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Exam 1 > Cell Bio > Flashcards

Cell Bio Flashcards

1
Q

relative sizes of cytoskeleton

A

microtubules > intermediate filaments > microfilaments

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2
Q

subunit of microtubules

A

tubulin

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3
Q

accessory protein of microtubules

A

tau

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4
Q

hyperstable structures of microtubules

A

axonemes (cilia, flagella), centrioles

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5
Q

motors of microtubules

A

dynein (retrograde)

kinesin (orthograde)

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6
Q

functions of microtubules

A

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

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7
Q

subunit of microfilaments

A

actin

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8
Q

hyperstable structures of microfilaments

A

sarcomere (muscle)

microvilli

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9
Q

motor of microfilaments

A

myosin

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10
Q

functions of microfilament

A

phagocytosis, cytokinesis, cell motility, force generation (muscle), membrane stabilization (RBC)

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11
Q

subunits of intermediate filaments

A

lamin (all nucleated cells), keratin (epithelial cells), desmin (muscle cells), neurofilamin (neurons), vimentin (mensenchymal cells, including endothelial cells and microblasts), GFAP (glial cells, astrocytes)

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12
Q

hyperstable structures of intermediate filaments

A

desmosome

hemidesmosome

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13
Q

motors of intermediate filaments

A

none

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14
Q

functions of intermediate filaments

A

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

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15
Q

cell type: lamins

A

all nucleated cells

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16
Q

cell type: vimentin

A

mesenchymal cells, endothelial cells, fibroblasts

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17
Q

cell type: desmin

A

muscle cells

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18
Q

cell type: glial fibrillary acidic protein (GFAP)

A

glial cells (astrocytes)

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19
Q

cell type: neurofilamin

A

neurons

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20
Q

cell type: keratin

A

epithelial cells

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21
Q

Kartagener’s/Primary Ciliary Dyskinesiea/Immotile Cilia Syndrome

A

MT disease.
No dyenein arm.
Motor cannot function, cilia cannot move.

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22
Q

Taxol

A

Binds to microtubules and freezes them in place.
Stops mitosis.
Anticancer therapy.

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23
Q

vinca alkaloids

A

Binds tubulin and prevents the assembly of microtubules.

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24
Q

Tau protein

A

Regulates microtubule length.
“Caps” microtubules.
Associated with dementia.

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25
Q

Listeria/Variola (smallpox)/ Vaccina

A

MF disease.
Bacterium is phagocytosed, but not digested.
Hijack actin machinery of host cell to propel themselves from one cell to another.
Are never exposed to the immune system.

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26
Q

Hereditary Spherocytosis

A

Mutated actin.
RBCs cannot get as small as the need to pass through tiny splenic blood vessels.
Inflexible RBCs are trapped in spleen and get targeted for destruction.
Symptoms: low RBC count (anemia), splenomegaly.

27
Q

Blistering diseases

A

Intermediate filaments are mutated–> cannot function in a hemidesmosome.
Epithelial cells detach from basal lamina, causing painful/fatal blisters.

28
Q

Huntington Disease

A

Autosomal dominant trinucleotide repeat.
Added glutamine residues.
Mutation causes protein to be cleaved.
Small fragments diffuse from the cytoplasm to the nucleus.
More severe forms have more protein fragments in the nucleus.

29
Q

SINEs (Selective Inhibitors of Nuclear Expression)

A

Block binding site of exportin-1 so it cannot export tumor supressors.
Tumor suppressors stay in the nucleus and function as normal.
Anticancer drug.

30
Q

Progeria

A

Laminopathy.
Defective lamin (lamin A/Progerin) causes nucleus to lose structure.
Unstable nucleus makes cell die younger–> premature ageing.

31
Q

Restrictive Dermopathy

A

Defective lamin only in skin.
No signs until birth.
Baby suffocates in skin.

32
Q

HIV/measles

A

Take advantage of the fusogenic properties of the plasma membrane.
Bind to CD4 receptors on a cell and enter by fusing membranes.
Then the pathogen replicates its genome.
HIV can produce the glycoprotein recognized by CD4, so it can fuse with other cells without external virus.

33
Q

the plasma membrane is more fusogenic if…

A

kinky (double bond)

34
Q

carbohydrate functions on membrane

A

Blood type antigens.
Pathogen recognition sites.
Reservoir for cytokines/growth factors.

35
Q

coccidia

A

Binds to glycoproteins in GI tract.
Each strain binds specifically and we can determine the strain by the location of the pain.
If stomach, it is from the water supply.
If intestines, it is from food.

36
Q

Toxoplasmosis

A

Protozoan binds to glycoproteins and causes severe birth defects in unborn children.
Infected woman has no symptoms and does not know she is affected.
From cat feces.

37
Q

mycoplasma pneumonia

A

Mycoplasma attach to cilia and extract cholesterol.
Cilia become fluid/floppy and cannot beat.
Mucus accumulates, which is a rich medium to propogate in, causing secondary infections.

38
Q

lysosomal storage disease

A

An enzyme is deficient, some substance accumulates, lysosome is clogged/unusable.
Treated by enzyme replacement therapy.

