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STEP 1 Review > Molecular and Cellular Biochemistry Review > Flashcards

Molecular and Cellular Biochemistry Review Flashcards

1
Q

Chromatin structure

A

Negatively charged DNA loops twice around histone octamer to form a bead, composed of H2A, H2B, H3, and H4 (each x2). Linker has H1 outside of nucleosome core.

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2
Q

Histone methylation

A

Usually represses DNA transcription, can activate in some cases.

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3
Q

Histone acetylation

A

Makes DNA relax and available for transcription.

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4
Q

GC bond has XXX H-bonds

AT has?

A

GC has 3. More GC, higher melting point

AT has 2.

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5
Q

How to make uracil from cytosine?

A

Deaminate

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6
Q

Amino acids necessary for purine synthesis

A

Glycine, aspartate, glutamine

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7
Q

Nucleoside?

A

Base plus sugar,

Nucleotide has phosphates.

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8
Q

Leflunomide

A

Blocks dihydroorotate dehydrogenase

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9
Q

Mycophenolate and ribavirin

A

Inhibits IMP dehydrogenase, prevents GMP creation from IMP

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10
Q

Hydroxyurea

A

Inhibits ribonucleotide reductase

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11
Q

What drugs work like methotrexate in bacteria and protozoa

A

Trimethoprim, pyrimethamine

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12
Q

Amino acids necessary for pyrimidine synthesis

A

Glutamine, aspartate.

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13
Q

Lesch-Nyhan syndrome

A

No HGPRT, XR inheritance. Causes hyperuricimia, gout, pissed off, retarded, dystonia. Treat with allopurinol or febuxostat.

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14
Q

Which AA’s are coded by only one codon?

A

Methionine and tryptophan

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15
Q

DNA polymerase III

A

Prokaryotic only, builds in 5-3 direction. Has 3-5 exonuclease activity which will proofread.

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16
Q

DNA polymerase I

A

Prokaryotic. Degrades RNA primer and replaces it with DNA. Has 5-3 exonuclease.

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17
Q

Frameshift mutations cause…

A

Shorter proteins due to deletion or insertion of nucleotides not dividuble by 3. Duchenne muscular dystrophy is a good example

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18
Q

Transition vs transversion

A

Purine to Purine (A to G) or pyrimidine to pyrimidine (C to T) is transition

Transversion is purine to pyrimidine, or pyrimidine to purine

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19
Q

Nucleotide excision repair

A

Specific endonucleases remove entire damaged nucleotide sequence. DNA polymerase and ligase fill in. Repairs bulky helix-distorting lesions like pyrimidine dimers.

Defective in xeroderma pigmentosum

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20
Q

Xeroderma pigmentosum

A

Defective nucleotide excsion repair cannot remove thymidine dimers due to UV exposure. Increased risk of cancer.

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21
Q

Base excision repair

A

Base specific glycosylase recognizes the altered base and cuts JUST the base out creating an AP site. AP endonuclease cuts out the rest of the nucleotide and DNA polymerase B fills in the gap.

Repairs spontaneous deamination

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22
Q

Mismatch repair

A

Newly synthesized strand is recognized and mismatched nucleotides are removed. Faulty in HNPCC.

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23
Q

Double stranded DNA repair…

A

Nonhomologous end joining. If there is a DS break like in radiation.

Mutated in ataxia telangiectasia.

Also NHEJ is done in VDJ recombination. so ATM has immunodeficiency too.

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24
Q

Stop codons

A

UAG
UAA
UGA

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25
Q

Where does promoter sit?

Where is enhancer?

A

Usually 70 bp upstream, usually at TATA and CAAT sequences. Promoter mutation decreases transcription.

Can be anywhere, same with silencers.

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26
Q

RNA polymerase 1
RNA polymerase 2
RNA polymerase 3

A

Makes ribosomal RNA
Makes mRNA
Makes tRNA

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27
Q

Alphaamanitin

A

Blocks RNA polymerase II, and causes severe hepatotoxicity.

28
Q

Prokaryotic RNA polymerase

A

Has only 1 type that makes all 3 kinds of RNA

29
Q

RNA processing

A

Nucleus there is 7G cap at 5’ end
Polyadenylation and splicing out of introns.

Then transported out of nucleus. where it is translated

30
Q

P-bodies

A

Where mRNA quality control occurs. Contains exonucleases, decapping enzymes, and microRNAS.

31
Q

Splicing

A

snRNPs combine with RNA to form spliceosome, creates lariat intermediate, and lariate is removed to join the exons.

32
Q

Anti U1 RNP antibodies

A

Seen in mixed connective tissue disease

33
Q

Anti-Smith Antibodies

A

Anti-snrnp seen in SLE

34
Q

tRNA

A

90 nucleotides with a cloverleaf form. AA binds at 3’ end where CCA sits.

T-arm has thymidine pseudouracil and cytosine, which is necessary for tRNA and ribosome binding

D arm: has dihydrouricil residues for tRNA recognition by appropriate aminoactyl tRNA synthetase.

