8. biochem - straight up uw aswers - part 1
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BIOCHEMISTRY STRAIGHT UP UW ANSWERS Bchem. Part 1– UW -Out of Time to Organize
REPLICATION, TRANSCRIPTION, TRANSLATION ETC:
• M !hr""m P"#!"$#$%: & GI L#'erLab increased AST, ALT. Most likely inhibited by toxinA! Me!!e$%er RNA
"Amatoxin inhibits RNA P"()mera!e * # sto$s mRNA !)$the!#! %
• RNA Pr#mer!&racil is only in RNA "'hich enzyme in(ol(ed in )*A synthesis catalyzesformation of +*A strands% in rokaryote )*A +e$lication. PRIMASE "+*A
rimase% makes Sh"rt RNA Pr#mer
Pr#ma!e is )*A de$endent +*A olymerase that incor$orates Short +*A$rimers into +e$licating )*A
mRNA Pr"ce!!#$% + Re% (at#"$: -m+*A inalizing! / ca$$ing, oly A-Tail add, 0ntron s$lice1. /c)t" (a!m hasI$teract#"$ 0#thP&BO IES for m+*A translation regulation and m+*A degradation
NA Re (#cat#"$: Lea2#$% a$2 La%%#$% Stra$2!: $2 .)*A rimase 3 )*A Ligase 3"#$! NA 4ra%me$t! 5) L#%a!e
")*A +e$lication is 67 t" 87 2#rect#"$ . Lead Strand # 4ontinuous Synthesis.Lag Strand # )iscontinuous S5O+T RNA Pr#mer stretches. 3 *67Synthesized )*A Segments 8Okazaki ragments9. Lag Strand Synthesisre:uires re$etiti(e action of )*A rimase and )*A Ligase%
• E 9ar)"t#c Ce(( NA Re (#cat#"$:6urkaryotic 4ells ha(e +e$lication more (olume, ast )*A re$lication bc of!A! M (t# (e Or#%#$! " Re (#cat#"$
• ;er"2erma P#%me$t"! m: $.2;Rec rre$t !9#$ (e!#"$! , face, limbs. 7hich enzymes likely $"$ $ct#"$a(<A! . E$2"$ c(ea!e f/d
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"&?-6ndonuclease +6MO?6S Th)m#$e T=T 2#mer! PYRIMI INES. CUT %@*icks/"6ndonuclease do *OT +6MO?6 urines A-B%. "Then olymerase, Ligase+e$laces )*A%
H"me"5"> Ge$e!:
5omeobox codes 'hich $rotein ty$esA! Tra$!cr# t#"$ Re% (at"r! "alters gene ex$ression%
Ra2#at#"$ a$2 Ce(( eath:0rri-Ra2#at#"$ for Metastatic Testicular 4ancer. +etro$eritonealnodes1.decreased size. Cest eDect of treatmentA! " 5(e Stra$2e2 NA Brea9!
" or +a$id )i(iding 4ells E B0, E Skin.%"+adiation NA ama%e (ia 2! NA 4ract re! # orms +66 +A)04ALS%"(s. )*A )amage from ! $ U? ra2#at#"$ P)r#m#2#$e&P)r#m#2#$e
IMERS Th)m#$e )m er! T=T, C=C, U=U@. CUT
R#5"!"me Str ct re – rRNA: $.2Frokaryote ribosomes ha(e G ty$es r+*A. 7hich best ex$lains function of
1-S rRNA in rokaryotic +ibosomesA! C"$ta#$! N c(e"t#2e Se e$ce C"m (eme$tar) t" a$ mRNA!e e$ce 1
"1.to initiate rotein Translation # Shine-)algarno on m+*A%
O9a a9# 4ra%me$t!:1> 2a %hter !tra$2! "rme2 . )aughter strand synthesized in o$$ositedirection of gro'ing fork uni:ueA! S)$the!#! " MULTIPLE SHORT NA 4ra%me$t!
• S#(e$c#$% RNACurkitt Lym$homa, 7estern blot. &ntreated cells! Cig blot. Treated cells! Thinblot. See on gel.7hich r"ce!! (#9e() #$terr te2<
A! mRNA Tra$!(at#"$• tRNA W"55(e: D
t+*A molecule 'ith &4& anticodon can eDecti(ely bind COT5 ABA and ABBm+*A codons. The Hnding is called! WOBBLE
"Means! More codons 2< than AA->I. 6ach t+*A molecule is S 640 04 for a
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single AA. MA*J t+*A anticodons can bind to a fe' )iDerent codons1.codingthe SAM6 AA%
• tRNA D :+es$onsible for amino acid binding - t+*A Structure.A! /87 e$2
• St" C"2"$!:5emolytic Anemia defecti(e enzyme < 2 AA instead of 1'hich follo'ing m+*A code changes likely occurA! UCA UGA
"Sto$ 4odons! UGA, UAG, UAA %
"(s! &AA &AB1'on/t change $rotein structure COT5 A+6 STO 4O*)O*Sthus Silent Mutation
• HC?:5e$ 4. Lacks roof reading in 87 t" 67 e>"$ c(ea!e act#'#t) in its +*A)e$endent +*A olymerase # causes 0nstability in 5e$ 4 (irus.
