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Biochemistry > Cellular Biochemistry > Flashcards

Cellular Biochemistry Flashcards

1
Q

What are the phases of the cell cycle?

A

G0 (quiescence), G1 (growth), S (DNA synthesis), G2, M (mitosis and cytokinesis)

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2
Q

What modulates G1 restriction point?

A

p53 (evaluates for DNA damage), and hypophosphorylated Rb (holds E2F).

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3
Q

What are CDKs?

A

Cyclin dependent kinases regulate cell cycle – constituitive and inactive.

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4
Q

What do cyclins do?

A

Activate CDKs. Cyclin-CDK complexes phosphorylate other proteins to coordinate cell cycle progression.

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5
Q

What causes Li-Fraumeni syndrome?

A

p53 mutation –> cancers

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6
Q

What is the result of Rb mutation?

A

Retinoblastoma.

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7
Q

What are “permanent” cell types?

A

Cells that remain in G0, ie neurons, skeletal, cardiac muscle, and RBCs.

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8
Q

What are “stable/quiescent” cell types?

A

Cells that enter G1 from G0 when stimulated. Hepatocytes, lymphocytes

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9
Q

What are labile cells?

A

Cells that never go to G0, divide rapidly with short G1. Bone marrow, gut epithelium, skin, hair, germ cells.

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10
Q

What is rough endoplasmic reticulum for?

A

Site of synthesis of proteins that will be exported, and of N-linked oligosacc addition to many proteins

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11
Q

What are NISSL bodies?

A

RER in neurons. Synthesize peptide neurotransmitters for secretion

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12
Q

What are free ribosomes?

A

Unattached to any membrane, site of synthesis of cytosolic and organellar proteins

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13
Q

Why do goblet cells and plasma cells have a lot of RER?

A

Mucus secretion from goblet cells, antibody secretion from plasma cells

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14
Q

What is smooth endoplasmic reticulum for?

A

Synthesis of steroids and detoxification of drugs and poisons. Lacks surface ribosomes.

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15
Q

What are two cell types that are rich in smooth ER?

A

Liver hepatocytes and steroid-hormone secreting cells of the adrenal cortex

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16
Q

What are peroxisomes?

A

Membrane enclosed organelle involved in catabolism of 1) very long chain fatty acids, 2) branched-chain fatty acids, and 3) amino acids.

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17
Q

What are proteasomes?

A

Barrel shaped protein complexes that degrades damaged or ubiquitin-tagged proteins

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18
Q

In what disease have ubiquitin-proteasome defects been detected?

A

Parkinson’s.

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19
Q

What is the Golgi apparatus? What modifications does it make?

A

Distribution center for proteins and lipids from the ER to the vesicles and plasma membrane. Modifications:

1) N-oligosaccharides on aspargine
2) O-oligosaccharides on serine and threonine
3) Mannose-6-phosphate addition to proteins for trafficking to lysosomes.

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20
Q

What are endosomes?

A

Sorting centers for material from outside the cell or from the Golgi; send to lysosomes for destruction or back to the Golgi/plasma membrane for further use.

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21
Q

What is cis-Golgi vs trans-Golgi?

A

cis-side is side closest to ER. trans-side is outward facing side.

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22
Q

What is COPI?

A

Vesicular trafficking protein, marks: Golgi–>golgi (retrograde) and cis-Golgi -> ER

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23
Q

What is COPII?

A

Vesicular trafficking protein, marks: ER -> cis-Golgi (anterograde).

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24
Q

What is clathrin?

A

Vesicular trafficking protein, marks: trans-Golgi to lysosomes, plasma membrane to endosomes (receptor mediated endocytosis, eg LDL receptor activity).
NB: Also stabilizes spindle in mitosis.

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25
Q

Via which enzyme does Golgi add mannose-6-phosphate to glycoproteins?

A

N-acetylglucosaminyl-glucosaminyl-1-phosphotransferase

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26
Q

What is Inclusion Cell disease?

A

Failure of Golgi to phosphorylate mannose residues on glycoproteins (defect in N-acetylglucosaminyl-glucosaminyl-1-phosphotransferase). Proteins secreted extracellularly instead of to lysosomes. Sx: coarse facial features, clouded corneas, restricted joint movement, high plasma levels of lysosomal enzymes. Often fatal in childhood.

27
Q

What is an SRP?

A

Signal recognition particle. Abundant, cytosolic ribonucleoprotein that traffics proteins from the ribosome to the RER. Absent SRP -> proteins accumulate in cytosol.

28
Q

Predominant function of Microfilaments?

A

Muscle contraction, cytokinesis. Eg, Actin.

29
Q

Predominant function of intermediate filaments?

A

Maintain cell structure. Vary by cell type.

30
Q

Predominant function of microtubules?

A

Movement, cell division. Eg, cilia, mitotic spindle, centrioles axonal trafficking.

31
Q

Which cell type has +immunohistochemical staining for vimentin?

A

Connective tissue

32
Q

Which cell type has +immunohistochemical staining for desMin?

A

Muscle.

33
Q

Which cell type has +immunohistochemical staining for cytokeratin?

A

Epithelial cells

34
Q

Which cell type has +immunohistochemical staining for GFAP?

A

neuroGlia

35
Q

Which cell type has +immunohistochemical staining for neurofilaments?

A

Neurons

36
Q

What are the key features of microtubule structure?

A
  1. Cylindrical structure composed of helical array of polymerized alpha and beta tubulin.
  2. Each dimer has 2 GTP bound
  3. Has positive end, negative end.
  4. Grows slowly, collapses quickly
37
Q

What are two molecular motor proteins?

