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Foundations > Cell Biology > Flashcards

Cell Biology Flashcards

1
Q

Nuclear localization signals are rich in which AA

A

Proline, Arginine, Lysine

To get in you need a PAL

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2
Q

What proteins inactivate cyclin-CDK complexes

A

p21, p27, p57

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3
Q

G1 to S phase cyclins and CDK

A

Cylcin D –CDK4 –> phosphorylation of Rb –> Rb released from E2F –> with E2F unbound cell can now transcribe
Cyclin E binds to CDK 2 allows progression to S phase

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4
Q

G2 to M phase cyclins and CDK

A

Cyclin A – CDK2 –>mitotic prophase

Cyclin B – CDK1 activated by cdc25 –> breakdown of nuclear lamins

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5
Q

Deficiency in Mannose phosphorylation leads to

A

I-ceel disease

  • No mannose-6-phosophate to target lysosome
  • corneal clouding, coarse facies, hepatosplenomegaly, skeletal abnormalities, joint movement prob
  • Death by 8
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6
Q

Peroxisomes purpose

A

Beta-oxidation of long chain FA and branched chain FA

  • Synthesis of plasmalogens
  • oxidases and catalase for metabolizing ethanol
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7
Q

Plasmalogens

A

Important phospholipids in myelin

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8
Q

COP II

A

RER –> cis golgi

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9
Q

COP I

A

cis Golgi –> RER

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10
Q

Clathrin

A

Trans Golgi –> lysosomes

-Plasma memb into cell

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11
Q

Golgi post-translational modifications

A
  • modifies N-oligosaccharide on ASPARAGINE

- adds O-oligosaccahrides to SERINE and THREONINE

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12
Q

Rx for MT

A

Vincristine, Vinblastine (prevents growth)
Paclitaxol, Docetaxel (prevents breakdown)
Benzimidazoles (worm inf, worms are BENDY)
Griseofulvin (fungal inf)
Colchicine (anti-infl, phagocytes use MT to move)

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13
Q

Dynein

A

+ to - retrograde back towards center of cell

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14
Q

Kinesin

A
  • to + away from nucleus anterograde
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15
Q

Kinase

A

adds phosphate with ATP

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16
Q

Phosphatase

A

Removes Phosphate

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17
Q

Phosphorylase

A

Adds Pi without ATP

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18
Q

Carboxylase

A

Adds COOH requires BIOTIN

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19
Q

Decarboxylase

A

Removes carboxyl group

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20
Q

Hydroxylase

A

Adds OH

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21
Q

Dehydroxylase

A

Removes OH

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22
Q

Dehydrogenase

A

Oxidize a substrate using electron acceptor (NAD+ or NADP+)

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23
Q

PDGF and GF receptor type

A

Tyrosine Kinase rec

-SIngle-pass transmembrane protein

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24
Q

Insulin and IFG-1 receptor

A

Tyrosine Kinase rec

  • 2 alpha subunits (disulfide bonds) bind extrecellular ligand [harsh conditions need the disulfide bonds]
  • 2 beta subunits: tyrosine kinase activity
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25
Q

Receptor-mediated endocytosis

A

-Molecules bind to receptors –> receptors interact with clathrin by adaptin protein –> clathrin polymerizes with other clathrin molecules to form a vesicle –> Dynamin pinches vesicle off –> vesicle is uncoated –> vesicle fuses with lysosome –> receptor recycled and lysosome breaks down contents

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26
Q

Histologic signs of apoptosis

A

-Pyknosis (condensation of nuclear chromatin), membrane blebbing, karyorrhexis (nuclear fragmentation), apoptotic bodies, phagocytosis, NO inflammation

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27
Q

Intrinsic pathway of apoptosis

A

Bcl-2 is anti-apoptotic –> DNA damage of apoptotic signals activates Bax (pro-apoptotic) –> Bax creates channels in mitochondrial membrane –> Cytochrome C moves from mitochondria to cytsol –> activates caspases –> caspases intitate apoptosis

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28
Q

Extrinsic pathway of apoptosis using the Death receptor

A

TNF receptors and Fas receptors are located on cell membrane –> TNF-alpha and Fas ligand activate receptors –> activated receptors lead to acctivation of caspases

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29
Q

Extrinsic pathway of apopptosis using Cytotoxic T cells

A

CD8+ T cells release perforin and granzyme B –> perforin punches holes in membrane and granzyme enters and activates caspases

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30
Q

Necrosis def

A

Cell death not orderly

-Spilling out of cytoplasmic contents –> inflammation

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31
Q

Coagulative Necrosis

A
  • gelatinous substance in dead tissue
  • common in heart, liver, kidneys
  • caused by ischemia (MI, wedge ischemia in liver)
  • histo: “death cells” cells with no nuclei
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32
Q

Liquifactive Necrosis

A
  • viscous liquid mass
  • common in brain, bacterial abscess, pleural effeusion
  • histo: homogenous eosinophilic (lots of MP)
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33
Q