39
Q

Gauchers

A

Sphingolipid metabolism defect.

Successfully treated by recombinant enzyme therapy.

40
Q

Fabry

A

Sphingolipid metabolism defect.

First LSD treated with enzyme replacement therapy.

41
Q

Tay-Sachs

A

Sphingolipid and glycosaminoglycan (GAG) metabolism defect.
Prevalent in Ashkenazi Jews.
Common on US east coast.

42
Q

prostaglandins

A

Vasodilation, vasoconstriction, uterine contraction.

43
Q

PGE2

A

induces uterine contractions.

44
Q

Leukotrienes

A

Role in asthma and anaphalaxis.

Vasodilation, bronchoconstriction.

45
Q

Thromboxanes

A

Induces platelet aggregation, vasoconstriction.

46
Q

lipid rafts

A

Enriched in cholesterol/sphingolipids.
More rigid than the rest of the membrane.
Concentrate ligand-receptor complexes for RME.
Localize components for signal transduction.
Mobilize matrix-modifying enzymes for migrating cells.

47
Q

RME

A

Lipid rafts concentrate ligand-receptor complexes in clathrin pits.
Clathrin pit invaginates and becomes an endosome.
Endosome acidifies, causing clathrin to leave/receptor to dissociate/ prepares it to fuse with a lysosome.

Many viruses take advantage of this process.
Are recognized by virus receptor, RME via endosome, virus fuses with endosome, releases viral genome into cell.

48
Q

phagocytosis

A

Fc receptors on membrane recognize foreign particles (IgG).
Plasma membrane evaginates to engulf particle (driven by actin).
Phagosome is acidified to help fusion with lysosome.

49
Q

cystic fibrosis

A

Mutation in CFTR gene causes defective ABC-ATPase.

Cl- transport is not regulated.

50
Q

familial hypercholesterolemia

A

Extremely high cholesterol, likely to dies before 30 years.
Faulty LDL receptor.
Cholesterol cannot be transported out of the blood.
Causes arteriosclerosis.

51
Q

rabies/influenza/viruses

A

Use RME to enter cells.

Cause infections.

52
Q

MDR complex

A

ABC-ATPase is capable of pumping out toxins.
Some cells overexpress this –> can pump out drugs and survive.
Typical in some cancer cells.

53
Q

Streptococcus

A

Evolved a carbohydrate coat on the cell surface so it is not recognized as foreign.
Is not phagocytosed by macrophages and can proliferate.

54
Q

Legionnaire’s Disease

A

Bacterium is phagocytosed by epithelial cells in respiratory tract.
In phagosome, bacterium rapidly neutralizes the acidification process, preventing binding with lysosome.
Bacteria proliferates.

55
Q

Leishmania/Leprosy

A

Cells phagocytose these organisms, but are not destroyed by acidity.
Thrive in acidity and cause serious consequences.

56
Q

Tuberculosis

A

Modify phagosome wall so it cannot fuse with the lysosome.

57
Q

Tangier Disease

A

Extremely low HDL levels.
ABC-ATPase transporter is defective, so it cannot pump cholesterol out of the cell.
Cholesterol accumulates in various tissues, causing severe cardiac disease.
Helped reveal link between HDL levels and cardiovascular disease.
Swollen, large, tonsils.

Enabled researchers to determine which chromosome was involved, the process of reverse cholesterol transport.

58
Q

signal hypothesis

A

The first 20-25 AA determine where the protein will be finished being translated (ER or cytoplasm).
From the ER, the protein can go to the PM, golgi, lysosomes, or secretion.
From the cytoplasm. the protein can go to the nucleus, mitochondria, peroxisome, or cytoplasm.

59
Q

lysosome biogenesis

A

Lysosomal enzyme is phosphorylated in the cis-golgi (mannose-6-phosphate).
The mannose-6-P is recognized by receptors and buds off in a clathrin coated vesicle in the trans-golgi.
The vesicle acidifies, so the receptor and clathrin leave.
Many vesicles can fuse together to form a new lysosome.
Or a vesicle can join an already-established lysosome.

60
Q

NALD/Zellweger Syndrome

A

Due to a mutation in the SKL sequence that targets formed proteins to peroxisomes.
Have empty peroxisomes that cannot function normally.

61
Q

Mucopolysaccharides

A

Most common LSDs.
Defect in enzyme needed to break down mucopolysaccharides.
Lysosome becomes engorged and inactive.
Treated with enzyme replacement.

62
Q

I-Cell Disease

A

Defect: phophotransferase enzyme that phosphorylates the 6 position on mannose.
Lack the phospho-mannose address label, so enzymes get lost and do not make it to the lysosome.
Accumulation of polymers in lysosome, and highly elevated secretion of lysosomal enzymes.
Revealed mechanisms for LSDs and lysosomal biogenesis.

The only non-amino acid targeting label used by the cell.

63
Q

targeting sequences

A 
SKL --- peroxisome (Zellweger, NALD).
Short, basic AA --- nucleus.
75 AA near N-terminus --- mitochondria.
Mannose-6-P --- lysosome (I-Cell Disease).
KDEL --- ER (dilated cardiomyopathies.

Exam 1 (3 decks)

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