ライフサイエンスコーパス: microcystin

1 L) and Muskegon Lake without a HAB (<1 mug/L microcystin).

2 d elevated concentrations of the hepatotoxin microcystin.

3 notoxins often rely on the quantification of microcystin.

4 bability of a beach sample exceeding 4 mug/L microcystin.

5 de of 12-18 product ions for each identified microcystin.

6 on sites was unaffected by MgCl(2), EDTA, or microcystin.

7 hatase that is inhibited by okadaic acid and microcystin.

8 more linear with time and was unaffected by microcystin.

9 t affected by the intracellular perfusion of microcystin.

10 rine/threonine protein phosphatase inhibitor microcystin.

11 actions induced by the phosphatase inhibitor microcystin.

12 urified with A and C subunits on immobilized microcystin.

13 phorylation was increased by the addition of microcystin.

14 ffects on cyanobacterial blooms as source of microcystins.

15 ides such as lantibiotics, thiopeptides, and microcystins.

16 )R (5) and MC-M(O)R (7), as well as 20 other microcystins.

17 everal conventional methods for detection of microcystins.

18 pment of innovative methods for detection of microcystins.

19 to identify peaks corresponding to candidate microcystins.

20 thiol to the alpha,beta-unsaturated amide of microcystins.

21 ens from all over the world commonly produce microcystins.

22 des dominated (>80%) over cyanopeptolins and microcystins.

23 ated nanobody of broad cross-reactivity with microcystins.

24 echanism, since the effect was reproduced by microcystin (10 microM in pipette solution), which is a

25 while the non-specific phosphatase inhibitor microcystin (250 nM) increased channel activity by 218%.

26 ed method for measuring the concentration of microcystin, a group of toxins associated with cyanobact

27 The transport of microcystin, a hepatotoxin produced by cyanobacteria (e.

28 influence harmful algal blooms, exposure to microcystin, a known hepatotoxin and a byproduct of cyan

29 Intracellular application of microcystin, a membrane-impermeable inhibitor of phospha

30 Intracellular perfusion with microcystin, a potent phosphatase 1 and 2a inhibitor, in

31 ts in pull-down experiments with immobilized Microcystin, a PP2A inhibitor.

32 ones, intracellular application of 20 microM microcystin, a protein phosphatase 1/2A inhibitor, prolo

33 Nuclear extracts were subjected to microcystin affinity chromatography to recover phosphata

34 by Mono Q anion exchange chromatography and microcystin affinity chromatography.

35 R was verified by co-immunoprecipitation and microcystin affinity purification.

36 Microcystin-affinity chromatography was used to purify 1

37 Third, microcystin-agarose depletes mitotic extracts of both PP

38 Microcystin-agarose pull-downs suggested that a phosphat

39 phosphatase-specific activity or binding to microcystin-agarose.

40 onine phosphatase inhibitors calyculin A and microcystin also stimulated SOCs in isolated outside-out

41 effects of EET persisted in the presence of microcystin, an inhibitor of protein phosphatases 1 and

42 This microcystin analog and potent hepatotoxin has previously

43 s approach simplifies detection of candidate microcystin analogues even in the presence of complex mi

44 More than 150 microcystin analogues have been reported from cultures,

45 Because the effects of microcystin and EDTA were additive, and microcystin did

46 New information was obtained using (a) microcystin and okadaic acid to inhibit serine/threonine

47 d Anabaena to Microcystis and an increase of microcystin and saxitoxin occurred.

48 Binding of PP2Ac to microcystin and to alpha-4 increased with temperature, c

49 to the toxins calyculin A, okadaic acid, and microcystin and to thiophospho-DARPP-32.

50 cate that the ELISA has broad specificity to microcystins and also detects nodularin, providing a sen

51 tides, including the widespread hepatotoxins microcystins and nodularins.

52 protein phosphatase inhibitors okadaic acid, microcystin, and protein phosphatase inhibitor-2.

53 ed LC-MS approach to identify Dhb-containing microcystins, and allowed identification of LC-MS peaks

54 Cyclosporin, microcystins, and nodularins are all notable pharmacolog

55 Microcystins are a group of cyclic heptapeptides origina

56 Microcystins are a major group of cyanobacterial heptape

57 Microcystins are cyclic heptapeptides produced by a rang

58 Microcystins are potent toxins that are responsible for

59 One suggestion is that microcystins are siderophores (i.e., ligands with an ext

60 Microcystins are the most worldwide extended and common

61 ated with the most toxic incidents involving microcystins, are within the cyanobacteria (intracellula

62 icrocystin-leucine-tryptophan (MC-LW) 63.7%, microcystin-arginine-arginine (MC-RR) 60.1% and nodulari

63 CLR (microcystin-leucine-arginine) and MCRR (microcystin-arginine-arginine) at a sublethal dose (10 m

64 public health organizations have categorized microcystins as a kind of neurotoxin and carcinogen.

