characteriza.on of the ac.vity and kine.cs of guanine

1
IC50 Determina.on for GDA IC50 values were determined with G at 0.5 µM under normal microplate assay condi<ons (30 min reac<on). AICA showed modest inhibi<on, 2,6-diaminopurine (2,6-DAP) showed no inhibitory ac<vity, while the an<viral Acyclovir showed very mild inhibitory ac<vity. -10 -5 0 50 100 log-dose vs GD Activity log[Test], M % Enzyme Activity AICA 4.8 2,6-DAP >1 m Acyclovir 427 2,6-DAP >1 mM Guanine deaminase, also known as “nedasin “ or “cypin”, catalyzes the purine catabolic commitment step from guanine (G), through xanthine (X), to the elimina<on product, uric acid. In rabbit, mouse and human, the enzyme appears to exist predominantly cytoplasmic as a homodimer, with cataly<c domains for the Zn +2 -dependent hydroly<c deamina<on of guanine to xanthine plus ammonia. Genomic details for the GDA gene are mapped for several species, and expression profiling in certain <ssues and organisms has been ini<ated, although the complement of various transcript variants is incomplete. Structure: c. 50 kDa subunits with sequences that vary at internal and terminal sites, due to exon selec<on; at least 4 significant forms predic<ng proteins of various lengths are known. Interac<ons: tubulin, snapin, and the post-synap<c domain protein 95 (PSD-95). PSD-95 binding is through the PDZ binding mo<fs present at the C-terminus of the dimeric structure. Sequence variants occur mostly at the protein binding domains, although minor variants lack the deaminase cataly<c site. In mammalian brain, high enzyma<c levels are in telencephalic brain regions; very low levels in white maYer and cerebellum; moderate levels in liver and certain other organs. low levels in plasma/serum, notably altered by liver dysfunc<on. The S- transcript is predominant, coding for a 51 kDa monomer. Actual role of guanine deaminase in specialized organ metabolism and synap<c physiology is uncertain, and rela<vely liYle is known about the enzyme characteris<cs outside of rabbit, with significant detail available detail on gene expression paYerns, but not at the protein level. Available protein expression surveys have suggested extensive post-transla<onal modifica<ons, that have not yet been detailed with certainty. Few useful inhibitors have been described for the enzyme, and the biochemical pharmacology is confused, in part due to poorly characterized enzyme proper<es. Presented at ASMS 2019 WP 509 Characteriza.on of the Ac.vity and Kine.cs of Guanine Deaminase Jus<n M. Godinho , Ben Libert, and Barry E. Boyes Advanced Materials Technology Inc., Wilmington, DE Introduc.on Purpose Efficient Separa.ons of Highly Polar Purine Metabolites Standard Microplate Enzyme Assay and LC/MS Condi.ons Comparison of Kine.cs Between Brain and Liver and Recombinant GDA INNOVATION YOU CAN TRUST – PERFORMANCE YOU CAN RELY ON fused-core.com Previous enzyme assays are problema<c, using either spectrophotometry (spectral shic of G to X, or ammonium capture), or coupled fluorometric enzyme assay of X (via Xanthine Oxidase produced H 2 O 2 ), with aYendant problems in kine<c parameter es<ma<on. Available assays have poorly characterized analy<cal specificity, reproducibility and sensi<vity, genera<ng broad reported ranges for basic kine<c parameters (Km values and specific ac<vi<es vary widely), and inhibitor characteris<cs. To measure <ssue enzyme levels, follow purifica<on processes, define enzyme