Caseous Necrosis

A
  • combination of coagulative and liquifactive
  • MP walling off the infecting organism
  • “clumpy cheese”
  • seen in TB and systemic fungal infections
  • histo: acellular cells in the middle of a granuloma with multinucleated giant cells
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34
Q

Fat necrosis

A
  • Damaged cells release lipase, breaks down triglycerides in fat cells
  • seen in pancreatitis (enzymatic) and breast trauma (nonenzymatic)
  • histo: white fat spots and inflammatory giant cells, dark blue on H&E stain
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35
Q

Fibrinoid necrosis

A
  • seen in blood vessels
  • typically immune-mediated vascular damage
  • histo: area of fibrosis with eosinophils
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36
Q

Gangrenous necrosis

A
  • Distal extremity after chronic ischemia
  • Wet: bacterial infection, extremities (liquefaction and coag)
  • Dry: ischemia, toes and feet (coag)
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37
Q

Why do we get reperfusion injury?

A
  • Drastic free radical production and massive influx of calcium
  • free radicals –> cell damage through membrane lipid peroxidation, protein modification and DNA breakage
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38
Q

MOI in cyanide poisoning

A

ATP depletion

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39
Q

Enzymes responsible for free radical degradation

A
  • Catalase
  • Superoxide dismutase
  • Glutathione Peroxidase
  • Antioxidants
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40
Q

Granuloma

A

cluster of MP, lymphocytes and fibroblasts, typically contains multinucleated giant cells

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41
Q

Neutrophil Extravasation rolling molecules

A

selectins

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42
Q

Neutrophil Extravasation Tight binding

A

ICAM-1 (endo) and LFA-1 (integrin on NP)

43
Q

Neutrophil Extravasation Diapedesis

A

PECAM-1

44
Q

NP chemotactic signals

A

C5a, IL-8, LTB4

45
Q

Acute inflammation mediators

A

IL-1
IL-6
TNF-alpha

46
Q

Vasodilation and increased vascular permeability –> fluid exudation caused by

A

Histamine
Serotonin
Bradykinin

47
Q

Tissue remodeling occurs by

A

Metalloproteinases (Req ZINC)

48
Q

ESR

A

Erythrocyte Sedimentation Rate

  • rate at which RBCs sediment to bottom of test tube
  • inflammatory debris coat RBCs to cause them to clump faster, increased in inflammatory states
49
Q

C-reactive protein

  • synthesized
  • why
A

synthesized by the liver with acute inflammation

-Part of innate immune response: opsonized bacteria and activates complement (C-reactive protein, Complement)

50
Q

Cells that generate fibrinogen and C-reactive protein

A

Heaptocytes LIVER

51
Q

Type I Collagen

A

Bones, skin, dentin, scar tissue

Strong, slippery, stretchy, BM
SCAB

52
Q

Type II Collagen

A

Cartilage, virtreous body, nucleus pulposos

Strong, slippery, stretchy, BM
SCAB

53
Q

Type III Collagen

A

blood vessels, skin,uterus, embryonic, fetal, granulation tissue

Strong, slippery, stretchy, BM
SCAB

54
Q

Type IV Collagen

A

Basement Membrane

Strong, slippery, stretchy, BM
SCAB

55
Q

Collagen Synthesis

A
  1. Basic peptide synthesis in RER of Fibroblasts (Preprocollagen, becomes alpha chain)
  2. Hydroxylation of lysine and proline (req VITAMIN C)
  3. Glycosylation of Hydroxylated Lyzine (Procollagen)
  4. Exocytosis
  5. Cleave terminal regions of procollegen (Tropocollagen)
  6. Cross link tropocollagen mol to make collagen fibrils (covalent bonds to form a triple helix)
56
Q

Angiogensis

A
  • Grow new branch off existing vessel
  • uses metalloproteinases (w ZINC) –> remodeled ECM
  • VEGF causes vascular endothelium to proliferate
  • FBGF
57
Q

Which metal facilitate generation of free radials

A

Iron and Copper

58
Q

Wound healing

A

0-3 hrs: hemorrhage and clotting
12-24 hrs: acute inflmmation NP
1-3 days: MP, granulation tissue (fibroblasts and vascular endothelial cells), Epitherlializations
wks-months: Collagen production (type III then Type 1 to form scar

59
Q

AA high in collagen

A

Proline, Glycine, Hydroxyproline

60
Q

AA high in elastin

A

Proline, Glycine

-elastin held together by fibrillin

61
Q

Lipofuscin granules

A

Residual body with yellow-brown pigment –> incomplete free radical-infuced lipid oxidation

62
Q

Remain in G0 regenerate from stem cells

A

Permanent cell types

63
Q

Ex of permanent cell types

A

Neurons, skeletal and cardiac muscles, RBCs

64
Q

Enter G1 from G0 when stimulated

A

Stable (quiescent cells)

65
Q

Examples of stable cells

A

Hepatocytes, lymphocytes

66
Q

Never go to G0, divide rapidly with a short G1, most affected by chemo

A

Labile cells

67
Q

Examples of labile cells

A

Bone marrow, gut epithelium, skin, hair follicles, germ cells

68
Q

The RER in neurons

A

Nissl bodies

-synthesis peptide NT for secretion

69
Q

Site of N-linked oligosaccharide addition

A

RER

70
Q

Cells rich in RER

A
  • Mucus-secreting goblet cells of the SI

- Ab-secreting plasma cells

71
Q

Where is glucose-6-phosphatase located and what does it do?

