Biochem Block 2 Enzymes
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- Phosphocreatine
-
in skeletal muscle
uses ATP to store E - Maltose
- reducing disacchride of made of 2 glucoses
- Lactose
- reducing sugar made of glactose and glucose
- Sucrose
- non-reducing sugar made of glucose and fructose
- law of mass action
- Vmax is proportional to collisons btwn reactants
- Competitive Inhibitor
-
I binds to E
I inc apparent Km
Vmax is unaffected - Non-Competive Inhibitor
-
binds E and ES
Vmax is decreased
Km can remain unchanged - Uncompetitive Inhibitor
-
I binds to ES
apparent Km dec
Vmax dec - GLUT 1 & GLUT 3
-
basal glucose uptake
Km = 1
all cells - GLUT 2
-
live and B-cells
Km = 15-20
glu uptake prop [blood glu]
inc glu uptake = inc insulin = carb storage - GLUT 4
-
Km = 5
skeletal muscle & fat cells
insulin inc = translocation to plasma memb - GLUT 5
- fructose uptake in small intestine
- SGLT 1
-
sodium glucose cotransporter
small intestine
glucose & galactose uptake - Hexokinase
-
low Km
use Mg-ATP
inhibited by product inhibitied by G6P - Glucokinase
-
liver and pancreatic b-cells
higher Km
not inhibited by G6P - Glycogen Phosphorylase
-
cleaves alpha 1-4 bonds
non-reducing ends >4 from branch
uses PLP
releases G1P - Phospholucomutase
- G1P --> G6P
- Glucose-6-phosphotase
- in liver, hydrolyzes G-6-P to glucose
- debranching enzyme
-
transfers block of 3 glu from a-1,6 branch to diff a-1,4 AND hydrolyzes the remaining a-1,6 glucose unit
releases 1 free glucose - UDP-glucose pyrophosphorylase
- rxn is readily reversible driven by hydrolysis of pyrophosphate
- pyrophosphatase
- hydrolyzes pyrophosphate PPi
- Glycogen Synthase
- catalyzes the elongation of non-reducing termini of glycogen forming a-1,4 linkages
- nucleoside diphosphate kinase
-
UDP --> UTP
readily reversible Km ~1 - Glycogenin
- tyrosine dimer
- Branching enzyme
- 7 glu residues to a 6 position on a nearby chain
- Factors that increase glycogen breakdown
- epinephrine, glucagon, AMP, Ca++
- Factors that decrease glycogen synthesis
- insulin, ATP, G-6-P, glucose (liver)
- Glycogen Phosphoylase
-
dimer
T-state = inactive
R-state = active
a - phosphorylated - active
b-not phos - inactive - Phosphorylase Kinase
-
phos glycogen phosphorylase a
activated by Ca & PKA phos -
Phosphoprotein phosphatase 1
PP1 -
dephos glycogen phosphorylase
inactivated by PKA P of I
activated by insulin TRK P of R -
Phosphofructose Kinase
activators?
Inhibitors? -
ATP, Citrate, dec pH - feedback inhib changes Km
AMP, ADP, Pi - allosteric activators that compete w/ ATP for binding site
F26BP => activator - Fructose 2,6 Bisphosphate
-
made by PFK2 + ATP
degraded by FBPase 2 - Phosphofructokinase 2
- makes F26BP and is stimulated by insulin activation of phosphoprotien phosphotase
- Fructose bisphosphatase 2
-
breaks F26BP -> F6P
Activated by glucagon activation of cAMP dependent PKs - Aldolase
- (glycolysis) uses Schiff base
- Triosephoasphate isomerase (TIM)
-
ketose -> aldose
driven by removal of GAP
(glycolysis) - Glyceraldehyde-3-phosphate dehydrogenase
-
(glycolysis)
ox-red
makes NADH
makes high E phosphate bond (mixed anhydride)
inactivated by heavy metals (arsenate) - Phosphoglycerate Kinase
-
(glycolysis)
substrate level phosphorylation -> ATP - Phosphoglycerate Mutase
-
(glycolysis)
shifts Phos from C3 to C2 - Enolase
-
(glycolysis)
dehydration creating high E posphoenol bond
driven by entropy (H2O loss) - Pyruvate Kinase
-
(glycolysis)
substrate level phosphorlyation -> ATP - Pyruvate Kinase Regulation
-
feedforward activation by F16BP
feedback inhibition by ATP & alanine
inactivated by phos by cAMP PKs - Enzymes Required for Fructose to enter glycolysis (3)
-
fructokinase
fructose 1 phospate aldolase
triose kinase - Enzymes Required for Glactose to enter glycolysis (3)
-
galactose kinase
gal-1-phos uridyl transferase
UDP gal 4 epimerase -> UDP glu -
Effects of insulin on glycolysis?
glycagon? -
insulin - stimulates
glucagon - inhibits - Pyruvate Carboxylase
- allosterically regulated biotin dependent enzyme -> OAA
- PEP carboykinase
- decarboylates OAA -> PEP at expense of GTP
- Fructose-1,6-Bisphosphatase
-
F-16-BP -> F6P
inhibited by AMP
activated by ATP - Glucose-6-phosphatase (G6Pase)
-
G6P -> Glu
rich in liver but absent in muscle
luminal side of ER facilitated by memb transporters in ER memb