"+*A olymerase de$ends on +*A%
PATHWAYS S#%$a( Tra$!2 ct#"$ Path0a)!:
• RAS&MAP F#$a!e Path0a):
+as $rotein stays A4T0?6 (ia! GTP -+as
PI8F A9t Mt"r:B B -+ 0 G hos$ho0nositide-GNinase O* rotein Ninase C O* mTOR TRANSLOCATION t" N c(e ! a$2 Ge$e Tra$!cr# t#"$
"#4ell Bro'th, roliferation, Anti-A$o$tosis1. # 4ancer athogenesis.%"Mutation in B -+, N-C, mTO+1 causes cancer%
Te(m"era!e $2 !
4ell has high re(erse transcri$tase acti(ityA! E #2erma( Ba!a( Ce((! "skin %
"Telomerase has +e(erse Transcri$tase acti(ity! NA P"()mera!e thatde$ends on +*A%1 adds TTABBB re$eats to G/end. &ses AA&444becomes TTABBB ss+*A1. Te("mera!e !e! !!RNA as tem$late thenMAN6S !! NA %
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E. C"(# – Lac O er"$ C"$ce t:
• E. C"(# – Lac O er"$ $22!A22 G( c"!e Cug sto$s fermenting Lactose. Cc Blucose 0nhibits LacO$eron bc it )e$letes cAM . 4ausing!A! ca !e LOW cAMP
"Add G( c"!e 0nhibits LA4 O$erone1.bc uses u$ cAM %
• E. C"(# – Lac O er"$ $22.!M tate2 OPERATOR L"c ! on Lac o$eron no' re$ressor rotein can/tbind it to sto$ lac o$eron # increased lac o$eron function
• Lac O er"$ -- !
Cacteria m+*A 6. 4oli has "()c#!tr"$#c m+*A "#can code se(eral $roteins%.6. 4oli can u$regulate Ceta-galactosidase and galactoside $ermease. Cestex$lains synchronous $roduction of both enzymesA! There #! ONE mRNA c"2#$% "r BOTH e$ )me!
BIOCHEM ISEASES
• HNPCC C"("$ Ca$cer & M#!match Re a#r: & GI# N c(e"t#2e M#!match that e!ca e! Re a#r
• 4a5r) #!ea!e .11 !Skin Lesions. ibroblasts a#( t" meta5"(# e Ceram#2e Tr#he>"!#2e . This $tis at risk for de(elo$ing!A! Re$a( 4a#( re
• A(9a t"$ r#a:Clack helix ear, Clack urine. Cro'n s$ots in sclera. 6nzyme deHcientA! H"m"%e$t#!#c Ac#2 O>#2a!e
• L)!#$e O>#2a!e: $.;; Lung"Al$ha )(a!e # 4ross-links e!m"!#$e&L)!#$e # E(a!t#$ 4#5er! 1stretch al(eolar 'all-inhaleP+ecoild-6xhale. ro$erty is ex$lained by!A! I$tercha#$ CROSS&LINFS #$'"('e! LYSINE
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• 4#5r#((#$ A$2 Mar a$ S2.:# 6lastin-associated glyco$rotein lots in zona Hbers of lens, $eriosteum,aortic media
BIOCHEM GENETICS
• S" ther$ B("tt#$%:# )etects NA M tat#"$!
• 4rame!h# t M tat#"$:)eletion or additions of Case airs *OT a multi$le of G # 4RAMESHI4T mutation occurred.
"Sibling 2 b$. atient Q b$. 7hat/s res$onsible 4RAME&Sh# tM tat#"$ 1.here is >b$ deleted%
•
We!ter$ B("t:Co(ine ex$osure case. Pr#"$ #!ea!e 1.antibody-$rotein com$lex. 7hichbest describes testA! We!ter$ B("t Test roteins
RAN OM
M)e(" r"(# erat#'e #!"r2er!: 3AF* M tat#"$:allor, fatigue, Lost 'eight. 6! 5e$atomegaly, s$lenomegaly. Tyrosinehos$horylation acti(ity. Acti(ation of STAT Pr"te#$! "Signal Transducers
and Acti(ators of Transcri$tion%t likely suDers from
A! M)e(" 5r"!#!
"4hronic Myelo$roliferati(e )isorders! -?era itchP0ncreased +C4. 6ssential Thrombocytosis # 0ncreased ThrombosisP6asy bruise, MyeloHbrosis#CM
ibrosisPdecreased 5emato$oiesisPTear )ro$ 4ells%"These ha(e mutation in CYTOPLASM T)r"!#$e F#$a!e, 3a$ ! F#$a!e *
3AF*J 1.results in TJ+OS0*6 Ninase Acti(ity1.cytokine 0nde$endent
acti(ation of STAT Transcri$tion factors%
• Ra!5 r#ca!e: .-K )LC4 Lym$homa# !e Lar%e B&Ce(( L)m h"ma . 4hemo. )ecreased &rine Out$ut.
0ncreased C&*, T 'a(es. 7hich Med +6?6*TS this $t/s +6*AL 0m$airmentA! Ra!5 r#ca!e
"*OT robenecid%
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"TUMOR LYSIS S2 . BO&T $ath'ay% see action of Ra!5 r#ca!e@.#$h#5#t!URATE O;I ASE 1 "sto$$ing con(ersion " Ur#c Ac#2 to Allantoin excretionto urine1.STO S BO&T%
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