65 Microcystins, as secondary metabolite of cyanobacteria (

66 ents' serum, and postmortem liver tissue for microcystin assays.

67 the first known report of a recombinant anti-microcystin avian antibody.

68 rential effects of the two nucleotides since microcystin, beta-glycerol phosphate, or okadaic acid co

69 Polymeric microcystin binding iron may be related with a toxic cel

70 imulated the dephosphorylation of NPR-A, and microcystin blocked the temperature-dependent dephosphor

71 Protein sequencing revealed that the microcystin-bound proteins with the greatest reduction i

72 nine phosphatase inhibitors okadaic acid and microcystin, but is inhibited by the tyrosine phosphatas

73 stence and the production of the hepatotoxin microcystin, but the physiological mechanisms to explain

74 en they enter directly into the circulation, microcystins can lead to fatal clinical syndromes rangin

75 Michigan: Mona Lake during a severe HAB with microcystin concentrations (>200 mug/L) well above the E

76 In 48 (26.4%) samples we observed microcystin concentrations as measured by ELISA that exc

77 Microcystin concentrations decline by approximately 98%

78 hat addresses these issues and that predicts microcystin concentrations from summer mean total nitrog

79 del accounts for 69% of the variance in mean microcystin concentrations in lakes and reservoirs of th

80 more robust and useful metric for predicting microcystin concentrations than qPCR measurements enumer

81 Mean microcystin concentrations were more strongly associated

82 enrichment yielding significant increases in microcystin concentrations.

83 Enrichment of hydrophobic microcystin congeners (e.g., microcystin-LR) was observe

84 agment displayed cross-reactivity with seven microcystin congeners (microcystin-leucine-arginine (MC-

85 also to minimize specificity for particular microcystin congeners.

86 RR and a range of other [Mdha(7)]-containing microcystin congeners.

87 rocedure that allows LC-MS identification of microcystins containing methionine and methionine sulfox

88 This suggests that microcystins containing methionine sulfoxide are primari

89 C-MS analysis, clearly discriminated between microcystins containing the isobaric [Dhb(7)]- and [Mdha

90 as sufficiently large that derivatization of microcystin-containing samples with mercaptoethanol, fol

91 (6), which comprised about half of the total microcystin content in the bloom, and ferintoic acids C

92 et under low N and a significant decrease in microcystin content per Microcystis cell demonstrating t

93 of chlorophytes over cyanobacteria and lower microcystin content.

94 The effect of microcystin could be blocked by co-applying PKA inhibito

95 s, the calculated photochemical half-life of microcystin decreased 6-fold with increasing salinity al

96 The efficiency of current microcystin detection methods has been hampered by the l

97 e to achieve sensitive and congener-specific microcystin detection with detection limit as low as 10

98 targeting molecules and their application in microcystin detection.

99 s of microcystin and EDTA were additive, and microcystin did not block the magnesium-dependent desens

100 freshwater, while enrichment of hydrophilic microcystin (e.g., microcystin-RR) was lower.

101 production of other cyanopeptides along with microcystins emphasizes the need to make them available

102 Thus, in conclusion, microcystin exposure in NAFLD could significantly alter

103 n vivo and in vitro experiments we show that microcystin exposure in NAFLD mice cause rapid alteratio

104 imulated the dephosphorylation of NPR-A, and microcystin failed to inhibit this process.

105 ediated photodegradation in future models of microcystin fate in freshwater-estuarine systems.

106 However, (15) N was incorporated into microcystins from all N sources.

107 More than 100 microcystins have been identified, of which MC-LR is the

108 A competitive assay with microcystin-horseradish peroxidase conjugate was optimiz

109 ICl,CaMK by okadaic acid (IC50 = 1.5 nM) and microcystin (IC50 = 0.15 nM); these data lead to the nov

110 Inside cells, with microcystin implicated in the fitness of the photosynthe

111 Previous research identified the toxin microcystin in blooms, but we wanted to better understan

112 Contractions induced by microcystin in Ca2+-free solution were associated with i

113 pounds corresponded with greater turnover of microcystins in cells grown on urea compared to nitrate

114 The limit of quantitation for microcystins in drinking water is 0.04 mug/L, well below

115 to monitor cyanobacterial blooms and detect microcystins in freshwater bodies.

116 rea on cellular physiology and production of microcystins in Microcystis aeruginosa NIES-843.

117 evealed the presence of only trace levels of microcystins in the edible parts.

118 The ELISA can be used for quantifying total microcystins in various matrices, including drinking wat

119 eawater halides increased quantum yields for microcystin indirect photodegradation by factors of 3-6.

