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Can fats be converted to glucose during starvation? What about glucose converted to fats?
No, humans don’t have the enzymes to do so. Yes, in the liver: glu = converted to FAs, which are converted to triacylglycerides
Can bases catalyze peptide bond hydrolysis?
Yep —> can lose enzyme activity
PROKS HAVE CIRCULAR DNA AND EUKS HAVE LINEAR Ds DNA
YOU BETTER REMEMBER THIS AND KNOW WHICH ENZYMES ACT ACCORDINGLY
Bohr effect
Hemoglobin’s affinity to O2 based on pH and CO2; its affinity to O2 dec when low pH and high CO2
GLUT1 vs GLUT2 vs GLUT4
glucose transporter into cell vs glucose transporter into cell; found in liver, intestines, kidneys, beta islet cells of pancreas vs glucose transporter into cell, insulin-regulated, found in adipose tissue and striated muscle (ie. skel and cardiac muscle). All to do glycolysis
What does it mean to be a colligative property?
depends on amount of molec, not identity
What’s the general idea of Michaelis and Menten? What’s the eqn? What are the 4 asmptns?
find K_M at 1/2Vmax. V = (Vmax*[S])/(Km+[S]) where V=initial vel
COFACTORS ARE NOT PART OF M-M KINETICS
1) this eqn = only used to describe initial rxn vel
2) steady state approximation (ie. [S]»>[P])
3) free ligand approximation (ie. [S]»>[E])
4) rapid equil approximation (ie. Lower Km means higher enzyme-substrate affinity)
What are prostaglandins? What can prevent their production?
Unsaturated CAs derived from arachidonic acid that act as autocrine and paracrine signal molecs; they help regulate synthesis of cAMP; also help with inflammation, pain and smooth muscle function. NSAIDS like aspirin
x-ray crystallography vs fluorescence in situ hybridization (FISH)
determines proteins’ 3D structure vs molec technique that uses fluorescent probes to bind to DNA to visualize their action)
Gs vs Gi vs Gq
Activates adenylate cyclase to inc cAMP vs inhibits adenylate cyclase to dec cAMP vs activates phospholipase C to cleave phospholipid from membrane into PIP2 which then gets cleaved into DAG and IP3, IP3 opens Ca channels in ER which inc Ca in cell
Pos inducible operon vs pos repressible operon vs neg inducible operon vs neg repressible operon
activator protein nmlly can’t bind to DNA; inducer molec binds to activator –> activator binds to DNA –> transcpxn vs activator protein always bind to DNA –> constant transcpxn until inducer molec binds to activator protein –> stop transcpxn vs absence of lactose –> repressor binds to operator –> no transcpxn; presence of lactose –> (allo)lactose binds to repressor –> repressor can’t bind to operator –> transcpxn (this described lac operon coding proteins for lactose metab) vs low conc of trp –> repressor can’t bind to operator –> transcpxn; high conc of trp –> trp (as inducer molec) binds to repressor –> repressor binds to DNA –> stops transcpxn (this described trp operon coding proteins for trp biosynthesis)
What are operons? Pos vs neg control in gene expression
Inducible or repressible cluster of genes transcribed as single mRNA IN PROKS; no euks!
Presence of activator protein —> turn on gene expression vs gene expression will stay on till a repressor protein turns it off
G protein receptors
Have alpha, beta and gamma subunits; when activated, alpha dissociates and binds w/ GTP and activate necessary enzymes (like adenylate cyclase); after doing its function, GTP becomes GDP —> alpha rebinds to beta and gamma subunits. Initiates second messenger cascade like enzyme linked receptors
Transition mutation. Are translocations frameshift mutations?
a type of point mutation; changes from purine to purine, pyr to pyr
nope
DeltaG for anabolic (monomer to polymer) vs catabolic (polymer to monomer) rxns
> 0, energy-requiring rxns vs < 0, energy-releasing rxns
A 3-base system can code how many aa?
64 aa: 4-nitrogen-bases^3-letter-codon