kine<cs and effects of inhibitors, highly specific and sensi<ve methods would be useful. Direct genera<on of product xanthine uses fast separa<on of highly polar purine metabolites by a new reversed-phase material, HALO® AQ- C18. High sensi<vity and selec<ve detec<on uses selected reac<on monitoring (SRM) LC-MS/MS. Analy<cal benefit was assessed across a range of substrate concentra<ons, in the presence of known and poten<al compe<<ve inhibitors. The features of the assay are explored for the only two known substrates for guanine deaminase, Guanine and 8-Azaguanine. We have also ini<ated comparison of na<ve GDA from bovine brain and liver <ssue, to recombinant bacterial expressed human GDA. 0.25 0.50 0.75 1.00 1.25 1.50 1.75 min 0.00 0.25 0.50 0.75 1.00 1.25 1.50 1.75 uV (x100,000) 0.00 0.25 0.50 0.75 1.00 1.25 1.50 1.75 min 0.0 0.5 1.0 1.5 2.0 2.5 uV (x100,000) 0.00 0.25 0.50 0.75 1.00 1.25 1.50 1.75 min 0.00 0.25 0.50 0.75 1.00 1.25 1.50 uV (x100,000) 1,2 3 5 6 7 8 4 9 1,2 3 5 6 7 8 4 9 1,2 3 5 6 7 8 4 9 Peak Iden<<es 1: 5-Amino-imidazole-4-carboxamide (AICA) 2: Azepinomycin 3: Guanine - Substrate 4: 2,6-Diaminopurine (2,6-DAP) 5: Uric Acid 6: Xanthine - Product 7: 8-Azaxanthine 8: 8-Azaguanine 9: Allopurinol LC Condi<ons Columns: 2.1 x 100 mm Mobile Phase: 0.1% Formic Acid Flow Rate: 0.5 mL/min Temperature: 35 °C Detec<on: UV 254 nm Injec<on: 1 µL Instrument: Shimadzu Nexera HALO 90Å, AQ-C18, 2.7 µm Compe<tor (B) 2.7 µm SPP Aqueous C18 Compe<tor (A) 2.6 µm SPP Aqueous C18 A selec<on of C18 phases stable in 100% Aqueous condi<ons were screened. The HALO 90Å, AQ-C18, 2.7 µm column was chosen for its ability to resolve the highly polar purine metabolites and inhibitors of interest. Under the current use condi<ons, the AQ-C18 column is stable for many thousands of samples, including <ssue homogenates. Panels A-D represent steps taken for selec<ve detec<on of the enzyme reac<on product, xanthine and 8-azaxanthine. Panel A shows a chromatogram of a 10 pmol injec<on of X or AzX using the extracted ions from 150 to 152 m/z. Panel B shows the spectra with xanthine and azaxanthine precursor ions [M−H] at 151 m/z (X) or 152 (AzX) chosen for fragmenta<on. Panel C shows the extracted ion chromatograms centered at dominant fragment ions, and Panel D shows the product ions 108 m/z monitored for X and 109 m/z for AzX. Xanthine Theore<cal Mass [m/z] 152.033 Da monoisotopic, [151.025 m/z (-) ] 8-azaxanthine Theore<cal Mass [m/z] 153.029 Da monoisotopic, [152.021 m/z (-)] ITMS [50-200 m/z] 0.875 1.000 1.125 1.250 0 50000 100000 150000 200000 260000 10pmol Xanthine inj. XIC (-) 150-152 m/z Precursor Ion 151 m/z ITMS [106.00-110.00 m/z] 0.875 1.000 1.125 1.250 0 5000 10000 15000 20000 26000 XIC (-) 107.8- 108.2 m/z Product Ion 108 m/z 55.0 75.0 100.0 125.0 150.0 0 20 40 60 80 100 120 108.01 m/z % 120.0 140.0 160.0 180.0 0.0 5.0 10.0 15.0 20.0 25.0 28.0 151.01 m/z % 0.875 1.000 1.125 1.250 0 10000 20000 30000 40000 ITMS [106.00-110.00 m/z] XIC (-) 108.8- 109.2 m/z Product Ion 109 m/z 55.0 75.0 100.0 125.0 150.0 0 20 40 60 80 100 120 109.08 124.01 m/z % 0.875 1.000 1.125 1.250 0 50000 100000 150000 200000 ITMS [50-200 m/z] XIC (-) 10pmol 8-Azaxanthine inj 151- 153 m/z Precursor Ion 152 m/z 120.0 140.0 160.0 180.0 0.0 5.0 10.0 15.0 20.0 25.0 28.0 151.99 m/z % A B C D SRM MS^2 151.00 @cid30 SRM MS^2 152.00 @cid30 Selec.ve Detec.on of Enzyme Reac.on Products Using SRM in the Ion Trap Shimadzu Nexera HALO® AQ-C18 2.1x75mm 