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M2M - Niswander > Unit III Week 3 > Flashcards

Unit III Week 3 Flashcards

1
Q

Microtubule structure and function

A

tubular, 25 nm diameter
tubulin (a and ß)
movement (cilia/flag and organelles), scaffold
cell division

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2
Q

Microtubule accessory proteins and nucleotide

A

motor proteins: kinesin and dynein

GTP for growth

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3
Q

Microfilament (actin filament) structure and function

A

helical filament 5-9 nm diameter
actin
cell movement, contraction

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4
Q

Intermediate filament structure and function

A

staggered tetramer of c-c dimers, 10 nm diameter
keratin, vimentin, neurofilaments, nuclear lamins
mechanical stability

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5
Q

Intermediate filament accessory proteins

A

crosslinking, membrane anchor

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6
Q

Microtubule dynamics/regulation

A

GTP cap, GDP in base
Severing proteins: katanin, spastin, fidgetin, VPS4
All ATPases (NSF like) which pull on C’ end sticking out
Disease: hereditary spastic paraplesia

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7
Q

Microfilament (actin filament) formation

A
  1. G-actin concentration (profilin)
  2. ADP to ATP exchange (profilin)
  3. Capping (gelsolin)
  4. Depolymerization/severing (ADF/cofilin)
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8
Q

Microfilament (actin filament) nucleation

A
  1. FH2 nucleation mimic actin and bind two more (bundle)
  2. Arp2/3 complex with WASP and binds one more (branch)
    Both paths activates by GTPase (Ras, Rho, Rac etc)
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9
Q

Actin filaments _____ at + end and ______ at - end

A

grow

shrink

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10
Q

Examples of asymetric cell division

A

erythroblast (eject nucleus)
platelets (polypliod megakaryocyte)
spermatogonia (long chain of almost pinched)
epithelial cells (apical side larger)

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11
Q

Regulation of actomyosin ring

A

Rho activated by high conc. microtubules (only middle)
RhoGDP - RhoGTP cycle (phos by Ect2)
RhoGTP activates ROCK
ROCK activates myosin

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12
Q

Types of communication between cells

A

Paracrine/autocrine
Endocrine
Contact dependent
Synaptic

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13
Q

Types of signaling molecules

A

Lipophilic: steroids, no vesicles, slow
Hydrophilic: peptide, vesicles, fast

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14
Q

Types of signal termination

A

Constitutively active terminators (PDEs)
Signal induced terminators (GAP enhanced GTPase)
Negative feedback mechanism terminators (Ca2+ pumps)

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15
Q

PDE5

A

Converts cGMP to GMP
two binding site (cooperative binding)
Targeted by drug Sildenafil (continued Ca2+ release, smooth muscle relaxation)

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16
Q

Neworks and pathways: nodes

A

multiple inputs and/or outputs

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17
Q

Tyrosine kinase activation

A

Ligand binding drives dimerization (homo or hetero)

Results in cross phosphorylation and activation

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18
Q

RasGTP regulation

A

RasGTP = active
GAP - activates hydrolysis ->RasGDP
GEF - exchanges GDP -> RasGTP

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19
Q

Ras activation example

A

Receptor dimer binds Grb2 (adaptor protein)
Sos binds Grb2 (GEF) (critical step, need Sos near PM)
PROXIMITY
Grb2 (GEF) results in RasGTP activation

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20
Q

Two classes of blocking tyrosine kinase

A

Antibodies - block ligand biding to receptor

Tyrosine kinase inhibitors - bind substrate site on kinase

21
Q

EGFR role in some cancers

A

Overexpressed
Increased EGFR = poorer clinical outcome
Stimulates more ligand (autocrine signaling)

22
Q

Response to EGFR targeted therapy

A

Depends on amount of EGFR expression in cancer

Determine by FISH/IHC

23
Q

Resistance to tyrosine kinase inhibition

A

Primary resistance: mutation is further down pathway

Secondary resistance: new mutation in receptor blocks inhibitor, or activation of other receptors with same effect

24
Q

ß1-AR pathway

A

Sympathetic, NE binds
Gs(a) activates AC, ATP->cAMP, PKA, Ca2+ channels
Cardiac muscle contraction

