review exam 1 Flashcards

exam 1

1
Q

Hemidesmosome

A

specialized IF structure that anchors skin cells

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2
Q

Desmosomes

A

specialized IF structures

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3
Q

cell type of lamins

A

all nucleated cells

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4
Q

cell type of vimentin

A

mesenchymal cells: endothelial cells and fibroblasts

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5
Q

cell type of desmin

A

muscle cells

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6
Q

cell type of glial fibrillary acidic protein

A

glial cells- astrocytes

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7
Q

cell type of neurofilamin

A

neurons

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8
Q

cell type pf keratin

A

epithelial cells

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9
Q

cytoskeleton sizes

A

microtubules> IF? microfilaments

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10
Q

Microtubules subunit

A

tubulin

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11
Q

Microfilaments subunit

A

actin

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12
Q

intermediate filaments subunit

A

lamins, keratin, desmin, neurofilamin, vimentin, GFAP

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13
Q

MT accessory proteins

A

TAU

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14
Q

MT hyperstable structures

A

cilia, flagella, centrioles

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15
Q

MF hyperstable structures

A

sarcomere, microvilli

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16
Q

IF hyperstable structure

A

desmosome, hemi-desmosom

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17
Q

MT motors

A

dyenin (retrograde)

kinesin (orthograde)

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18
Q

MF motor

A

myosin

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19
Q

IF motor

A

none

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20
Q

MT functions

A

cilia/flagella functions, mitotic spindle, organele/cargo transport

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21
Q

MF functions

A

phagocytosis, cytokenisis,
cell motility,
force generation,
membrane stabilization

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22
Q

IF function

A

mechanical integrity (nucleus, cell-cell, cell-matrix)

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23
Q

MT drugs

A

taxol. vinca alkaloids/ colchine/vinblastine

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24
Q

MT medical significance

A

kartageners, cancer chemotherapy, dementias

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25
Q

MF medical significance

A

hereditary spherocytes, listeria infection, smallpox/vaccinia

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26
Q

IF medical significance

A

laminopathies, blistering diseases, cancer diagnosis

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27
Q

lamins are responsible

A

connecting chromatin to the nuclear membrane

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28
Q

progeria

A

laminopathy

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29
Q

Restrictive dermopathy

A

laminopathy

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30
Q

when the nuclear envelope is intact in what state are the lamins?

A

dephosphorylated state

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31
Q

interphase

A

intact nuclear envelope

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32
Q

lamins are phosphorylated by a ______ during ______

A

lamins are phosphorylated by a kinase during early mitosis

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33
Q

early in mitosis what happens once lamins are phosphorylated?

A

the chromatin-nuclear membrane connection to breaks apart beginning the process of nuclear membrane disassembly and chromosome condensation

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34
Q

correlation between Hnt severity and age

A

severity of symptoms is inversely related with age

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35
Q

Sines blocks what for which purpose?

A

they block exportin-1, because exportin-1 is used by cancer cells to pump out tumor suppressors but by blocking exportin-1 the tumor suppressors stay in the nucleus. Anti-cancer drug

36
Q

Leukotrienes

A

induces bronchoconstriction and vasodilation

37
Q

lipid rafts are critical for (3):

A

(1) signal transduction
(2) endocytosis
(3) rapid re-organization of the membrane

38
Q

Glucose permease…. tell me more about it

A

it is a way to transport small molecules against their concentration gradient. Here we are trying to move glucose from the intestinal lumen to the blood. First it need to pass the intestinal epithelium, and which is high in glucose. We use a glucose/ sodium simporter to get into the cell and then glucose will travel to the permease channel to go into the blood. Sodium is pumped out by a sodium/potassium ATPase

39
Q

Factors affecting membrane fluidity (4)

A

(1) Double bonds
(2) acyl chain length
(3) temperature (heat)
(4) cholesterol

40
Q

measles virus

A

phospholipid fusogenicity

41
Q

lipid rafts are critical for (3):

A

(1) signal transduction
(2) endocytosis
(3) rapid re-organization of the membrane for extracellular matrix modification and motility

42
Q

what happens at the Cis Golgi?

A

mannose gets phosphorylated at the 6th position

43
Q

Where does mannose-6-phosphate goes?

A

lysosome!!!

44
Q

do we recycle the M6P receptor?

A

Yes! it is transported back to the trans golgi

45
Q

do we recycle the M6P receptor?

A

Yes! it is transported back to the trans golgi

46
Q

what is the Key point of Lysosomal storage diseases

A

they are due to a single enzyme deficiency…..

I-CELL DISEASE IS AN EXCEPTION!!!!!