2.7µm 90Å, or HTP assay using 2.1 x 30 mm. A=0.1%Formic Acid B=Acetonitrile 0.5ml/min, 35°C, 265nm, MTP, autosampler 25°C Gradient: 0%B 0-1.5min to 70%B @1.7-2.2min to 0%B @2.3-4.2min Thermo Orbitrap Velos Pro ETD MS Run Time (min): 1.7; divert first 0.8 min from MS source ITMS (-) 0.7 to 1.7min HESI Source Type; Capillary 350°C; Heater 325°C; Sheath Gas 40; Aux Gas Flow 10 ITMS Full AGC 50K; ITMS SIM AGC 100K; ITMS MSn AGC 50K Source Voltage (-kV) 2.70; Ion Trap Full Max Ion Time (ms) 200; Segment (SEG) Informa<on/Scan Event Details: ITMS - c low injrf=70.0 ·(151.00000)->oS(98.00-118.00) MS/MS: AT CID CE 30.0% Q 0.350 Time 10.000 IsoW 1.5, CV = 0.0V Assay Condi<ons 50 mM Bicine pH 7.8, 5 µg/mL BSA, varying Guanine or 8-azaGuanine. Reac<on at 25°C for >15 minutes, typical volume of 100 µL Stop Reac<on by addi<on of 0.1 volume of 10% Formic Acid. All purine reagent stocks are maintained in 15 mM NaOH/0.15 mM MgCl 2 un<l dilu<on. Enzyme incuba<ons are conducted in standard 96 well reac<on plates, which are directly loaded in the Nexera Autosampler, for LC/MS analysis of reac<on products. Enzyme ac<vity is linear over 4 orders of dilu<on, in this example, an enzyme concentra<on of 1 in 12,000 (50 mU/rx), X produc<on is linear with incuba<on <me to 300 minutes, consuming less than 10% of substrate at 100 uM G. Observed for 10 uL injec<on; LOQ for X < 1 fmol and linearity to > 10 pmol injected. 0 10 20 30 40 50 0 100 200 300 pmol of X Produced Time (min) 0 10 20 30 40 50 0 500 1000 pmol of X Produced Enzyme Dilu<on (x10 -6 ) Conclusions Deconvolu<on resulted in a subunit MW of 50866. This is 193 Da from the predicted mass using genomic data, 51059, for the S isoform of the enzyme. Chromatograms and SDS PAGE show high enzyme purity. Column: HALO 1000 Å Diphenyl, 2.7 µm, 2.1 x 150 mm QExac<ve HF and Nexera X2 A: 0.1% DFA B: 0.1% DFA 1:1 nPropanol:ACN 0.25 mL/min 30%B 0-20min 0 50 100 0 2 4 6 Saturation Kinetics Recombinant Human Enzyme Activity (m mol/min/mg) 0 20 40 60 0.00 0.05 0.10 0.15 0.20 Saturation Kinetics Bovine Liver Enzyme Activity (pmol/min) 0 20 40 60 0.0 0.5 1.0 1.5 2.0 Saturation Kinetics Bovine Brain Enzyme Activity (m mol/min/mg) Km values for bovine brain and liver are similar, 0.286 ± 0.035(SEM) µM and 0.31 ± 0.03(SEM) µM respec<vely, and are much lower than literature values. This emphasizes the importance of highly specific and sensi<ve LC/MS enzyme assays. The Km values for bovine <ssues are much lower than the assayed recombinant human enzyme, Km of 6.2 ± 0.2(SEM) µM. Vmax of bovine brain compares favorably with literature reports at 1.36 ± 0.04(SEM) µmole/min/mg but differs significantly from the recombinatnt, 5.2 ± 0.2(SEM) µmole/min/mg. AzG is a much poorer substrate. A sensi<ve and specific LC/MS approach to study enzyme kine<cs is demonstrated. Results differ from literature reports that use spectrophotometric methods highligh<ng the importance of the assay’s specificity. The HALO® AQ-C18 phase provides robust separa<on in 100% aqueous condi<ons for these highly polar purines. High purity enzyme from <ssue exhibited much lower Km than bacterial expressed recombinat enzyme and a subunit mass that diverges from DNA derived value. This work was supported in part by NIGMS[GM116224 to BEB]. The content is solely the responsibility of the authors and does not necessarily represent the official views of the Na<onal Ins<tute of Health LC/MS of GDA [G] µM [G] µM [G] µM µM µM

