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MS1 - MCBD > Week 1 Review > Flashcards

Week 1 Review Flashcards

1
Q

Which AAs are negatively charged?

A

The ones with “acid” in the name.

Glutamic acid (E) and aspartic acid (D).

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2
Q

Which AAs are negatively charged?

A

The ones with acid in the name.

Glutamic acid and aspartic acid.

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3
Q

What is the difference between a nucleoside and a nucleotide?

A

NucleoTides have phosphaTes

NucleoSides are a base + Sugar

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4
Q

What are the steps in DNA replication?

A
  1. Helicase unzips
  2. SSBs keep strands apart
  3. Primase makes RNA primer
  4. DNA polymerase alpha comes in
  5. Polymerase happens in 5’ to 3’ direction
  6. Ligase stitches together Okazaki fragments in lagging strand
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5
Q

What are the steps in transcription?

A
  1. GTFs bind at promoter, making a transcription bubble
  2. RNAPII comes in and binds GTFs
  3. Other TFs bind enhancer sequences
  4. Activating TFs bind to coactivators that loop around to contact RNAPII for activation and transcription initiation
  5. Transcription goes until terminator sequence is reached
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6
Q

Explain the structure of a mammalian gene.

A

DNA strands associate with proteins called histones which assemble to form nucleosomes, DNA in between nucleosomes are called linker DNA sections. DNA/nucleosome complexes form 10nm chromatin fibers —> 30nm chromatin fibers —> looped domains —> heterochromatin —> chromosome

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7
Q

Describe the processing reactions that occur to a mRNA transcript.

A
  • 5’ cap is added to protect mRNA against exonuclease and it signals to translation machinery that it is indeed a mRNA.
  • poly-A tail is added as a signal that it should go to the cytosol and it also controls the stability of the mRNA in the cytoplasm.
  • splicing: leave exons, throw away introns.

EXons are EXpressed.

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8
Q

Describe the processing reactions that occur to a mRNA transcript.

A
  • 5’ cap is added to protect mRNA against exonuclease and it signals to translation machinery that it is indeed a mRNA.
  • poly-A tail is added as a signal that it should go to the cytosol and it also controls the stability of the mRNA in the cytoplasm.
  • splicing: leave exons, throw away introns.

EXons are EXpressed.

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9
Q

What are the amino acids with nonpolar side chains?

A

GLAM VIP WYF

(G) glycine
(L) leucine
(A) alanine
(M) methionine
(V) valine
(I) isoleucine
(P) proline
(W) tryptophan
(Y) tyrosine
(F) phenylalanine
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10
Q

Name two protein modifications that are typically only found on extracellular proteins (cell surface proteins, secreted proteins).

A

Glycosylation - addition of sugar

Disulfide bonding

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11
Q

Define Kd and how it relates to Koff and Kon. What does it mean if Kd is a small number?

A

Kd is the dissociation constant and is equal to Koff/Kon. Small Kd = high affinity

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12
Q

Where is the cellular location of hormone receptors?

A

Inside the cell, sometimes in the nucleus.

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13
Q

Name five types of receptors and their corresponding effectors.

A
  1. GPCR - adenylyl cyclase
  2. Hormone receptors - gene products are the effector
  3. Cytokine receptors - tyrosine kinase via JAK/STAT
  4. Ligand-gated ion channel (it is the effector)
  5. GF receptors have intrinsic tyrosine kinase activity (they are the effector)
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14
Q

What units are on the x and y axises of a dose-response curve?

A

y: % max effect
x: log[agonist]

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15
Q

What is EC50?

A

The concentration of drug that produces 50% max effect - a measure of potency. Lower EC50 = higher potency.

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16
Q

Kd is a measure of _______. The lower the Kd, the _________.

A

Kd is a measure of affinity. The lower the Kd, the higher the affinity

17
Q

Describe physical and chemical antagonists.

A
  • physiological antagonists produce an opposing effect through an alternate biological pathway
  • chemical antagonists interact directly with the agonist to prevent receptor binding
18
Q

How do competitive antagonists shift the dose-response curve?

What about noncompetitive antagonists?

What about allosteric antagonists?

A

Competitive antagonists are surmountable and if enough agonist is added Emax can be achieved. So the D-R curve is shifted to the right.

Noncompetitive antagonists = IRREVERSIBLE antagonists and are not surmountable. D-R curve is shifted down.

Allosteric antagonists shift the D-R curve down.

19
Q

What is the equation for therapeutic index?

A

TI = TD50/ED50

toxic dose for 50% of pop./effective dose for 50% of the pop.

20
Q

Is a drug with a high therapeutic index safe?

A

Yes!

21
Q

In what congenital disorder are patients overly friendly? What is the genetic defect?

A

Williams Syndrome - microdeletion of 26 genes of 7q

22
Q

In Prader-Willi, which gene is imprinted and which gene is deleted?

A

Mom’s gene is imprinted and there is a 4-5 mega base-pair deletion of the PWS-AS critical region on the Paternal chromosome 15.

23
Q

In Angelman’s syndrome, which gene is imprinted and which gene is deleted?

A

Dad’s gene is imprinted and there is a 4-5 mega base-pair deletion of the PWS-AS critical region on Mom’s (angels are females) chromosome 15.

24
Q

In Angelman’s syndrome, which gene is imprinted and which gene is deleted?

A

Dad’s gene is imprinted and Mom’s (angels are females) is deleted.

25
Q

Which amino acids can be methylated? Which can be acetylated? What effect does this have on histone-DNA interactions and therefore on gene expression?

A

LAM - lysine, arginine can be methylated. Methylation adds positive charge to increase ionic interactions between DNA and histones - Mutes gene expression.

Lysine can be acetylated. Acetylation gets rid of positive charge on lysine to decrease ionic interaction between histones and DNA. Activates gene expression.

26
Q

Name the two readers and what they read.

A

Bromodomains read acetylated lysines (A-B).

Chromodomains read methylated lysines.

27
Q

Name the two readers and what they read.

A

Bromodomains read acetylated lysines (A-B).

Chromodomains read methylated lysines and arginines.

28
Q

What is the equation for catalytic specificity?

A

Catalytic specificity = kcat/Km

29
Q

What are Xist and Tsix?

A

Noncoding RNAs that are involved in X inactivation.

Xist is coded for on the to-be-inactivated X chromosome and physically coats the X chromosome, triggering silencing.

Xist is coded for on both chromosomes, but Tsix blocks it from inactivating one of the chromosomes.

MS1 - MCBD (17 decks)

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