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Cellular Flashcards

1
Q

Cell cycle phase

A

G1, S, G2, M = cell cycle
- Regulated by checkpoints (cyclins, cyclin-dependent kinases = CDKs, tumor suppressors)

G0 and G1 = variable length
Mitosis = shortest phase of cell cycle
- Prophase, metasphase, anaphase, telophase

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2
Q

CDKs

A

Cyclin-dependent kinases

- Constitutive and inactive

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3
Q

Cyclins

A

Regulatory proteins, activated CDKs, control cell cycle

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4
Q

Tumor suppressors

A

p53 and hypophosphorylated Rb

  • Inhibit G1 to S progression
  • Mutations -> unihibited cell division (Li-Fraumeni syndrome)
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5
Q

Permanent cells

A

Remain in G0 - regenerate from stem cells

- Neurons, cardiac muscle, skeletal muscle, RBCs

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6
Q

Stable (quiescent) cells

A

Enter G1 from G0 when stimulated; can regenerate

- Hepatocytes, lymphocytes

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7
Q

Labile cells

A

Never go to G0; divide rapidly w/ short G1

  • Chemo affects these most
  • Bone marrow, epithelium, skin, hair follicles, germ cells
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8
Q

Rough endoplasmic reticulum (RER)

A
  • Synthesis of secretory (exported) proteins here
  • Nissl bodies = RER in neurons -> make peptide NTs for secretion
  • Free ribosome - unattached to membrane, cytosolic + organeller proteins made here
  • Mucus-secreting goblet cells of SI + antibody-secreting plasma have lots of RER
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9
Q

Smooth endoplasmic reticulum

A

Steroids and detox of drugs/poisons here

  • Lack surface ribosomes
  • Seen in liver hepatocytes, steroid producing cells of adrenals/gonads
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10
Q

Golgi

A

Transports porteins/lipids from ER to vesicles/membrane

  • Modifies N-oligosacc on asparagine
  • Adds O-oligosacc on serine + threonine
  • Adds manose-6-phosphate to proteins for trafficking to lysosome (w/o this can’t destroy proteins)
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11
Q

Endosomes

A

Sorting center for material outside cell or Golgi

- Sends it to lysosomes for destructions or back to membrane/Golgi for further use

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12
Q

I-cell disease (inclusion cell disease)

A

Inherited lysosomal storage disease

  • Defective phosphotransferase –> Golgi can’t phosphorylate mannose on glycoproteins –> so proteins excreted extracellularly instead of brought to lysosomes
  • Sx: course facial features, clouded corneas, restricted joints, high plasma levels of lysosomal enzymes (fatal in childhood)
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13
Q

Vesicular trafficking proteins

A

COP I: Golgi to Golgi (retrograde); Golgi to ER
COP II: Golgi to Golgi (anterograde); ER to Golgi
Clathrin: trans-Golgi to lysosomes; or plasma membrane to endosomes (receptor-mediated endocytosis)

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14
Q

Peroxisome

A

Membrane-enclosed organelle used for catabolism of very long chain fatty acids, branched chain fatty acids, and AA

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15
Q

Proteasome

A

Barrel-shaped protein complex –> degrades damaged or ubiquitin-tagged proteins
- Defects in ubiquitin-proteosome system = Parkinson’s

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16
Q

Microtubule

A

Helices of a and B-tubulin heterodimers
+ end, protofilaments, - end

  • Each dimer has 2GTP
  • See these in flagella, cilia, mitotic spindles
  • Grow slow, collapse quickly
  • Do slow axoplasmic transport in neurons (move into/out of neuron cell body)
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17
Q

Molecular motor proteins

A

These transport cell cargo down microtubule “tracks”

  • Dynein = retrograde to microtubule (+ to -)
  • Kinesin = anteriograde to microtubule (- to +)
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18
Q

Drugs that act on microtubules

A

“Microtubules Get Constructed Very Poorly”

  • Mebendazole (anti-helminthic)
  • Griseofulvin (anti-fungal)
  • Colchicine (anti-gout)
  • Vincristine/Vinblastine (anti-cancer)
  • Paxlitaxel (anti-cancer)
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19
Q

Cilia structure

A

9+2 arrangement of microtubules

- Axonemal dynein - ATPase that links peripheral 9 doublets and causes bending of cilium by sliding doublets

20
Q

Kartagener syndrome

A

Primary ciliary dyskinesia

  • Immotile cilia from dynein arm defect
  • Male/female infertility bc immobile sperm or disfxnal fallopian tube cilia
  • Incr risk of ectopic pregnancy
  • Other: bronchiectasis, recurrent sinusitis, situs inversus (dextrocardia on CXR)
21
Q

Cytoskeleton elements

A
  • Actin and myosin
  • Microtubule
  • Intermediate filaments
22
Q

Actin and myosin

A
  • Muscle contraction, microvilli, cytokinesis, adherens jxn
  • Actins = long, structured polymers
  • Myosins = dimeric, ATP-driven motor proteins that move along actins
23
Q