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IC50Determina.onforGDA

IC50valuesweredeterminedwithGat0.5µMundernormalmicroplateassaycondi<ons(30minreac<on).AICAshowedmodestinhibi<on,2,6-diaminopurine(2,6-DAP)showednoinhibitoryac<vity,whilethean<viralAcyclovirshowedverymildinhibitoryac<vity.

-10 -50

50

100

log-dose vs GD Activity

log[Test], M

% E

nzym

e A

ctiv

ity AICA 4.8 mM

2,6-DAP >1 mM

Acyclovir 427 mM

-10 -50

50

100

log-dose vs GD Activity

log[Test], M

% E

nzym

e A

ctiv

ity AICA 4.8 mM

2,6-DAP >1 mM

Acyclovir 427 mM

-10 -50

50

100

log-dose vs GD Activity

log[Test], M

% E

nzym

e A

ctiv

ity AICA 4.8 mM

2,6-DAP >1 mM

Acyclovir 427 mM

-10 -50

50

100

log-dose vs GD Activity

log[Test], M

% E

nzym

e A

ctiv

ity AICA 4.8 mM

2,6-DAP >1 mM

Acyclovir 427 mM

Guanine deaminase, also known as “nedasin “ or “cypin”, catalyzes the purine cataboliccommitmentstepfromguanine(G),throughxanthine(X),totheelimina<onproduct,uricacid.In rabbit, mouse and human, the enzyme appears to exist predominantly cytoplasmic as ahomodimer,withcataly<cdomainsfortheZn+2-dependenthydroly<cdeamina<onofguaninetoxanthineplusammonia.GenomicdetailsfortheGDAgenearemappedforseveralspecies,andexpression profiling in certain <ssues and organisms has been ini<ated, although thecomplementofvarioustranscriptvariantsisincomplete.

•  Structure:c.50kDasubunitswithsequencesthatvaryatinternalandterminalsites,duetoexonselec<on;atleast4significantformspredic<ngproteinsofvariouslengthsareknown.

•  Interac<ons:tubulin,snapin,andthepost-synap<cdomainprotein95(PSD-95).•  PSD-95binding is through thePDZbindingmo<fspresentat theC-terminusof thedimeric

structure.•  Sequencevariantsoccurmostlyattheproteinbindingdomains,althoughminorvariantslack

thedeaminasecataly<csite.•  Inmammalianbrain,highenzyma<clevelsareintelencephalicbrainregions;verylowlevels

inwhitemaYerandcerebellum;moderatelevelsinliverandcertainotherorgans.lowlevelsin plasma/serum, notably altered by liver dysfunc<on. The S- transcript is predominant,codingfora51kDamonomer.

•  Actualroleofguaninedeaminaseinspecializedorganmetabolismandsynap<cphysiologyisuncertain, and rela<vely liYle is knownabout theenzyme characteris<csoutsideof rabbit,with significant detail available detail on gene expression paYerns, but not at the proteinlevel. Available protein expression surveys have suggested extensive post-transla<onalmodifica<ons,thathavenotyetbeendetailedwithcertainty.

•  Few useful inhibitors have been described for the enzyme, and the biochemicalpharmacologyisconfused,inpartduetopoorlycharacterizedenzymeproper<es.

PresentedatASMS2019WP509

Characteriza.onoftheAc.vityandKine.csofGuanineDeaminaseJus<nM.Godinho,BenLibert,andBarryE.Boyes

AdvancedMaterialsTechnologyInc.,Wilmington,DE

Introduc.on

Purpose

EfficientSepara.onsofHighlyPolarPurineMetabolites StandardMicroplateEnzymeAssayandLC/MSCondi.ons ComparisonofKine.csBetweenBrainandLiverandRecombinantGDA

INNOVATION YOU CAN TRUST – PERFORMANCE YOU CAN RELY ON fused-core.com

•  Previousenzymeassaysareproblema<c,usingeitherspectrophotometry(spectralshicofGtoX,orammonium capture), or coupled fluorometric enzyme assay of X (via Xanthine Oxidase producedH2O2),withaYendantproblemsinkine<cparameteres<ma<on.

•  Available assays have poorly characterized analy<cal specificity, reproducibility and sensi<vity,genera<ngbroadreportedrangesforbasickine<cparameters(Kmvaluesandspecificac<vi<esvarywidely),andinhibitorcharacteris<cs.

