KB
51
I-KB
Binds/sequesters NFKB. When stimulated, releases NF-KB so that it can translocate to the nucleus to stimulate transcription of certain genes
52
functions of apoptosis
1. sculpting/morphogenesis 2. deleting unecessary structures 3. control cell numbers 4. eliminate bad cells
53
caspase
cysteine protease
54
initiator caspase
begins the apoptotic process (caspase 8 or 9)
55
effector caspase
activated by upstream caspase (3, 6 or 7)
56
cytochrome c
* in intrinsic apoptototic pathway * released from mitochondria into cytosol * causes Apaf 1 to oligomerize into apoptosome * apaf recruits caspase 9
57
CAD (caspase dependent deoxyribonucleosomes)
inactivated by ICAD (inhibitor); caspase 3 inactivates ICAD so that CAD can cut up the chromosomal DNA between nucleosomes
58
FLIP
dimerizes with caspase 8 in the DISC (death inducing signaling complex) preventing apoptosis
59
Bcl-2
regulates intrinsic pathway of apotosis by controlling cytochrome c relase; involved in both pro and anti apoptosis
60
guardians
prosurvival - bind and inhibit effectors
61
sensors
proapoptosis - inhibit guardians; can't kill without effectors; response to environmental cues
62
effectors
proapoptosis; perturb mito intracellular membranes. need to be primed/activated
63
bax and bak
respond to cytotoxic signals; confirmational change causes membrane to release apoptotic mediators
64

Block 2: Fundamentals of Medicine (11 decks)

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