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M2M - Niswander > Unit III Week 2 > Flashcards

Unit III Week 2 Flashcards

(59 cards)

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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)

Study These Flashcards
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
Co-translational translocation (multiple transmembrane domains)
SRP binds/translocates mRNA through translocon Many start/stop sequences Simple N linked glycosylation occurs in ER lumen
26
Major functions of the Golgi complex
Sphingolipid synthesis Additional post-translational modification Finishing/complex N linked glycosylation Proteolytic processing Sorting of proteins/lipids via membrane thickness
27
Three vesicle coats and transport
COPII - ER to Golgi (forward) COPI - ER to Golgi (backward) Clathrin - Golgi to PM (endocytosis)
28
Clinical features of Cholera
Non-inflammatory diarrhea Severe, acute, watery, no blood (rice water stool) Dehydration or asymptomatic
29
Leading cause of death with Cholera
Dehydration
30
What bacterial molecules contribute to Cholera and mechanism
CT, AB5 toxin produced by bacteriophage Ganglioside GM1 on ß-subunit attaches, A transmits Irreversibly binds CFTR (cAMP path) until death of cell
31
How to distinguish between Cholera strains
O-specific polysaccharide of the lipopolysaccharide
32
Molecules that protect against Cholera
water, gastric acid (H. pylori), O blood, antibodies, CFTR mutation (heterozygote advantage), oral rehydration solution
33
Vaccines against Cholera
Dukoral - kill v. cholerae 01 x2 and CTxB Shanchol - kill v. cholerae 01 and 0139 antibodies to OPS of LPS
34
Two major routes for small volume endocytosis
Phagocytosis (macrophages and neutrophils) | Pinocytosis (clathrin and caveolae)
35
Clathrin mechanism
Transmembrane receptor binds adaptor proteins Adaptor proteins bind clathrin Buds off/ dynamin pinches Rapid disassociation Receptor recycling and (ex) LDL breakdown
36
Caveolae
Small vesicles that from without coat proteins Important with lipid rafts Animal viruses and cholera toxin use caveolae
37
Proteasome breakdown
Cap bind Ub and unfolds protein Cylinder does actual protein breakdown (a and ß) a - regulates entry into chamber ß - cleaves
38
Ubiquitin mechanism
E1: binds and activates (Activation) E2: transfers to E3 complex or forms complex with E3 (Conjugation) E3: attaches string of Ub >4 (Ligation)
39
Lysosome
Breakdown, pH=5 Proton pumps need to be protected Lysosomal storage diseases: Tay Sachs, Gaucher's, Niemann-Pick
40
Apoptosis - nuclear events
``` superocondensing of heterochromatin/euchromatin DNA cleaved into nucleosomes (core histone + ~180bp) Many DSB (beyond repair, if apoptosis fails will not divide) ```
41
Apoptosis - cytoplasmic events
shrinkage | lose 1/3 volume in seconds
42
Apoptosis - plasma membrane events
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
Apoptosis vs. necrosis
Apoptosis: happens in phagocyte (no immune response) Necrosis: swelling from inability to maintain gradients, bursting, immune/inflammatory response
44
Apoptosis - intrinsic pathway
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
Anti and pro-apoptotic mitochondrial proteins
Anti: Bcl-2 and Bcl-XL Pro: Bim and PUMA (allow Bax to act)
46
Apoptosis - extrinsic pathway (Fas/CD95) - CTL
CTL upregulates Fas (CD95) ligand expression Binds abnormal cell receptor Recruits FADD which activates caspase-8 which activates caspase-3
47
Apoptosis - extrinsic pathway (Granzymes) - CTL
CTL secrete granzymes and perforin that deliver apoptosis inducing molecules
48
FLIP
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
Key parts of NPC structure
``` 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
Karyopherins
Import/export - regulate nuclear entry | a (adapter, complex) and ß (receptor) families
51
NTF2
Binds Ran.GDP and moves back into nucleus
52
NXF1/NXT1
Bind mRNA and rRNA to export via brownian ratchet
53
Ran
Binds GTP and GDP in both import/export High GDP in cytoplasm, High GTP in nucleus Hydrolysis leads to disassociation
54
Types of nuclear transport and location in channel
Size filtering diffusion (middle) Spontaneous migration of amphiphilic (sides) Facilitated transport (cargo proteins, sides)
55
Regulation of nuclear transport
``` 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
Macroautophagy vs. chaperone-mediated autophagy
MA: double membrane vesicle with cytosolic components CMA: Recognize specific protein sequence, protein complex and direct delivery to lysosome
57
Process of macroautophagy
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
Autophagy's protective action against neurodegeneration
Capture and degradation of aggregate prone proteins
59
Connection between autophagy and induction of apoptosis
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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