Tomeasure<ssueenzyme levels, followpurifica<onprocesses,defineenzymekine<csandeffectsofinhibitors,highlyspecificandsensi<vemethodswouldbeuseful.Directgenera<onofproductxanthineusesfastsepara<onofhighlypolarpurinemetabolitesbyanewreversed-phasematerial,HALO®AQ-C18. High sensi<vity and selec<ve detec<on uses selected reac<on monitoring (SRM) LC-MS/MS.Analy<calbenefitwasassessedacrossa rangeof substrateconcentra<ons, in thepresenceofknownand poten<al compe<<ve inhibitors. The features of the assay are explored for the only two knownsubstrates for guanine deaminase, Guanine and 8-Azaguanine.We have also ini<ated comparison ofna<veGDAfrombovinebrainandliver<ssue,torecombinantbacterialexpressedhumanGDA.

0.25 0.50 0.75 1.00 1.25 1.50 1.75 min 0.00 0.25 0.50 0.75 1.00 1.25 1.50 1.75 uV (x100,000)

0.00 0.25 0.50 0.75 1.00 1.25 1.50 1.75 min 0.0 0.5 1.0 1.5 2.0 2.5

uV (x100,000)

0.00 0.25 0.50 0.75 1.00 1.25 1.50 1.75 min 0.00 0.25 0.50 0.75 1.00 1.25 1.50

uV (x100,000)

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4 9

PeakIden<<es1:5-Amino-imidazole-4-carboxamide(AICA)2:Azepinomycin3:Guanine-Substrate4:2,6-Diaminopurine(2,6-DAP)5:UricAcid6:Xanthine-Product7:8-Azaxanthine8:8-Azaguanine9:Allopurinol

LCCondi<onsColumns:2.1x100mmMobilePhase:0.1%FormicAcidFlowRate:0.5mL/minTemperature:35°CDetec<on:UV254nmInjec<on:1µLInstrument:ShimadzuNexera

HALO90Å,AQ-C18,2.7µm

Compe<tor(B)2.7µmSPPAqueousC18

Compe<tor(A)2.6µmSPPAqueousC18

Aselec<onofC18phasesstablein100%Aqueouscondi<onswerescreened.TheHALO90Å,AQ-C18,2.7µmcolumnwaschosenforitsabilitytoresolvethehighlypolarpurinemetabolitesandinhibitorsofinterest.Underthecurrentusecondi<ons,theAQ-C18columnisstableformanythousandsofsamples,including<ssuehomogenates.

PanelsA-Drepresentstepstakenforselec<vedetec<onoftheenzymereac<onproduct,xanthineand8-azaxanthine.PanelAshowsachromatogramofa10pmolinjec<onofXorAzXusingtheextractedionsfrom150to152m/z.PanelBshowsthespectrawithxanthineandazaxanthineprecursorions[M−H]−at151m/z(X)or152(AzX)chosenforfragmenta<on.PanelCshowstheextractedionchromatogramscenteredatdominantfragmentions,andPanelDshowstheproductions108m/zmonitoredforXand109m/zforAzX.

XanthineTheore<calMass[m/z]152.033Damonoisotopic,[151.025m/z(-)]

8-azaxanthineTheore<calMass[m/z]153.029Damonoisotopic,[152.021m/z(-)]

ITMS[50-200m/z]

0.875 1.000 1.125 1.250 0

50000

100000

150000

200000

260000 10pmolXanthineinj.XIC(-)

150-152m/z

PrecursorIon151m/z ITMS[106.00-110.00m/z]

0.875 1.000 1.125 1.250 0

5000

10000

15000

20000

26000 XIC(-)107.8-108.2m/z

ProductIon108m/z

55.0 75.0 100.0 125.0 150.0

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120 108.01

m/z

%

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151.01

m/z

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0.875 1.000 1.125 1.250

0

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40000 ITMS[106.00-110.00m/z]

