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92 Cards in this Set

  • Front
  • Back
alpha 1
uses q
alpha 2
i
beta 1
s
beta 2
s
M1
q
M2
i
M3
q
D1
s
D2
i
H1
q
H2
s
V1
q
V2
s
fxn V1
vascular sm m cxn
fxn V2
increase H20 perm and reabsorption in collecting tubules in kidney
fxn H1
mucus production (nasal and bronchial), cxn bronchioles, pruritis, pain
fxn D1
relaxes renal vascular sm m
fxn D2
modulates transmitter release, esp in brain
fxn M3
incr exocrine gland sxns
fxn M2
decr HR
fxn M1
CNS
fxn alpha 1
vascular sm m cxn GI, sphincter constriction, mydriasis, ejac,
fxn alpha 2
decr symp outflow, decr insulin, decr aq humor
fxn beta 1
incr HR, contractility, incr aq humor, incr renin, incr lipolysis
fxn beta 2
vasodilation BF to organs and mscls, bronchodilation, relax GI, incr glucagon, epp + NE rel
Gq path
phospholipase C converts lipids to PIP2
1) IP3->incr Ca internally
2) DAG->protein kinase C
Gs path
adenylcyclase convert ATP to cAMP->protein kinase A
Gi path
adenylcyclase decr cAMP->decr protein kinase A
which R use Gi
alpha 2, M2, D2
which R use Gs
beta 1,2, D1, H2, V2
which R use Gq
alpha 1, M1, H1, V1, M3
what need for nuclear transport?
NLS, NES
what need for ER
SRP
specific fxns of ER
-N link glycosyl
-folding by chaperones
-disulfide
-GPI anchor
KDEL=ER retention
what's signal for ER
KDEL means ER retention
fxn golgi
O link glyc and trim N link, if lyso add mannose6P
where syn of tg occur
in SER
golgi's role
protein sorting and packaging
getting into mito
uses TOM/TIM
Progressive Opthal
ANT to import ATP, mito poly delta, twinkle helicase
MELAS
aminoacyl of Lys nec to import (assoc w bipolar)
MNGIE
thymidphosphorylase to make nucleotide, resents with diarrhea/constipation
name 3 mito dz
Progress Ophthal, MNGIE, MELAS
what 3 things happen to start transcript
demethyl Histones, acetyl histones, demeth promoter
competit agonist: change Km
increases Km (need more substrate to compete)
competit agonist: Vmax
same
noncompetit agonist changes in Km, Vmax
Vmax lower, Km same
on plot, how do competit and noncompetit lines appear
competit=increase slope same x intercept (Vmax same)
noncompetit=increase x intercept, y intercept same (increasing slope)
is Km related to binding affinity?
no, to speed
exn use to plot enzyme rxn
1/v= 1/vmax + Km[S]/(Km + [S])
describe forms DNA when see them
A=R 10bp/turn, most DNA
B=11bp in RNA:DNA, dsRNA, or dehydration
Z=L hand turn
genomic library
has introns, nontranscribed regions, promoter
if wanted to make protein, and have the sequence stored, what use to make it from
cDNA (can use polyT to get mRNA
cDNA
no introns, only the sequence that codes mRNA
describe how, where splicing occurs
in splicesomes by snRNPs
describe difft choices vectors
plasmid=5kb
phage=20kb
YAC=1000kb
role peroxisome
detox
b oxidation LCFA
syn: cholesterol, plasmalogen (myelin) and bile acid
name peroxisomal dz
Zelweger (empty perox)
ALO (defect transport LCFA)
Phytanic acid problem
Phytanic acid problem presents with? tx?
decr night vision, tx by diet
problem in Zelweger
unable to import into peroxisomes
ALO (peroxisome dz) presents with what symptoms? what's the problem?
(peroxisome dz) neuro symptoms bc fa degradation myelin,
problem is transport LCFA
peroxisome have mem?
yes, 1 mem
how peroxisomes import? what do they need to import?
PEX5, need to import all proteins bc has none of its own DNA
role lysosomes
intracellular digest
what cell has lots and lots of lysosomes
phagocyte
if lysosomes leak what happens?
nothing bc the lysosomes are very acidic and the lysosome enz only work at acidic pH, not cell pH
lipofucsion
residual bodies after phago
is proteasome mem bound
nom soluble
role of proteasome
degrade protein labeled with Ubq
lipid anchored proteins on C face mem
fa, isoprenoid
lipid anchored proteins on E face
GPI
O linked gly occurs
golgi
T/F disulfide bonds formed in ER
T
what can use passive transport
small nonpolar like O2,CO2
hydrophobic-benzene
small polar uncharg ETOH, H2O
T/F thymidine dimers are across strands
F SAME STRAND
excision repair defect in xeroderma pigmentosum
uvr ABC endonuclease (can't repair thymidine dimers after exposure UV light)
alpha amanitin does what?
inhibits RNA poly II
describe initiation translation
RNA pol II opens DNA at promoter site (AT rich upstream seq, TATA, CAAT)
name types RNA poly
I makes rRNA
II makes mRNA
III makes tRNA
largest RNA? most abundant? smallest?
largest=mRNA
abundant=rRNA
smallest=tRNA
Massive, Rampant, Tiny
what charges tRNA
aminoacyl-tRNA synthetase, using ATP
all tRNA's have what seq
CCA at 3 end where aa is linked
describe ribosome steps
met sits in P site, incoming aa comes into A site,
hydrolyzes Met bond to tRNA, forms Met-aa bond and transfers that to E site
A=aminoacyl
P=peptidyl
E=
is GTP or ATP used for charging aa? for translocation?
ATP for activation
GTP for gripping and going places
if tRNA bond is incorrect what happens?
synthetase hydrolyzes
DNA poly used in prokaryo
DNA poly III elongates 5-3 and proofreads with 3-5 exonuclease,
DNA poly I excises RNA primer with 5-3 exonuclease
how many origins of replication in bac? virus? plasmid?
all 1, euk only with mutliple
describe single strand DNA repair
glycolase reognizes and removes damaged base, endo nuclease makes a break, exonuclease removes several neighboring bases, DNA poly fills in gap and DNA ligase seals
Bloom's syndrome
can't repair DNA s/p radiation
ataxia telangiectasia has repair problem with what
xrays
Fanconi's anemia
defect in DNA repair from cross-linking agents
name DNA repair dz
Xeroderma Pigment (UV light)
atxia-telangiectasia (x-ray)
Bloom's (radiation)
Fanconi's anemia (cross linking agents)