25
Q

a1-AR pathway

A

Sympathetic, NE binds
Gq(a) activates PLC, PIP2->IP3 and DAG
DAG, PKC, L-Ch (and IP3) Ca2+ release
Peripheral vasoconstriction (increase return, BP)

26
Q

propanolol, metoprolol

A

beta-blockers

decrease heart rate and blood pressure

27
Q

prazosin

A

alpha-blocker

decrease blood pressure

28
Q

m2-MR pathway

A

Parasympathetic, acetylcholine
Gi(a) activates and inactivates AC (from Gs(a)/ß1-AR)
Still need PDE to convert existing cAMP to AMP
ßy binds GIRK and opens K+ (decreases excitability in heart)

29
Q

ß2-AR pathway

A

Sympathetic, NE binds
Gs(a) activates AC, ATP->cAMP, PKA, Ca2+ channels
Smooth muscle relaxation - bronchodilation

30
Q

m3-MR pathway

A

Sympathetic, NE binds
Gq(a) activates PLC, PIP2->IP3 and DAG
DAG, PKC, L-Ch (and IP3) Ca2+ release
Bronchoconstriction

31
Q

ipratropium inhalation (m3-MR antagonist)

A

inhibit bronchoconstriction

32
Q

albuterol (ß2-AR agonist)

A

support bronchodilation

33
Q

GRK kinase

A

binds ßy (independent of a) and phosphorylates receptor
ß-arrestin binds phos-GPCR
Desensitization and re-integration or degradation

34
Q

Humans have _____ kinases and _____ phosphatases

A

518, 130

35
Q

Structure of ATP

A

Purine base
Ribose sugar
Phosphates with PAH bonds (phosphate donor)
Can be converted to 2nd messenger

36
Q

Conserved structure of kinases

A 
beta sheet group
alpha helix group
helix C
activation loop (phosphorylated when in correct position, not all kinases have this)
action happens between groups
37
Q

Open/close movement of kinases

A

Both needed for activity

Different position of glycine loop

38
Q

Differences in kinases for drug development

A

More differences in inactive state (2 of 4)

  1. activation loop
  2. c helix
  3. glycine rich loop
  4. ATP binding pocket
39
Q

MAP kinase pathway

A

Input, MAPKKK, MAPKK, MAPK, ouput

(eg glycerol synthesis or IL-2)

40
Q

IL-2 pathway (MAP kinase contribution)

A

T-cell receptor, RasGTP pathway, Raf-1 (MAPKKK), MEK (MAPKK), erk (MAPK), NFATn
Still need NFATc

41
Q

IL-2 pathway (Calcineurin contribution)

A

T-cell receptor, PIP2 to DAG (PKC), IP3, increase Ca2+
Inhibit calcineurin, stop phosphorylating NFATc
NFATc enter and binds with NFATn
IL-2

42
Q

IL-2 T-cell proliferation pathway

A

IL-2 binds T-cell, mTOR/Cdk2 = proliferation

43
Q

Excitatory CNS synapse

A

AMPA-R (glutamate receptor) opens, Na+ in
Opens NMDA-R, eject Mg2+, Ca2+ in
Stimulates AMPA-R proliferation
POTENTIATION (positive feedback)

44
Q

Sources of androgen in body

A

Testis
Adrenal glands
Intracrine (in prostate cells)

45
Q

Androgen receptor structure

A

N’ transactivation domain
DNA binding domain
Hinge region
C’ ligand binding

46
Q

Androgen receptor function

A

in cytoplasm
binds ligands and disassociates chaperones
enters nucleus, homodimerizes, binds DNA
recruits coactivators and gene expresson

47
Q

Mechanisms of resistance to traditional prostate cancer therapies

A

AR activation via non-testis androgen
Overexpression of AR
AR mutation (gain of function)
Truncated AR with constitutively active LBD

48
Q

Abiraterone

A

inhibits CYP 17 (androgen formation)
Side effects: hypokalemia, edema, hypertension
due to excess mineralcoracoids

49
Q

Enzalutamide

A

antiandrogen

inhibits binding of T to AR (inhibits downstream)

M2M - Niswander (4 decks)

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