XIC(-)108.8-109.2m/z

ProductIon109m/z

55.0 75.0 100.0 125.0 150.0

0

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120 109.08

124.01

m/z

%

0.875 1.000 1.125 1.250

0

50000

100000

150000

200000 ITMS[50-200m/z]

XIC(-)10pmol8-Azaxanthineinj151-153m/z

PrecursorIon152m/z

120.0 140.0 160.0 180.0 0.0

5.0

10.0

15.0

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151.99

m/z

%

A B C D

SRMMS^2151.00@cid30

SRMMS^2152.00@cid30

Selec.veDetec.onofEnzymeReac.onProductsUsingSRMintheIonTrap

ShimadzuNexeraHALO®AQ-C182.1x75mm2.7µm90Å,orHTPassayusing2.1x30mm.A=0.1%FormicAcid B=Acetonitrile0.5ml/min,35°C,265nm,MTP,autosampler25°CGradient:0%B0-1.5minto70%[email protected]%[email protected](min):1.7;divertfirst0.8minfromMSsourceITMS(-)0.7to1.7minHESISourceType;Capillary350°C;Heater325°C;SheathGas40;AuxGasFlow10ITMSFullAGC50K;ITMSSIMAGC100K;ITMSMSnAGC50KSourceVoltage(-kV)2.70;IonTrapFullMaxIonTime(ms)200;Segment(SEG)Informa<on/ScanEventDetails:ITMS-clowinjrf=70.0·(151.00000)->oS(98.00-118.00)MS/MS:ATCIDCE30.0%Q0.350Time10.000IsoW1.5,CV=0.0VAssayCondi<ons50mMBicinepH7.8,5µg/mLBSA,varyingGuanineor8-azaGuanine.Reac<onat25°Cfor>15minutes,typicalvolumeof100µLStopReac<onbyaddi<onof0.1volumeof10%FormicAcid.Allpurinereagentstocksaremaintainedin15mMNaOH/0.15mMMgCl2un<ldilu<on.Enzymeincuba<onsareconductedinstandard96wellreac<onplates,whicharedirectlyloadedintheNexeraAutosampler,forLC/MSanalysisofreac<onproducts.

Enzymeac<vityislinearover4ordersofdilu<on,inthisexample,anenzymeconcentra<onof1in12,000(50mU/rx),Xproduc<onislinearwithincuba<on<meto300minutes,consuminglessthan10%ofsubstrateat100uMG.Observedfor10uLinjec<on;LOQforX<1fmolandlinearityto>10pmolinjected.

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EnzymeDilu<on(x10-6)

Conclusions

Deconvolu<onresultedinasubunitMWof50866.Thisis193Dafromthepredictedmassusinggenomicdata,51059,fortheSisoformoftheenzyme.ChromatogramsandSDSPAGEshowhighenzymepurity.Column:HALO1000ÅDiphenyl,2.7µm,2.1x150mmQExac<veHFandNexeraX2A:0.1%DFAB:0.1%DFA1:1nPropanol:ACN0.25mL/min30%B0-20min

0 50 1000

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Saturation Kinetics Recombinant Human

[G] mM

Enz

yme

Act

ivity

(mm

ol/m

in/m

g)

0 20 40 600.00

0.05

0.10

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0.20

Saturation Kinetics Bovine Liver

[G] mM

Enz

yme

Act

ivity

(pm

ol/m

in)

0 20 40 600.0

0.5

1.0

1.5

2.0

Saturation Kinetics Bovine Brain

[G] mM

Enz

yme

Act

ivity

(mm

ol/m

in/m

g)

Kmvaluesforbovinebrainandliveraresimilar,0.286±0.035(SEM)µMand0.31±0.03(SEM)µMrespec<vely,andaremuchlowerthanliteraturevalues.Thisemphasizestheimportanceofhighlyspecificandsensi<veLC/MSenzymeassays.TheKmvaluesforbovine<ssuesaremuchlowerthantheassayedrecombinanthumanenzyme,Kmof6.2±0.2(SEM)µM.Vmaxofbovinebraincomparesfavorablywithliteraturereportsat1.36±0.04(SEM)µmole/min/mgbutdifferssignificantlyfromtherecombinatnt,5.2±0.2(SEM)µmole/min/mg.AzGisamuchpoorersubstrate.

Asensi<veandspecificLC/MSapproachtostudyenzymekine<csisdemonstrated.Resultsdifferfromliteraturereportsthatusespectrophotometricmethodshighligh<ngtheimportanceoftheassay’sspecificity.TheHALO®AQ-C18phaseprovidesrobustsepara<onin100%aqueouscondi<onsforthesehighlypolarpurines.Highpurityenzymefrom<ssueexhibitedmuchlowerKmthanbacterialexpressedrecombinatenzymeandasubunitmassthatdivergesfromDNAderivedvalue.ThisworkwassupportedinpartbyNIGMS[GM116224toBEB].ThecontentissolelytheresponsibilityoftheauthorsanddoesnotnecessarilyrepresenttheofficialviewsoftheNa<onalIns<tuteofHealth

LC/MSofGDA

[G]µM

[G]µM [G]µM

µM µM