120 The observed sensitivity of the microcystin-induced contraction to various protein kinas

121 the phosphatase inhibitors okadaic acid and microcystin inhibit transport mediated by the import rec

122 ine/threonine protein phosphatase inhibitor, microcystin, inhibited the desensitization of NPR-A in m

123 detectable cross-reactivity to okadaic acid, microcystin-LA, and microcystin-YR.

124 Microcystin-leucine arginine (MC-LR), associated with th

125 microcystin-tyrosine-arginine (MC-YR) 79.7%, microcystin-leucine-alanine (MC-LA) 74.8%, microcystin-l

126 reactivity with seven microcystin congeners (microcystin-leucine-arginine (MC-LR) 100%, microcystin-t

127 The sensing surface consisted of microcystin-leucine-arginine (MCLR) covalently immobiliz

128 neation exposure of adult zebrafish to MCLR (microcystin-leucine-arginine) and MCRR (microcystin-argi

129 , microcystin-leucine-alanine (MC-LA) 74.8%, microcystin-leucine-phenylalanine (MC-LF) 67.5%, microcy

130 ocystin-leucine-phenylalanine (MC-LF) 67.5%, microcystin-leucine-tryptophan (MC-LW) 63.7%, microcysti

131 bed is the total synthesis of the cyanotoxin microcystin-LF (MC-LF, 1a) and two derivatives thereof.

132 Microcystin LR (MCLR) was covalently bound to the dextra

133 ition of PP2A activity by okadaic acid (OA), microcystin LR (mLR), or fostriecin (Fos) leads to perik

134 Detection limits of 0.4 mug/L for microcystin LR and 10(0) and 10(1) cfu/mL for Salmonella

135 brary against the cyanobacterial hepatotoxin microcystin LR and its selection using competitive panni

136 phatases (sodium fluoride, okadaic acid, and microcystin LR).

137 A protein phosphatase inhibitor, microcystin LR, also induced contraction in the absence

138 r quality inputs was comparable in detecting microcystin-LR (91% correct), as was UV(254) in predicti

139 igate unexplored molecular pathways by which microcystin-LR (MC-LR) acts on hepatocytes to elucidate

140 A novel electrochemical microcystin-LR (MC-LR) biosensor based on the inhibition

141 a novel electrochemical sensing platform for microcystin-LR (MC-LR) detection.

142 ined selective capture and SERS detection of Microcystin-LR (MC-LR) in blood plasma has been develope

143 waveguide immunosensor for the detection of microcystin-LR (MC-LR) in lake water.

144 ntitative and time-integrated measurement of microcystin-LR (MC-LR) in waters.

145 264.7 macrophages, we showed the potency of microcystin-LR (MC-LR) to stimulate production of pro-in

146 The presence of the potent cyanotoxin, microcystin-LR (MC-LR), in drinking water sources poses

147 lindrospermopsin (CYN), nodularin (NOD), and microcystin-LR (MC-LR), in parallel, with the limit of d

148 xpressing a recombinant antibody specific to microcystin-LR (MC-LR), the environmental toxin pollutan

149 ork, we explore proton and iron binding with microcystin-LR (MC-LR).

150 The compounds chosen for this study were microcystin-LR (MLR), phenobarbital (PB), lipopolysaccha

151 rd other coexistent cyanobacterial toxins of microcystin-LR and Anatoxin-a.

152 To immobilize microcystin-LR antibody and improve the electrical condu

153 dropped on the electrode surface and finally microcystin-LR antibody was covalently connected to the

154 Microcystin-LR binds also Mo(6+), Cu(2+), and Mn(2+).

155 The phosphatase inhibitor microcystin-LR blocked rescue of microtubule sliding, in

156 r and before incubation with 2.0x10(-15)M of microcystin-LR can retain 95% over a 20-weeks storage pe

157 inked immunosorbent assay (ELISA) format for microcystin-LR detection was developed, achieving a dete

158 ptamer assembled on a graphene electrode for microcystin-LR detection was developed.

159 It has been successfully applied to the microcystin-LR determination in water samples with a spi

160 or the presence of the active site inhibitor microcystin-LR did not interfere with binding of PP2Ac t

161 Using atomic force microscopy, 40% of microcystin-LR dimers were observed, and the presence of

162 meaningful environmental pHs values shows a microcystin-LR dissociaton constant for Fe(2+) and Fe(3+

163 protein kinase, but did require inclusion of microcystin-LR during cell lysis, implying that phosphor

164 We demonstrate that quantification based on microcystin-LR equivalents can introduce an error of up

165 ses on the immobilized phosphatase inhibitor microcystin-LR identified histone deacetylase 1(HDAC1),

166 effective, and suitable for the detection of microcystin-LR in buffer and spiked tap and river water

167 m would facilitate the routine monitoring of microcystin-LR in real samples.