Microtubules

A

Made of tubules, part of cytoskeleton, allow movement intracellularly (move within cell along “tracks”)
- Cilia, flagella, mitotic spindle, axonal trafficking, centrioles

24
Q

Intermediate filaments

A

Part of cytoskeleton, give structure

- Vimentin, desmin, cytokeratin, lamins, glial fibrillary acid proteins (GFAP), neurofilaments

25
Plasma membrane composition
Asymmetric lipid bilayer - Cholesterol, phospholipids, sphingolipids, glycolipids, proteins - Fungal membranes have ergosterol
26
Immunohistochemical stains for intermediate filaments
``` Vimentin = connective tissue - Tells you sarcoma DesMin = Muscle Cytokeratin = epithelial cells - Tells you carcinoma GFAP = neuroGlia Neurofilaments = neurons ```
27
Na+ K+ pump
Na+K+ATPase is on plasma membrane --> ATP on cytosol side | - Each 1 ATP gets: 3 Na+ out, 2 K+ in
28
Na+K+ pump inhibitors
Ouabain - inhibits by binding K+ site Cardiac glycosides = digoxin and digitoxin - Directly inhibits Na+K+ ATPase --> indirectly inhibits Na+/Ca++ exchange --> incr Ca(intracell) --> incr cardiac contractility
29
Collagen
Most abundant protein in human body! - Modified by posttranslational modif - Organizes/strengthens extracellular matrix - Order Type I-IV = "Be (So Totally) Cool, Read Books"
30
Type I Collagen
``` In BONE (has 'one' in it) Most common collagen (90%) - BONE (made by osteoblasts) - Skin, Tendon - (dentin, fascia, cornea, late wound repair) ``` Osteogenesis imperfecta = decr T1 collagen production
31
Type II Collagen
``` In CARTILAGE (carTWOlage) - Cartilage (including hyaline), vitreous body, nucleus pulposus ```
32
Type III Collagen
``` In RETICULIN (pliability) - Skin, blood vessels, uterus, fetal tissue, granulation tissue ``` Defect seen in vascular Ehlers-Danlos syndr (ThreE D)
33
Type IV Collagen
In basement membrane, basal lamina, lens
34
Collagen synthesis and structure
Occurs inside and outside fibroblasts - Inside fibroblast = synthesis, hydroxylation, glycosylation, exocytosis - Outside fibroblast = proteolytic processing, cross-linking
35
Synthesis of collagen
- In RER - Collagen a-chains translated = preprocollagen (Gly-X-Y) - Glycine content good measure of collagen synthesis (collagen 1/3 glycine)
36
Hydroxylation of collagen
- In RER - Hydroxylation of specific proline and lysine residues (Requires VitC; deficiency = scurvy)
37
Glycosylation
- In RER - Glycosylation of pro-a-chain hydroxylysine residues --> forms triple helix of 3 collagen a-chains = procollagen - Problems forming triple helix = osteogenesis imperfecta
38
Exocytosis
Exocytosis of procollagen into extracellular space
39
Proteolytic processing
Procollagen disulfide terminal regions cleaved --> get insoluble tropocollagen
40
Cross-linking
Cross-link tropocollagen to make collagen fibrils | - Problems here = Ehlers-Danlos
41
Osteogenesis imperfecta
Genetic bone d/o, w/ brittle bones - AD most common, decreased production of T1 collagen - Sx: multiple fractures (in birth), blue sclera bc translucent connective tissue, hearing loss (abn ossicles), dental imperfections (no dentin)
42
Ehlers-Danlos syndrome
Faulty collagen synthesis - skin hyperextensible, bleed easily (bruise), hypermobile joints - 6 types: inheritance/severity varies; can be assoc w/ joint dislocations, berry/aortic aneurysms, organ rupture - Hypermobility type = joint instability; most common - Classical type = joint/skin sxs; mutation in type V collagen - Vascular type = vasc/organ rupture; deficient type III collagen
43
Menkes disease
Connective tissue disease - impaired copper absorp/transport - Decreased lysyl oxidase activity (Cu = cofactor) - Get brittle, "kinky" hair, growth retardation, hypotonia
44
Tissue repair
Starts with granulation tissue (T3 collagen, pliable), then will later form scar (T1 collagen, stronger) - Needs collagenase (w/ zinc cofactor) to do this
45
Elastin
Stretchy protein in skin, lungs, large arteries, elastic ligaments, vocal cords, ligamentum flava - Rich in proline/glycine - Tropoelastin w/ fibrilling scaffolding - Get cross-linking extracellularly - get elastic properties - Elastase - breaks down, inhibited by a1 antitrypsin Wrinkles = decr collagen + elastin production
46
Marfan syndrome
Defect in fibrillin | - Fibrillin = glycoprotein that forms sheath around elastin
47
Emphysema
Can be caused by a1-antitrypsin deficiency --> excess elastase activity - Remember, elastase is inhibited by a1-antitrypsin

Biochemistry (6 decks)

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