35
Q

T Arm vs D Arm

A

T arm for ribosomal binding

D arm for charging

36
Q

Protein synthesis initiated by

A

GTP hydrolysis and initiation factors building the 40S with 60S.

37
Q

What is ATP used for in translation?

A

Charging

GTP is used for translocation

38
Q

Chaperone protein

A

Facilitates or maintains folding.

39
Q

Are CDKs always active?

A

No they are always around, but need cyclins to be activated.

40
Q

Rough ER, cells that half a lot of it

A

Site of synthesis of secretory proteins. Also site of N-linked oligosaccharide addition.

Neurons, goblet cells, plasma cells

41
Q

Free ribosomess

A

Where cytosolic and organellar proteins are made

42
Q

Smooth SR

A

Site of steroid synthesis and detoxification. Liver hepatocytes and steroid hormone producing cells of the adrenal cortex and gonads are rich in SER

43
Q

N-oligosaccarides added to

O-oligosaccharides added to

A

Asparagine

Serine/threonine

44
Q

Mannose 6 phosphate added to

A

Proteins that are going to be trafficked to lysosomes.

45
Q

I cell disease

A

Lysosomal storage disorder that is due to a defect in phosphotransferase. Golgi does not phosphorylate mannose, so proteins are secreted extracellularly rather than sent to the lysosome for degradation.

Results in coarse facial features, clouded corneas, restricted joint movement, high plasma levels of lysosomal enzymes

46
Q

Signal recognition peptide

A

Abundant cytosolic ribonucleoprotein that traffics proteins to the RER. If there is no SRP then proteins accumulate in the cytosol

47
Q

COPI
COPII
Clathrin

A

Retrograde from golgi to ER
Anterograde from ER to golgi
Trans-golgi to lysosomes, or from plasma embrades to endosomes.

48
Q

Peroxisome

A

Site of very long chain fatty acid metabolism, lack of peroxisomes causes zellweger syndrome – which causes neurological deficits

49
Q

Microtubule structure

A

Alpha and beta heterodimers with GTP.

50
Q

Chediak-Higashi Synndrome

A

Defect in LYST, causes fucked upp microtubules. Albanism, increased infections, granular macrophages and neutrophils, neuropathy.

51
Q

Vimentin stains

A

Connective tissue

52
Q

Desmin

A

stains muscle tissue

53
Q

Cytokeratin stains

A

epithelial cells

54
Q

GFAP stains

A

Microglia

55
Q

Neurofilaments stain

A

Neurons

56
Q

Microtubule drugs

A

Mebendazole, griseofulvil, cochicine, vincristine/vinblastine, paclitaxel

57
Q

Ouabain

A

Inhibits Na-K ATPase by binding to K+ site.

58
Q

Type 1 collagen

A

Bone, skin, tendon, late wound repair.

59
Q

Type 2 collagen

A

In cartilage, nucleus pulposis

60
Q

Type 3 Collagen

A

Invessels, granulation tissue. Vascular type ehler’s danlos

61
Q

Type 4 collagen

A

Basement membranes, lens, basal lamina Defective in alport syndrome. Targeted by autoanibodies in goodpasture syndrome

62
Q

Synthesis of collagen

A

Inside fibroblasts:

Translation of collagen alpha chains (pre-pro-collagen), usually Gly-X-Y. Glycine content best reflects collagen synthesis.

Hydroxylation of some proline and lysine residues which requires vitamin C. (inhibted in scurvy)

Glycosylation of pro-alpha-chain hydroxylysine residues and formation of procollagen (triple helix) via hydrogen and disulfide bonds. (osteogenesis imperfecta can’t form triple chains)

Exocytosis into extracellular space.

Cleavage of disulfide rich terminal regions making it tropocollagen

Reinforcement of many staggered tropocollagen molecules by covalent lysine-hydroxylysine cross linking- by copper containing lysyl oxidase. Problems with cross linking =ehler’s danlos.

Decreases copper is menkes disease. Bad collagen

63
Q

Osteogenesis imperfecta

A

Problems forming triple helix with hydrogen bonds and disulfide bonds. Causes brittle bones. Can be autosomal dominant.

Multiple fractures, blue sclera, hearing loss, dental imperfections.

64
Q

Ehler’s Danlos syndrome

A

Problem with cross linking of collagen. Leads to hyperextensible skin, bleeding, easy bruising. Hypermobile joints.

Hypermobility type is most common.

Classical type (joint and skin) is caused by a mutation in type V collagen.

Vascular type (vascular/organ rupture) deficient type 3 collagen.

65
Q

Menkes Disease

A

Deficient lysyl oxidase due to impaired copper absorption and transport. Brittle kinky hair and growth retardation

66
Q

Elastin

A

Stretchy protein in skin, lungs, arteries, ligamenta flava. Rich in proline and glysine (nonhydroxylated). Tropoelastin with fibrillin scaffolding. Cross linking takes place extracellularly.

STEP 1 Review (21 decks)

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