DIT Biochem 1 Flashcards
What 5substance are going into purines? What donates what?
And what go into pyrimadines?
CAG
Glycine (C), Glutamine (N), Aspartate (N), CO2 (C) and tetrahydrofolate (C)
Pyr: Aspartate, carbamoyl phosphate (CO2 and glutamine and ATP make up carbamoyl phosphate)
What enzyme is rate limiting step of pyrimidine synthesis?
Carbamoyl phosphate synthetase II takes Glut and CO2 and 2 ATP to make carbamoyl phosphate
What does 5 FU block?
Thymidylate synthase (the enzyme to make dTMP from dUMP, the same one that needs THF)
Baby with failure to thrive, megaloblastic anemia, hyper segmented neutrophil, that can’t be cured with folate or B12 and no hyperammonemia? Tx?
Orotic aciduria is unable to make orotic acid into UMP.
Tx is UMP to bypass enzyme mutation
Prokaryotic polymerases?
DNA polym III is for making a leading strand and lagging strand
DNA polym I is to replace RNA primers
DNA ligase closes the last bit up
Eukaryotic polymerases?
DNA polym alpha needs no primers and is for lagging strands
DNA polym Delta is on leaDing strand
DNA polym Beta is Broken DNA repair
DNA polym gamma is for mitochondria
What type of DNA damage is repaired in nucleotide excision repair?
What if deficient?
Nucleotide Excision repair
Dimers cause kink in DNA
Endonuclease remove nucleotide
DNA polym inserts new nucleotide
DNA ligase closes it up
Xeroderma pigmentosa is deficiency and dimers happen from ultraviolet light
What type of damage is fixed with base excision repair?
Remove damaged base (apurine or apyrimadine site)
4 steps Glycosolase removes damaged base Endonuclase cuts DNA and removes sugar DNA poly puts in new nucleotide DNA ligase closes it up
(last three steps are just like nucleotide excision repair)
NEEDED to repair from toxic damage
What DNA repair is for fixing damaging to both strands?
Damage to this causes what?
Nonhomologu end joining problem causers ataxia telangiectasia
IgA deficiency, cerebellar ataxia, high AFP after 8 months of age. SENSITIVE to ionizing radiation (The A disease on page 213 FA)
Explain lac operon
There is a CAP which is to activate and a lac repressor. Each binds their metabolite and if no glucose (CAP is bound to DNA) and lactose is present (lactose metab binds repressor so it can’t bind DNA) and operon is on!
Where does aminoacylt tRNA synthetase work?
3’ end of tRNA to load it at the CCA
What allows for a tRNA to come in and bind to A site of 40s subunit in eukaryotes? and in prokaryotes?
GTP and
Euckaryotes: Elongation Factor 2 (diphtheria and exotoxin A in pseudomonas)
Prokaryotes is elongation factor G
What makes collagen and fibrillin and elastin?
fibroblasts (fibrous support network proteins)
Mnemonic for X recessive?
Be Wise Fools GOLD Heeds Silly Hope
Brutons X linked aggamagl Wiskot Aldrich Fabry G6PD Ocular albinism Lesch Nyhan Duchenne (and Becker) Hunter Syndrome Hemophilia A and B Ornithine transcarbomylase def
Angelman is what genetically?
MAMA Maternal gene Angelman Mood (inappropriate laugh) Ataxia
chromosome 15
happy puppet
What metastasizes to the brain? mnemonic alert
Lots of Bad Stuff Kills Glia
Lung Breast Skin (melanoma) Kidney (RCC) GI
Hexokinase vs glucokinase? locaiton?
Km?
Vmax?
Insulin induction?
Feedback inhib by Gluc6P?
Associated with MODY?
Glucokinase in glucose controlling tissue
G has higher Km (needs a lot of, duh, b/c don’t want liver to hog all the glucose)
G has high Vm (duh, if there is a ton of sugar, do something with it)
G is insulin induction, duh
G is inhibited b/c you don’t want to waste effort
G is associated with maturity onset diabetes of the young MODY