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FA: Biochemistry > cellular > Flashcards

cellular Flashcards

1
Q

Cell cycle phases are regulated by what?

A

cyclins, CDKs, tumor suppressors

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2
Q

how do CDKs regulate cell cycle?

A

cyclin dependent kinases that are constitutive and inactive

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3
Q

how do cyclins regulate cell cycle?

A

regulatory proteins that control cell cycle events;
phase specific;
activate CDKs

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4
Q

what must be both activated and inactivated for cell cycle to progress?

A

cyclin-CDK complexes

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5
Q

What are primary tumor suppressors and where is there primary action?

A

p53 and hypophosphorylated Rb normally inhibit G1 to S progression

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6
Q

what are the 3 different types of cell types? define where each is prevented in cell cycle

A

permanent: G0 and regenerate stem cells;
stable: enter G1 & G0 when stimulated;
labile: never go G0 & divide rapidly w/ short G1

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7
Q

what are the permanent cells?

A

neurons, skeletal, cardiac muscle, RBCs

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8
Q

what are the stable cells?

A

hepatocytes, lymphocytes

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9
Q

what are the labile cells?

A

bone marrow, gut epithelium, skin, hair follicle, germ cells

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10
Q

what is important of rough ER?

A

site of synthesis of secretory (exported) proteins and N-linked oligosaccharide addition to many proteins

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11
Q

What are the rER in neurons? what is their role?

A

Nissl bodies synthesize enzymes ChAT makes ACh and peptide neurotransmitters

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12
Q

what is the importance for free ribosomes?

A

unattaches to any membrane; site of synthesis of cytosolic and organellar proteins

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13
Q

what specific cells are rich in rER?

A

mucus-secreting goblet cells of small intestine and Ab secreting plasma cells

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14
Q

What is important for smooth ER?

A

site of steroid synthesis and detox of drugs and poisons

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15
Q

what cells are rich in smooth ER?

A

liver hepatocytes and steroid hormone-producing cells of adrenal cortex are rich in sER

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16
Q

importance of Golgi

A

distribution center for proteins and lipids from ER to vesicle and plasma membrane;
modifies N-oligosaccharide on asparagine;
adds O-sugar on serine and threonine;
adds mannose-6-phosphate to proteins for trafficking to lysosomes

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17
Q

What are endosomes used for?

A

sorting material from outside cell or from Golgi to send it back to lysosomes for destruction or Golgi/membrane for use

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18
Q

What is I cell disease?

A

inherited lysosomal storage disease;
failure of addition of mannose-6-phosphate to lysosome proteins=> enzymes secreted outside cell instead of targeted to lysosome

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19
Q

How will I cell disease present?

A 
often fatal in childhood
coarse facial features;
clouded corneas;
restricted joint movement;
high plasma levels of lysosomal enzymes
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20
Q

What are the vesicular trafficking proteins? and their actions

A

COP I: Golgi->Golgi (retrograde); Golgi->ER

COP II: Golgi->Golgi (anterograde); ER->Golgi

Clathrin: trans-Golgi->lysosomes;
plasma membrane->endosomes (receptor mediated endocytosis)

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21
Q

what is peroxisome

A

membrane-enclosed organelle involved in catabolism of very long fatty acids and amino acids

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22
Q

what is proteasome

A

barrell shaped protein complex that degrades damaged or unnecessary proteins tagged for destruction w/ ubiquitin

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23
Q

what are the drugs that act on microtubules?

A 
Mebendazole/thiabendazole=> antihelminthic;
Griseofulvin=> antifungal
vincristine/vinblastine => anti-cancer
paclitaxel=> anti-breast cancer
colchicine=> anti-gout
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24
Q

what is the structure of microtubules?

A

cylindrical structure composed of a helical array of polymerized dimers of alpha and Beta tubulin

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25
Q

What binds the dimers of microtubule?

A

2 GTP bound

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26
Q

Where are microtubles associated with?

A

flagella, cilia, mitotic spindles;

involved in slow axoplasmic transport in neurons

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27
Q

what are the molecular motor proteins of the cell? and how they moved

A

dynein=> retrograde to microtubule from (+) -> (-)

kinesin=> anterograde to microtubule (-) -> (+)

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28
Q

What causes Chediak Higashi syndrome?

A

mutation in lysosomal trafficking regulator gene (LYST) that is required for Mt dependent sorting of endosomal proteins into late multivesicular endosomes

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29
Q

what is the result of a mutation in lysosomal trafficking regulator gene?

A

recurrent pyoenic infections;
partial albinism;
peripheral neuropathy

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30
Q

How is a cilia arranged?

A

9+2 arrangement of Mt

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31
Q

for cilia to to bend, what must be present?

A

axonemal dynein=> ATPase links peripheral 9 doublets and causes bending of cilium by differential sliding of doublets

32
Q

What causes Kartagener’s syndrome?

A

immotile cilia due to dynein arm defect

33
Q

what are the results of kartagener’s syndrome

A

male infertility (immotile sperm) and decrease in female fertility;
bronchiectasis;
recurrent sinusitis (bacteria, particles not pushed out);
assoc w/ situs inversus

34
Q

What are actin and myosin found in cytoskeleton?

A

microvilli, muscle contraction, cytokinesis, adherens junctions

35
Q

What are microtubules used for?

A

movement;

cilia, flagella, mitotic spindle, axonal trafficking, centrioles

36
Q

What are intermediate filaments used for?

A

structure;
vimentin, desmin, cytokeratin, lamins,
glial fibrillary acid proteins, neurofilaments

37
Q

What is the composition of the plasma membrane?

