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M2M - Niswander > Unit III Week 2 > Flashcards

Unit III Week 2 Flashcards

1
Q

Structure of Na/K voltage channels

A 
4 transmembrane domains with 6 a-helices each
S4 has (+) lys/arg every 3 positions (sensor)
S5-S6 (P-loop) from passage
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2
Q

Structure of pentamer ligand gated channels (Cys-loop family)

A

Heteropentamers (2x a, 2x ß, y)
4 transmembrane a-helices (M1-M4)
M2 = passage
Cl- or cations Na+ (preference) and K+

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3
Q

Structure of ionotropic glutamate receptors

A

Tetrameric ligand gated

Ex. NMDA (2 units bind glutamate, 2 bind glycine)

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4
Q

Structure of chloride channels

A

CLC family - dimers (H+/Cl- exchangers same family)

Each subunit has own pathway (either/both can be stim)

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5
Q

Structure of aquaporin channels

A

Tetramers
Each subunit has own pathway (NO IONS)
Central pore will allow ions

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6
Q

Factors for channel selectivity

A

Charge
Size
Dehydration
Multiple binding sites

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7
Q

Gates and actions of Na+ and K+ voltage channels

A

K+: activation/deactivation, hinge movement of S6

Na+: activation/inactivation, two gates, cytoplasmic loop between III and IV = inactivation gate

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8
Q

Glucose and amino acid uptake

A

2nd active transport into cells from lumen

Otherwise - facilitated diffusion (glucose is phos in cell)

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9
Q

Transepithelial potential equation

A

TP = Basolateral - apical

with respect to inside of cell

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10
Q

Water, O2, CO2, urea movement across membranes

A

Always passive diffusion

Facilitated diffusion as well (open/close channels)

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11
Q

Excretion of non-volatile metabolic waste

A

GI does very little (absorbs all it can)
Kidney does most (concentrates beforehand)
Urea/protons, regulates ECF, requires ATP

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12
Q

Axons as conductors

A 
Cytoplasm = high resistance
Membrane = poor insulation
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13
Q

Refractory period

A

Absolute (no fire) vs. relative (hard to fire)
K+ hyperpolarization
unidirectionality

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14
Q

Accommodation of action potential

A

Slow depolarization, inactivation gates close first

Happens during hyperkalemia (cell can’t respond to physiological stimulus)

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15
Q

Myelination and conduction

A

Thick membranes = lower capacitance
Fewer channels = higher membrane resistance
Larger diameter axon = lower internal resistance

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16
Q

Calcium effect on action potentail

A

Ca2+ normally bound to (-) on outside of cell
Less Ca2+ means less membrane potential difference
Easier to depolarize (activation gates open easier)

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17
Q

CBIGK

A

C: give Ca2+ (bind - charge, increase potential difference)
B: HCO3 (eat H+, H/K exchanger, take K+ into cells)
I: Insulin
G: Glucose (Insulin/glucose mean ATP for Na/K pump)
K: Kaexalate (big anion that eats K+ in lumen and pulls out of body)

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18
Q

Consequences of demyelination (MS)

A

Neuronal damage
Slower conduction of action potentials
Proliferation of Na+ channels (lower membrane resistance)

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19
Q

Multiple Sclerosis treatments

A

No treatment
Some drugs improve nerve function:
Na+ channel blockers: phenytoin, flecainide
K+ channel blockers

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20
Q

Three mechanisms of protein transport

A 
Gated transport (cyto->nuc)
Transmembrane transport (cyto->organelle)
Vesicular transport (compartment to compartment)
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21
Q

Major functions of the ER

A 
Lipid synthesis (SER)
Cholesterol homeostasis
Ca2+ storage
Protein synthesis (RER)
Co-translational folding/early posttranslational modifications
Quality control
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22
Q

Signal recognition particle (SRP)

A

Six proteins and one RNA
Binds mRNA, ribosome, and translocon
Leaves once ribosome binds translocon

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23
Q

Co-translational translocation (soluble protein, no transmembrane domain)

A

SRP binds/translocates mRNA through translocon
Soluble portion enters ER and folds (help from BiP)
Hydrophobic portion moves laterally and degraded

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24
Q

Co-translational translocation (transmembrane domain)

A

SRP binds/translocates mRNA through translocon
“STOP” sequence on mRNA
Remainder of protein synthesized on outside
Type I = C’ in cyto, Type II = N’ in cyto (+)

25
Q

Co-translational translocation (multiple transmembrane domains)

A

SRP binds/translocates mRNA through translocon
Many start/stop sequences
Simple N linked glycosylation occurs in ER lumen

26
Q

Major functions of the Golgi complex

A

Sphingolipid synthesis
Additional post-translational modification
Finishing/complex N linked glycosylation
Proteolytic processing
Sorting of proteins/lipids via membrane thickness

27
Q

Three vesicle coats and transport

A

COPII - ER to Golgi (forward)
COPI - ER to Golgi (backward)
Clathrin - Golgi to PM (endocytosis)

28
Q

Clinical features of Cholera

A

Non-inflammatory diarrhea
Severe, acute, watery, no blood (rice water stool)
Dehydration
or asymptomatic

29
Q

Leading cause of death with Cholera

A

Dehydration

30
Q

What bacterial molecules contribute to Cholera and mechanism

A

CT, AB5 toxin produced by bacteriophage
Ganglioside GM1 on ß-subunit attaches, A transmits
Irreversibly binds CFTR (cAMP path) until death of cell

