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Foundations Test 1 > Membrane Transport and Disease > Flashcards

Membrane Transport and Disease Flashcards

1
Q

Simple diffusion

A

Small gases, water, lipophilic molecules

No transporters and no specificity

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2
Q

Facilitated diffusion

A

Specificity
Requires transporter
Saturation kinetics observed
No direct Energy

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3
Q

Ligate gated channels respond

A

Signaling molecule

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4
Q

Open channels respond to

A

Local concnetrations of solutes

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5
Q

Voltage-gated channels respond to

A

Membrane potential changes

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6
Q

Channels responding to covalent modification typically

A

Phosphorylation

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7
Q

Mechanosensitive channels respond to

A

Deformations in bilayer

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8
Q

Aquaporins role, location, regulation

A

Water translocation
Differnet tissues
Exo/endocytosis

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9
Q

Aquaporins exampel of

A

Mechano-sensitive channel

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10
Q

Aquaporin sturcture

A

Alpha-helical homotetramers…hourglass shape

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11
Q

NDI

A

Nephrogenic Diabetes insipidus

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12
Q

Most common form of NDI

A

Defect in vasopressin receptor making kidney tubules unresponsive to vasopression (X-dominant)

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13
Q

Other form of NDA

A

Defect in aquaporin-2 for water reabsorption (recessive)

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14
Q

Symptoms of NDI

A

Large urine output, dehyration

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15
Q

F class pump

A

H+ across inner mitochondrial membrane

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16
Q

V class pump

A

H+ across endosomal/lysosomal mebrnae

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17
Q

P class pump

A

H+, Na+, K+, Ca2+ across plasma membrane

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18
Q

ABC class pumps

A

Found in plasma and intracellular membrnaes…catalyze influx of lipids, peptides, ions, and drugs

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19
Q

Primary carriers

A

ATp or GTP driven

20
Q

Secondary carriers

A

Concentration driven

21
Q

Importance of nuclear pore membrane wrapping

A

Transport of membrane proteins back into nucleus from the ER

22
Q

Effective channel size of nuclear pore

A

9-26 nm

23
Q

Fast diffuson of nuclear pore

A

<5 kDa

24
Q

Slow diffusion of nuclear pore

A

6-50 kDa

25
Q

Active transport of nuclear pore

A

> 50 kDa

26
Q

NLS

A

Signal for import…string of basic amino acids (+ charged)

27
Q

NES

A

Hydrophobic amino acids

28
Q

NRS

A

Tell to stay in the nucleus

29
Q

Nuclear recycling mechanism

A

Binding of calcineurium marks NES of NF-AT and activates import signal via dephosphorylation…once back inside the nucleus, calcineurium leaves, NF-AT rephosphorylated, and NES exposed

30
Q

What causes calcineurium to bind to NF-AT outside fo cell

A

High Calcium concentration

31
Q

Small G proteins activated and inactivated by

A

Activated by GEF (guanine-nucleotide-exchange-factor)

Inactivated by GAP (GTPase-activating-protein)

32
Q

GEF reaction

A

Removes GDP from Ras and replaces with GTP

33
Q

Movement of ____ drives active nuclear transport

A

Ran - small G-protein

34
Q

Ran-GTP/Ran-GDP locations

A

Ran-GTP - nucleus

Ran-GDP - cytosol

35
Q

Ran-GAP

A

Ran GTPase-activating protein…dephosphorylates the Ran-GTP complex in cytosol

36
Q

Ran-GEF

A

Ran gunaine nucleotide exchange factor (bound to chromatin)

Phosphorylates RAN-GDP in the nucleus

37
Q

Importin steps

A

Importin binds cargo protein with NLS
Complex associates with fibrils and enters nucleus
RanGTP binds importin inside nucleus and displaces cargo
Importin and Ran-GTP exit nucleus
Ran Binding Protein displaces RanGTP and importin is free
RanGAP activates RanGTP and hydrolyses GTP
RanGDP recycles to nucleus where RanGEF promotes exchange of GDP for GTP

38
Q

Export steps

A 
Exportin binds target AND RanGTP
Complex moves out 
Ran binding protein displaces RanGTp
Exportin releases cargo
RanGTP released from RanBP
RanGAP activates RanGTP and hydrolyses 
Exportin and RanGDP back to nucleus 
RanGDP converted by to RanGTP by RanGEF
39
Q

ALS Very early symptoms

A

Fatigue, muscle weakness, poor concentration

40
Q

ALS early

A

Cramps, spasticity, limb onset, slurred or nasal speech, bulbar onset

41
Q

ALS late

A

Difficulty moving, dysphagia, dysarthia

42
Q

ALS terminal

A

Resp failure or penumonia

43
Q

Only small % of ALS is ____

A

inherited

44
Q

Only ALS therapy and what it does

A

Riluzole

Blocks voltage gated sodium channels to prevent glutamate release

45
Q

Most common mutation of ALS

A

C9orf72 (GGGGCC) hexanucleotide expansion

46
Q

ALS mutations of C9orf72

A

Haploinsufficiency due to reduced expression of gene copy on expanded repeat halotype
RNA gain-of-function toxicity because of aggregates formed
Abnormal bidirectional transcription of expanded repeat sequences followed by Non-AUG-initiated tranlation into aggregation prone proteins

47
Q

3 things the GGGGCC mutation does

A

1) Directly clog NPC
2) Bind to RanGAP preventing nuclear import
3) Abnormal form of tranlation to form toxic dipeptide rpeeat proteins (DPRs) that interphere with import through karyopherins

Foundations Test 1 (15 decks)

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