Biochemistry

Front 1

What is heterochromatin

Back 1

Condensed chromatin, appears dark in EM

Front 2

What is euchromatin

Back 2

Less condensed chromatin, appears lighter in EM

Front 3

Why is important dna methylation?

Back 3

Adenine and cytosine methylation in dna replication, allows mismatch repair enzymes to distinguish between old and new strands

Dna methylation at CpG represses transcription

Hint 3

CpG methylation makes dna mute

Front 4

What does histone methylation?

Back 4

It Usually represses transcription but can activate in some cases

Hint 4

Histone methylation mostly make dna mute

Front 5

What does histone acetylation

Back 5

Relaxes dna coiling, allowing transcription

Hint 5

Histone acetylation makes dna active

Front 6

Amino acids necessary for purine synthesis

Back 6

Glycine, aspartate, glutamine

Front 7

Why are histones positively charged

Back 7

A lot of lysine and arginine, dna is negatively charged due to phosphate groups

Front 8

Rate limiting enzyme for pyrimidine synthesis

Back 8

Carbamoyl phosphate snythtase II, requires atp, CO2 and nitrogen source is glutamine, cps II is found in cytosol

Front 9

Which are the nucleotide synthesis interfering drugs

Back 9

-Leflunomide inhibits dihydroorotate dehydrogenase

-hydroxyurea inhibits ribonucleotide reductase

-5Flourouracil inhibits thymidylate synthase (⬇dTMP)

-Methotrexate, trimethoprim amd pyrimethamine inhibit dihydrofolate reductase in humans, bacteria and protozoa respectively (⬇dTMP)

-Mycophenolate inhibits IMP dehydrogenase

- 6 mercaptopurine and prodrug azathioprine inhibit de novo synthesis of purines

Front 10

how does adenosine deaminase compromised deficiency?

Back 10

Adenosine deaminase increase ATP and dATP leading to inhibition of ribonucleotide reductase ->prevents DNA synthesis and decrease lymphocytes

Adenosine is toxic to lymphocytes decreasing humoral and cellular immunity

Front 11

What is Lesch-nyhan syndrome?

Back 11

X-Linked, absence of HGPRT, which converts hypoxanthine in IMP, guanosine in GMP, causing hyperuricemia, gout, self mutilation, intellectual disability and dystonia

Front 12

Origin of replication

Back 12

base pair in genome where DNA replication begins, single in procaryotes and multiple in eukaryotes

Front 13

Replication fork

Back 13

Y-shaped region along DNA template whereleading and lagging strands are synthesized

Front 14

Helicase

Back 14

Unwinds DNA template at replication fork

Front 15

Single-strandedbinding proteins

Back 15

Prevent strands from reannealing

Front 16

DNAtopoisomerases

Back 16

Create a single- or double-stranded break in thehelix to add or remove supercoils.

flouroquinolones topoisomerase II and IV

Etoposide/teniposide eukaryotic topoisomerase

Front 17

Primase

Back 17

Makes an RNA primer on which DNApolymerase III can initiate replication

Front 18

DNA Polymerase III

Back 18

DNA polymerase III has 5′ 3′ synthesis andproofreads with 3′ 5′ exonuclease.

Front 19

DNA polymerase I

Back 19

Degrades RNA primer;replaces it with DNA

Front 20

DNA ligase

Back 20

Catalyzes the formation of a phosphodiesterbond within a strand of double-stranded DNA

Front 21

Telomerase

Back 21

An RNA-dependent DNA polymerase that addsDNA to 3′ ends of chromosomes to avoid lossof genetic material with every duplication

Front 22

what is a transition

Back 22

purine to purine substitution or pyrimidine to pyrimidine

Front 23

what is a transversion

Back 23

purine to pyrimidine substitution or pyrimidine to purine

Front 24

severity of substitutions in DNA mutation

Back 24

severity of damage silent<

Front 25

What is a silent substitution

Back 25

Nucleotide substitution but codes for same(synonymous) amino acid; often base changein 3rd position of codon

Front 26

What is a missense substitution

Back 26

Nucleotide substitution resulting in changedamino acid.

Hint 26

sickle cell disease

Front 27

What is a nonsense substitution

Back 27

Nucleotide substitution resulting in early stopcodon. Usually results in nonfunctionalprotein.

Front 28

What is a frameshift mutation

Back 28

Deletion or insertion of a number of nucleotidesnot divisible by 3, resulting in misreading ofall nucleotides downstream. Protein may beshorter or longer, and its function may bedisrupted or altered

Front 29

What is a splice site mutation

Back 29

Mutation at a splice site-> retained intron inthe mRNA ->protein with impaired or alteredfunction

Front 30

Nucleotide excisionrepair

Back 30

Repairs bulky helix-distortinglesions. Occurs in G1. Specific endonucleases release theoligonucleotides containing damaged bases;DNA polymerase and ligase fill and reseal thegap

Xeroderma pigmentosum

Hint 30

single strand DNA repair

Front 31

Base excision repair

Back 31

Base-specific glycosylase removes altered baseand creates AP site (apurinic/apyrimidinic).One or more nucleotides are removed byAP-endonuclease, which cleaves the 5′ end.Lyase cleaves the 3′ end. DNA polymerase-βfills the gap and DNA ligase seals it.

Hint 31

single strand DNA repair

Front 32

Mismatch repair

Back 32

Newly synthesized strand is recognized,mismatched nucleotides are removed, occurs in G2

Hint 32

single strand DNA repair

Front 33

mRNA start codons

Back 33

AUG

Front 34

mRNA stop codons

Back 34

UGA, UAA, UAG