31
Q

How to distinguish between Cholera strains

A

O-specific polysaccharide of the lipopolysaccharide

32
Q

Molecules that protect against Cholera

A

water, gastric acid (H. pylori), O blood, antibodies, CFTR mutation (heterozygote advantage), oral rehydration solution

33
Q

Vaccines against Cholera

A

Dukoral - kill v. cholerae 01 x2 and CTxB
Shanchol - kill v. cholerae 01 and 0139
antibodies to OPS of LPS

34
Q

Two major routes for small volume endocytosis

A

Phagocytosis (macrophages and neutrophils)

Pinocytosis (clathrin and caveolae)

35
Q

Clathrin mechanism

A

Transmembrane receptor binds adaptor proteins
Adaptor proteins bind clathrin
Buds off/ dynamin pinches
Rapid disassociation
Receptor recycling and (ex) LDL breakdown

36
Q

Caveolae

A

Small vesicles that from without coat proteins
Important with lipid rafts
Animal viruses and cholera toxin use caveolae

37
Q

Proteasome breakdown

A

Cap bind Ub and unfolds protein
Cylinder does actual protein breakdown (a and ß)
a - regulates entry into chamber
ß - cleaves

38
Q

Ubiquitin mechanism

A

E1: binds and activates (Activation)
E2: transfers to E3 complex or forms complex with E3 (Conjugation)
E3: attaches string of Ub >4 (Ligation)

39
Q

Lysosome

A

Breakdown, pH=5
Proton pumps need to be protected
Lysosomal storage diseases:
Tay Sachs, Gaucher’s, Niemann-Pick

40
Q

Apoptosis - nuclear events

A 
superocondensing of heterochromatin/euchromatin
DNA cleaved into nucleosomes (core histone + ~180bp)
Many DSB (beyond repair, if apoptosis fails will not divide)
41
Q

Apoptosis - cytoplasmic events

A

shrinkage

lose 1/3 volume in seconds

42
Q

Apoptosis - plasma membrane events

A

membrane boiling
phospholipid phosphatidylserine evenly distributed by scramblase (usually confined to inner by flippase)
Phagocytes have receptors for PE so as to not activate macrophages (and inflammatory response)

43
Q

Apoptosis vs. necrosis

A

Apoptosis: happens in phagocyte (no immune response)

Necrosis: swelling from inability to maintain gradients, bursting, immune/inflammatory response

44
Q

Apoptosis - intrinsic pathway

A

Trigger: mt mmbr perturbation (withdraw GF)
Replacement of anti with pro-apoptotic proteins
Cytochrome C released into cytoplasm
Activates Apaf-1 which activates caspases

45
Q

Anti and pro-apoptotic mitochondrial proteins

A

Anti: Bcl-2 and Bcl-XL
Pro: Bim and PUMA (allow Bax to act)

46
Q

Apoptosis - extrinsic pathway (Fas/CD95) - CTL

A

CTL upregulates Fas (CD95) ligand expression
Binds abnormal cell receptor
Recruits FADD which activates caspase-8 which activates caspase-3

47
Q

Apoptosis - extrinsic pathway (Granzymes) - CTL

A

CTL secrete granzymes and perforin that deliver apoptosis inducing molecules

48
Q

FLIP

A

Can bind to FADD and prevent caspase-8 activation

v-FLIPs (herpes HHV-8 and Kaposi’s sarcoma) keep cell alive while use machinery

49
Q

Key parts of NPC structure

A 
Lumenal subunits (fuse inner/outer nuc membrane, anchor)
Ring subuints (both inner/outer on both cyto/nuc side)
Barrier layer (unfolded FG repeat nups in middle)
50
Q

Karyopherins

A

Import/export - regulate nuclear entry

a (adapter, complex) and ß (receptor) families

51
Q

NTF2

A

Binds Ran.GDP and moves back into nucleus

52
Q

NXF1/NXT1

A

Bind mRNA and rRNA to export via brownian ratchet

53
Q

Ran

A

Binds GTP and GDP in both import/export
High GDP in cytoplasm, High GTP in nucleus
Hydrolysis leads to disassociation

54
Q

Types of nuclear transport and location in channel

A

Size filtering diffusion (middle)
Spontaneous migration of amphiphilic (sides)
Facilitated transport (cargo proteins, sides)

55
Q

Regulation of nuclear transport

A 
Happens at NPC, transport receptor, or cargo
Entropy barrier of nups
Ran.GTP/GDP gradient
Cargo interactions with nups
Cargo mods that impact binding
56
Q

Macroautophagy vs. chaperone-mediated autophagy

A

MA: double membrane vesicle with cytosolic components
CMA: Recognize specific protein sequence, protein complex and direct delivery to lysosome

57
Q

Process of macroautophagy

A

PI3K complex that allows nucleation of membrane
Membrane extension
Capture (random or target) cargo into extending mmbr
Fuse membrane, transport, fuse lysosome
Recycle good stuff

58
Q

Autophagy’s protective action against neurodegeneration

A

Capture and degradation of aggregate prone proteins

59
Q

Connection between autophagy and induction of apoptosis

A

Same proteins regulate both (ex Bcl-2)
Caspases can cleave autophagy regulators (blocking)
Difficult to measure therapy due to interaction

M2M - Niswander (4 decks)

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