A
  • Smooth ER

- last step in gluconeogenesis

72
Q

Deficiency in Glucose-6-phosphatase

A

Von Gierke’s disease

73
Q

Purpose of an endoscope

A

Sorting center for material from outside cell or from Golgi –> sending to lysosomes for destruction of back to membrane/Golgi

74
Q

Cytosolic ribonucleoprotein that traffics protein from ribosome to the RER

A

Signal Recognition Particle

-now protein synthesis can continue in the RER

75
Q

Eukaryote ribosomal subunits

A

40S + 60S = 80S

76
Q

Prokaryotic Ribosomal subunits

A

30S + 50S = 70S

77
Q

Initiation factor role in protein sythesis

A
  • Help assemble 40S subunit with initiator tRNA and release when mRNA and 60S subunit assemble
  • initiated by GTP hydrolysis
78
Q

Purpose of ribozymes in protein synthesis

A

Catalyes peptide bond formation

79
Q

ATP in protein synthesis

A

tRNA Activation (charging of tRNA, the attachment of the AA)

80
Q

GTP in protein synthesis

A

TRNA Gripping and Going places: Translocation

81
Q

Removal of N or C terminal peptides from zygote not to generate mature protein

A

Trimming

82
Q

Chaperone proteins that prevent shock-stressed proteins from misfolding

A

-hsp70 and hsp90 (heat shock proteins)

83
Q

Fxn of muscle contraction and cytokinesis

A

Microfilaments

Ex: actin, microvilli

84
Q

Fxn of maintaining cell structure and ex

A

Intermediate filaments

Ex: Vimentin, Desmin, GFAP, neurofilaments, cytokeratin

85
Q

Fxn of movement and cell division and ex

A

Microtubules

-ex: cilia, flagella, mitosis spindle, centrioles

86
Q

Drugs that act on MT

A 
Microtubes Get Constructed Very Poorly
Mebendazole (anti helminthic)
Griseofulvin (antifungal)
Colchicine (antigout)
Vincristine/Vinblastine (chemo)
Paclitaxel (anticancer)
87
Q

Large component of Fungal membranes

A

Ergosterol

What you say to fungus: ERRRR GO STARE AT A WALL

88
Q

Toxin that inhibits binding to the K+ site in Na/K ATPase

A

Ouabain

89
Q

Relocates a functional group within a molecule

A

Mutate

90
Q

How does Bcl-2 prevent apoptosis?

A

Prevents cytochrome c release by binding to and inhibiting APAF-1
-APAF-1 normally binds cytochrome c and induces activation of caspase 9 initiating the cascade

91
Q

Which extrinsic death receptor pathway is used in thymic medullary negative selection?

A

Fas-FasL interaction

92
Q

Regions most vulnerable to hypoxia/ischemia in brain

A

ACA/MCA/PCA bound areas (watershed most likely)

93
Q

Regions most vulnerable to hypoxia/ischemia in heart

A

Subendocardium (LV)

94
Q

Regions most vulnerable to hypoxia/ischemia in kidney

A

Straight segment of PT (medulla), thick ascending limb (medulla)

95
Q

Regions most vulnerable to hypoxia/ischemia in liver

A

Area around central vein (zone III)

96
Q

Regions most vulnerable to hypoxia/ischemia in colon

A

Splenic flexure and rectum (both watershed areas)

97
Q

Red infarct

A
  • Hemorrhagic infarcts in venous occlusion and tissues with multiple blood supplies
  • common in liver, lung, intestine, testes, reperfusion injuries
98
Q

Pale infarct

A
  • anemic infarcts in solid organs with 1 blood supply

- heart, kidney, spleen

99
Q

Causes of exudate

A
  • Lymphatic obstruction (chylous)
  • Inflammation, infection
  • Malignancy
100
Q

Causes of Transudate

A

Increased hydrostatic pressure (HF, Na+ retention)

Decreased oncotic pressure (cirrhosis, nephrotic syndrome)

101
Q

Increased ESR assoc

A
  • Anemia
  • Infection
  • Inflmmation
  • Cancer
  • Renal disease
  • Pregnancy
102
Q

Decreased ESR levels

A
  • Sickle Cell anemia
  • Polycythemia (inc RBC dilute aggregation factors)
  • HF
  • Microcytosis
  • Hypofibrinogenemia
103
Q

Elastin is high in what areas of the body?

A

Skin, lungs, large arteries, Elastic ligaments, vocal cords, ligamenta flava

Foundations (6 decks)

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