A

asymmetric lipid bilayer;

contains cholesterol, phospholipids, sphingolipids, glycolipids, proteins

38
Q

Give stain and what cell type for different intermediate filaments

A 
vimentin=> connective tissue;
desmin=> muscle;
cytokeratin=>epithelial cells;
GFAP=> neuroglia;
neurofilaments=> neurons
39
Q

where are Na/K ATPase located?

A

cytosolic side

40
Q

How does ouabain work?

A

inhibits by binding to K+ site

41
Q

what types of drugs inhibit Na/K ATPase?

A

cardiac glycosides => digoxin and digitoxin

42
Q

How do cardiac glycosides (digoxin and digitoxin) help the heart?

A

inhibit Na/K ATPase leading to direct inhibition of Na/Ca exchange to increase intracellular Ca causing increase in cardiac contractility

43
Q

what is significant about collagen use in the body?

A

organizes and strengthens ECM => extensively modified by post-translational modification

44
Q

What is the most common type of collagen?

A

Collagen I: bone, skin, tendon => dentin, fascia, cornea, late wound repair

45
Q

defect in type I collagen results in what disease

A

osteogenesis imperfecta

46
Q

where is type II collagen found?

A

cartilage (including hyaline), vitreous body, nucleus pulposus

47
Q

Where is type III collagen found?

A

reticulin=> skin, blood vessels, uterus, fetal tissue, granulation tissue

48
Q

defect in type III collagen causes what?

A

Ehlers-Danlos

49
Q

what does type IV collagen make up?

A

basement membrane or basal lamina

50
Q

defect in type IV collagen causes what?

A

Alport syndrome

51
Q

What are the steps to collagen synthesis both inside and outside the fibroblasts?

A 
inside:
synthesis (RER);
hydroxylation (ER);
Glycosylation (ER);
exocytosis;

outside:
proteolytic processing;
cross-linking

52
Q

inside the fibroblasts, what occurs in first step of collagen synthesis?

A

Synthesis:
translation of collagen alpha chains
(preprocollagen)-usually Gly-X-Y
=> X & Y are proline or lysine

53
Q

what occurs in step 2 of collagen synthesis?

A

hydroxylation:

hydroxylation of specific proline and lysine residues => requires vitamin C

54
Q

what is the deficiency that leads to scurvy?

A

vitamin C

55
Q

what is the 3rd step of collagen synthesis?

A

Glycosylation of pro-alpha chain hydroxylysine residues & formation of procollagen via H+ and disulfide bonds => triple helix of 3 collagen alpha chains

56
Q

If problems forming the triple helix occur in glycosylation, what disease is associated?

A

osteogenesis imperfecta

57
Q

what is the 4th step of collagen synthesis?

A

Exocytosis of procollagen into extracellular space

58
Q

outside of the cell, what is the 5th step of collagen synthesis?

A

proteolytic processing:

cleavage of disulfide rich terminal regions of procollagen, transforming it into insoluble tropocollagen

59
Q

what is the last step of collagen synthesis?

A

cross-linking:
reinforcement of many staggered tropocollagen molecules by covalent lysine-hydroxylysine cross-linkage (Cu contains lysyl oxidase) to make collagen fibrils

60
Q

What disease is associated with problems in cross-linking?

A

Ehlers-Danlos

61
Q

genetic bone disorder (brittle bone disease) caused by variety of gene defects?

A

osteogenesis imperfecta=> autosomal dominant w/ abnormal type I collagen

62
Q

What does the most common form of osteogenesis imperfecta cause?

A
  • multiple Fx w/ minimal trauma; may be in birth
  • blue sclerae due to translucency of connectiv tissue over choroidal veins
  • hearing loss (abnormal middle ear bones)
  • dental imperfections due to lack of dentin
63
Q

define ehlers-danlos syndrome

A

faulty collagen synthesis causing hyperextensible skin,
tendency to bleed (easy bruising);
hypermobile joints

64
Q

There are 6 types of ehlers danlos syndrome. what are they typically associated with?

A

autosomal dominant or recessive
joint dislocation;
berry aneurysms;
organ rupture

65
Q

in severe, classic Ehlers-Danlos, what type of collagen is affected?

A

Type I or Type V collagen

66
Q

What type of collagen is associated w/ Alport syndrome?

A

XLR=> due to a variety of gene defects resulting in abnormal type IV collagen

67
Q

what is alport syndrome characterized?

A

progressive hereditary nephritis and deafness;

ocular disturbances

68
Q

Type IV collagen is important structurally in what areas?

A

basement membrane of kidney, ears, and eyes

69
Q

where is elastin typically found?

A

stretchy protein w/in skin, lungs, large arteries, elastic ligaments, vocal cords, ligamenta flava

70
Q

What is the ligamenta flava?

A

connects vertebrae => relaxes & stretched conformations

71
Q

What are amino acids found in elastin?

A

nonhydroxylated forms that are rich in proline and glycine

72
Q

what is the role in tropoelastin?

A

fibrillin scaffolding

73
Q

What gives elastin its elastic properties?

A

cross-linking extracellularly

74
Q

What breaks down elastin? what inhibits this breakdown?

A

elastase;

inhibited by alpha-1-antitrypsin

75
Q

what is a defect in fibrillin lead to?

A

Marfan’s syndrome

76
Q

What does an alpha-1-antitrypsin deficiency cause? what is it a result of?

A

emphysema => results in excess elastase activity

77
Q

What are wrinkles of aging due to?

A

reduced collagen and elastin production

FA: Biochemistry (5 decks)

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