A

Dynein (retrograde to tubule: positive to negative).

Kinesin (anterograde to tubule: neg to pos).

38
Q

Which key drugs act on microtubules?

A

Mebendazole (antihelminthic), Griseofulvin (antifungal), Colchicine (antigout), Vincristine/Vinblastine (anticancer), Paclitaxel (anticancer). “Microtubules Get Constructed Very Poorly).

39
Q

What are the key features of cilia structure? What causes bending?

A

9+2 arrangement of microtubule doublets. Axonemal dynein-ATPase links peripheral 9 doublets and causes bending by differential sliding of doublets.

40
Q

What is the defect in Kartagener’s syndrome?

A

Immotile cilia due to dynein arm defect.

1) Fertility issues. Male (sperm) AND female (fallopian tube cilia) infertility. Inc risk ectopic preg.
2) Resp/Pulm issues: Bronchiectasis, recurrent sinusitis due to mucociliary escalator defect.
3) Situs inversus (eg dextrocardia)

41
Q

Plasma membrane composition?

A

Asymmetric lipid bilayer. Contains cholesterol, phospholipids, sphingolipids, glycolipids, and proteins.

42
Q

What’s special about fungal plasma membranes?

A

Contain ergosterol.

43
Q

Describe location and configuration of Na/K+ ATPase.

A

Located in plasma membrane, ATP site on cytosolic side. For each ATP consumed, 3NA+ go out of cell (pump is phosphorylated), and 2K+ come into the cell (pump is dephosphorylated).

44
Q

What does Ouabain do?

A

Inhibits binding to K+ side.

45
Q

How does digoxin work?

A

Directly inhibits Na/K+ atpase, which leads to indirect inhibition of Na+/Ca2+ exchange (which uses Na+ gradient to bring 1Na+ in and 3Ca2+ out), leading to rise in intracellular calcium, and increased cardiac contractility.

46
Q

What is the most abundant protein in the human body?

A

Collagen. It organizes and strengthens extracellular matrices. Extensively modified by post-translational modification.

47
Q

Pneumonic for collagen types?

A

I: Be So Totally; II: Cool; Read Books (III)

48
Q

Where are the types of collagen found?

A

I (90%): Bone (made by osteoblasts), Skin, Tendons (dentin, fascia, cornea, late wound repair)
II: Cartilage (incl hyaline)
III. Reticulin (skin), Blood vessels. uterus, fetal granulation tissue.
IV: Basement membrane, basal lamina, lens.

49
Q

In what disease is Type I collagen production decreased?

A

Osteogenesis Imperfecta type I. Autosomal dominant. Brittle bones. Blue sclerae (translucency of connective tissue over choroidal veins). Hearing loss (abnormal ossicles). Dental imperfections (dentin). Caused by deficient formation of triple helix of alpha collagen.

50
Q

In what disease is Type III collagen deficient?

A

Vascular-type Ehlers-Danlos.

51
Q

In what disease is Type IV collagen defective?

A

Alport syndrome. Also targeted by Abs in goodpastures.

52
Q

What steps of collagen synthesis occur within fibroblasts?

A

Synthesis, Hydroxylation, Glycosylation, formation of triple helix (RER)

53
Q

What amino acid best reflects collagen synthesis? Which are other are involved?

A

Glycine (1/3 of collagen). Gly-X-Y, X/Y = proline/lysine.

54
Q

What does collagen hydroxylation require and what disease represents a defect in this requirement?

A

Vitamin C is required for hydroxylation or proline/lysine. Deficiency = scurvy.

55
Q

In what structure does collagen leave the fibroblast? What disease represents a defect of forming this structure?

A

Procollagen = triple helix of three alpha chains. Osteogenesis imperfecta = problems forming triple helix.

56
Q

What modifications to collagen occur outside the fibroblast?

A

Peptide cleavage –> insoluble tropocollagen. Cross-linking staggered tropocollagen with covalent bonds.

57
Q

How does cross-linking of tropocollagen occur?

A

Copper-requiring lysl oxidase makes covalent lysine-hydroxylysine bonds to make collagen fibrils.

58
Q

What are the three types of Ehlers-Danlos?

A

Hypermobility type (joint instability, most common), Classical type (joint and skin symptoms (type V collagen), Vascular type (vascular and organ rupture, deficient type III).

59
Q

What is Menkes disease.

A

X-linked recessive connective tissue disease. Defect in ATP7A protein, responsible for copper absorption and transport. Impairs lysl oxidase, thus impairs tropocollagen crosslinking. Results in brittle, kinky hair, growth retardation, and hypotonia.

60
Q

What is elastin and where is it found?

A

Stretchy protein in skin, lungs, large arteries, elastic ligaments, vocal cords, and ligamenta flava (connect vertebrae)

61
Q

How is elastin composed/structured?

A

Rich in non-hydroxylated proline, glycine and lysine. Tropoelastin stabilized with fibrillin scaffolding. Cross-linking takes place extracellularly and gives elastin its elastic properties.

62
Q

How is elastin broken down? What inhibits this?

A

Broken down by elastase. Elastase inhibited by alpha 1 antitrypsin.

63
Q

What is the defect in Marfan syndrome?

A

In fibrillin, a glycoprotein that forms a sheath around elastin.

64
Q

What does alpha 1 antitrypsin cause?

A

Emphysema, due to excess elastase activity.

Biochemistry (11 decks)

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