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