47
Q

what is the Key point of Lysosomal storage diseases

A

they are due to a single enzyme deficiency…..

I-CELL DISEASE IS AN EXCEPTION!!!!!

48
Q

______ returns lamins to the de-phosphorylated state

A

phosphatase returns lamins to the de-phosphorylated state

49
Q

What happens during nuclear membrane assembly/disassembly late in mitosis?

A

once lamins are phosphorylated, the nuclear membrane assembles and chromosomes decondensation occurs

50
Q

What happens to HNT proteins?

A

the protein acquires the ability to enter the nucleus of brain neurons and gum up the works and causing cell death

51
Q

membrane fluidity double bonds:

Cis vs trans

A

the more kinkier the cis double bond the more fluid it is.

Trans are not kinky and therefore are less fluid

52
Q

Membrane Fluidity: acyl chain length

shorter vs longer

A

shorter are more fluid

53
Q

membrane fluidity: temperature

low vs high

A

higher temperature are more fluid

54
Q

membrane fluidity:
Cholesterol

more vs less

A

more cholesterol less fluid

55
Q

membrane fluidity:
Cholesterol

more vs less

A

more cholesterol less fluid

56
Q

HIV enters by

A

Fusing with the plasma membrane using phospholipid fusogenicity

57
Q

Rabies enters through

A

RME and fuse with endosome membrane

58
Q

Influenza virus enters through

A

RME and fuse with endosome membrane

59
Q

major functional organizers of the membrane, bringing lipids and proteins together

A

lipid rafts

60
Q

Lipid rafts are composed of

A

specialized cholesterol and sphingolipid-rich lipid-protein allowing them to move rapidly within the membrane

61
Q

LDL-cholesterol uptake

A

ligand degraded, receptor recycled

62
Q

reveled the mechanism of cholesterol transport into cells and the role of LDL in CVD

A

familial hypercholesterolemia

63
Q

Tangier is caused

A

by a defect in ABC ATPase that pumps cholesterol out of cells

64
Q

led to our understanding of the role of HDL in CVD

A

Tangiers

65
Q

Targeting signal and organelle for:

Hnt

A

short basic aa sequence and nucleus

66
Q

Targeting signal and organelle for:

Zellweger/NALD

A

SKL tripeptide and peroxisome

67
Q

Targeting signal and organelle for:

mitochondriapathies

A

70-80 aa sequence near N- terminus and mitochondria

68
Q

Targeting signal and organelle for:

I-Cell

A

mannose-6-phosphate and lysosome

69
Q

Targeting signal and organelle for:

dilated cardiomyopathies

A

KDEL tetrapeptide and ER

70
Q

Required knowledge:

Fabry

A

Sphingolipid metabolism defect: first LSD successfully tx. with enzyme replacement therapy

71
Q

Required knowledge:

Gaucher

A

sphingolipid metabolism defect: also successfully tx. with enzyme replacement therapy

72
Q

Required knowledge:

Mucopolysaccharidoses

A

defect in one of the several enzymes needed to break down GAGs (aka mucopolysaccharides); several are now tx. with enzyme replacement or enzyme enhancement therapies

73
Q

Required knowledge:

I-Cell disease

A

defect in phospholytransferase which does not allow the phosphorylation of M6P

74
Q

key point of LSD

A

individual LSD is 1/100000 but overall likelihood is in 1/5000 due to the many enzymes in that pathway

75
Q

self-recognition

A

role of carbohydrates on membrane glycoproteins in determining blood types

76
Q

Coccidiosis/ toxoplasmosis mechanism

A

interaction of coccidial parasites with cell surface carbohydrates

77
Q

Mycoplasma pneumonia

A

sucks cholesterols out of the base of respiratory cilia

78
Q

lipid composition of membranes is

A

asymmetrical

79
Q

clathrin-coated pits _______ and pinck off to form an endosome

A

invaginates

80
Q

in phagocytosis the plasma membrane ______

A

evaginates

81
Q

critical fact in signal hypothesis

A

first 20-25 aa translated will determine if it will stay in the cytoplasm or be secreted

82
Q

All protein synthesis starts with the _________ aa

A

N-terminal

83
Q

protein that will be secreted contain a

A

hydrophobic signal peptide

84
Q

fates of proteins from cytosol ribosomes (4)

A

cytoplasm
nucleus
mitochondria
peroxisomes

85
Q

fates of proteins from ER ribosomes

A
plasma membrane
ER
Golgi
lysosomes 
secretion
86
Q

defects in KDEL lead to

A

dilated cardiomyopathies