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CU DENVER / Business / INTB 3611 / How a chemist speeds a reaction: increase temperature to go over barri

How a chemist speeds a reaction: increase temperature to go over barri

How a chemist speeds a reaction: increase temperature to go over barri


School: University of Colorado Denver
Department: Business
Course: General Cell Biology
Professor: Bradley stith
Term: Spring 2017
Tags: Biology and Cell
Cost: 50
Name: BIOL 3611 exam 2 study guide
Description: This guide gives an outline of what will be covered on exam 2. Be sure to look back at the figures provided by the professor when reading through and practice answering questions. Good luck!
Uploaded: 03/12/2017
4 Pages 85 Views 4 Unlocks

BIOL 3611 Exam 2 Study guide

How a chemist speeds a reaction: increase temperature to go over barrier?

❖ catalysts:

▪ speed up attainment of equilibrium (where ΔG = 0) so enzyme could speed up  forward reaction (a???? b) or reverse reaction (a????b).

▪ are not used up

▪ interact reversibly (< == >) with substrate (vs. irreversibly ????)

▪ lowers the activation energy barrier (Ea)

o see fig. 6-1

o how a chemist speeds a reaction: increase temperature to go over barrier o how an enzyme speeds up the reaction: lowers the barrier not average  energy of a molecule

o know what’s on the axes of the diagrams

How an enzyme speeds up the reaction?

If you want to learn more check out What causes cyclical unemployment?

❖ induces fit model

▪ substrate binds to the active site of the enzyme

▪ it forms new weak bonds with the r groups of the protein  

▪ weak bonds pull on the substrate and protein

▪ both substrate and the protein are distorted

o bond breaks more easily

❖ Km

▪ Km is a measure of the affinity between the substrate and the enzyme’s active site o Low Km means high affinity (lots of weak bonds)

o High Km means low affinity

∙ a competitive inhibitor can make Km higher  

o would reduce the affinity between substrate and enzyme

Why is enzyme regulation important?

We also discuss several other topics like What are the five ethics of research?

❖ Vmax

▪ maximal chemical reaction rate (initial reaction velocity)

o increases if you add more enzyme

∙ amount of enzyme/active sites is limiting

❖ Enzyme regulation Don't forget about the age old question of Which tissue allows our body to respond to stimuli?

▪ competitive inhibitors:

o resemble the substrate

∙ bind to the active site of an enzyme

∙ distort the protein to inhibit enzyme activity

o human body does not use or make competitive inhibitors

▪ allosteric regulation

o the body makes allosteric activators or inhibitors

o forms weak bonds to protein in the spaces between subunits of an enzyme  o allosteric regulator binds to site other than active site

o distorts the enzyme to turn it on or off

▪ phosphorylation

o add a phosphate group to a protein

∙ phosphate functional group is very negative Don't forget about the age old question of When does intraindustry trade happen?

o new weak ionic bonds will form and distort the protein

o this distortion can turn on the protein or turn it off Don't forget about the age old question of How does entry of ca ions into dendritic spine cause ampa receptors to move into postsynaptic membrane?

❖ Membrane fluidity

▪ if a membrane is too fluid or not fluid enough, the membrane will not function ▪ determined by:

o length of fatty acid chain If you want to learn more check out What is an example of a spontaneous mutation?

∙ longer chains mean more gel like, less fluid

∙ hydrophobic bond involved

o degree of unsaturation

∙ more double bonds mean more fluid

o cholesterol

o increase temperature means more fluid

❖ Membrane rafts

▪ Location of receptors, ion channels, and transporters

▪ Cholesterol, sphingolipids and glycolipids concentrated there

▪ Rafts are thicker

o sphingolipids have longer fatty acid tails that are saturated  

∙ straighter fatty acid chain means longer

▪ less fluid

o more hydrophobic interaction

❖ Types of movement across a membrane

▪ Simple diffusion

o Osmosis

o No energy

o –ΔG

o Jdiffusion = Jpassive transport = Jchemical + Jelectrical + Jconvection  

▪ Facilitated diffusion

o no ATP needed

o faster than simple diffusion

o charged molecule or ion moves down electrochemical gradient

o membrane protein involved

o two types

∙ channel

o like a big door (high flux)

▪ Porin

∙ carries water across membrane

o bacterial porin: a barrel of beta  

pleated sheets with a very wide pore

o human porin: four subunits

▪ ion channel

∙ only ions can cross

o changes the membrane potential

∙ two types

o ligand-gated ion channel

o voltage-gated ion channel

∙ carrier

o like a small door (low flux)

▪ slower than channel

▪ active transport

o indirect

∙ coupling of spontaneous (-∆G) sodium movement drives  

nonspontaneous +∆G movement of glucose into cell

∙ cotransport

∙ symport

∙ energy comes from movement of sodium (not ATP)

∙ carrier, not channel

o direct

∙ ATP drives nonspontaneous movement

❖ Membrane math

▪ Jtotal = [Jdiffusion or Jpassive transport] + Jactivet transport

▪ ∆G for movement across a membrane:

o ∆Ginward = RT ln ([x]in / [x]out) + ZFVm

o z is charge on ion (+1, -1, 0, etc.)

o f is 23062 (faraday’s number)

o Vm is membrane potential (volts)

▪ ∆Ginward = - ∆Goutward

▪ Nernst equation

o Vm = (RT/ZF) ln ([C]out/[C]in)

o Assumptions

∙ ignores active transport

∙ ignores convection

∙ only deals with the electrochemical gradient

❖ Signal transduction

▪ types

o Chemical mediators

∙ Hormones

o Kd = affinity of a receptor for a hormone

o Endocrine: through blood stream

o Paracrine: diffuses to nearby cells

o Autocrine: the secreting cell is the target cell

o Cell to cell contact

o Electrical

▪ Receptors

o Ligand gated

o G protein linked

o Kinase  

❖ Cell signaling pathways

▪ cAPM

o G proteins

∙ Hormone levels lower

∙ α subunit of G protein turns off

o GTP to GDP

∙ Beta and gamma subunits inhibit alpha  

∙ cAMP breaks down via phosphodiesterase

o Ion channel

∙ Nicotinic

o Binds ACH

o Na enters cell

o Membrane potential approaches 0 mV

o depolarize

∙ Muscarinic

o ACH binds to G protein coupled receptor

o Subunits bind K channel  

o K moves out of the cell

o Membrane potential approaches -90 mV

o hyperpolarize

o IP3-Ca release

∙ IP3 released by ACH and epinephrine

∙ PIP2

o NO (nitric oxide)

∙ No detail for exam 2

o Tyrosine kinase receptors

∙ No detail for exam 2

o Steroid

∙ No detail for exam 2

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