168 1.2%), sensitive electrochemical response to microcystin-LR in the range of 1.0x10(-16)-8.0x10(-15)M

169 immunosensor for ultrasensitive detection of microcystin-LR in water.

170 ymer (MIP) specific for Cyanobacterial toxin microcystin-LR is presented.

171 show that fluorescence spectra predict both microcystin-LR occurrence and DBP formation potential (D

172 classified 94% of test data with respect to microcystin-LR occurrence, with a 96% probability of cor

173 ility and stability when compared to present microcystin-LR sensors.

174 peak current, allowing the quantification of microcystin-LR through the measurement of peak current c

175 binding was eliminated by addition of excess microcystin-LR to the lysate, showing that binding at th

176 lyclonal antibodies (the detection limit for microcystin-LR using the MIP-based assay was found to be

177 A detection limit of 0.5 mug L(-1) for microcystin-LR was achieved.

178 novel immuno-sensing format can detect free microcystin-LR with a functional limit of detection of 0

179 sor also exhibited excellent selectivity for microcystin-LR with no detectable cross-reactivity to ok

180 of hydrophobic microcystin congeners (e.g., microcystin-LR) was observed in aerosol particles relati

181 hat exhibit high affinity and specificity to microcystin-LR, -YR, and -LA.

182 reated simultaneously with cycloheximide and microcystin-LR, a potent in vivo and in vitro inhibitor

183 Microcystin-LR, a PP1 inhibitor, also attenuated I-2 bin

184 ssociated PP1cbeta readily bound immobilized microcystin-LR, an active-site inhibitor of PP1c.

185 We found that okadaic acid, microcystin-LR, and calyculin A, which are known to spec

186 , the tumor-inducing agents okadaic acid and microcystin-LR, at 2.6 and 2.8 A resolution, respectivel

187 anobacterially produced cyclic heptapeptide, microcystin-LR, both potent inhibitors of mammalian PP1

188 50 with active site inhibitors okadaic acid, microcystin-LR, calyculin A, and cantharidin.

189 s insensitive to inhibition by okadaic acid, microcystin-LR, calyculin A, and cantharidin.

190 1, and several toxins, including tautomycin, microcystin-LR, calyculin A, and okadaic acid.

191 binding site for the toxins okadaic acid and microcystin-LR, in the beta12-beta13 loop with Trp, Phe,

192 AP-associated PP1cbeta did not interact with microcystin-LR, indicating that the active site of PP1cb

193 The cyanobacteria toxins anatoxin-a, microcystin-LR, microcystin-RR, microcystin-YR, and nodu

194 -type and mutant phosphatases to immobilized microcystin-LR, NIPP-1, and I-2 established that the bet

195 tly inhibit eucaryal PP1 and PP2A, including microcystin-LR, okadaic acid, tautomycin, and calyculin

196 The presence of microcystin-LR, on the other hand, caused a dose-respons

197 he visible light-driven rapid degradation of microcystin-LR, one of the most toxic compounds produced

198 ications to produce diagnostic antibodies to microcystin-LR, remove it from the environment by phytor

199 In support of this concept, okadaic acid and microcystin-LR, which are inhibitors of protein phosphat

200 Microcystin-LR-produced by cyanobacteria-is linked with

201 PP4) belongs to a family of okadaic acid and microcystin-LR-sensitive protein phosphatases.

202 ffered by previously reported biosensors for microcystin-LR.

203 or the detection of the cyanobacterial toxin microcystin-LR.

204 nt to hepatoxicity induced by phalloidin and microcystin-LR.

205 ctivated the Nek2::PP1 to the same extent as microcystin-LR.

206 ealing study was used in MIP preparation for microcystin-LR.

207 hy on the immobilized phosphatase inhibitor, microcystin-LR.

208 from a cyanobacterium that does not produce microcystins, M. aeruginosa UTEX 2063.

209 Although there have been numerous studies on microcystin (MC) accumulation in aquatic organisms recen

210 Our results showed that bloom growth and microcystin (MC) concentrations responded more frequentl

211 tification and sensitive quantitation of the microcystin (MC) congeners.

212 tudy examines the effects of electrolytes on microcystin (MC) electrospray ionization (ESI) mass spec

213 d what environmental parameters may regulate microcystin (MC) production and congener type.

214 Microcystin (MC), a cyanotoxin, is the most widely repor

215 The cyanotoxin, microcystin (MC), is known to accumulate in the tissues

216 and this was blocked by a PP1/PP2A inhibitor microcystin (MC)-LR or by mutation of the active sites i

217 The known microcystins (MC) MC-LR, MC-LA, [MeSer7]MC-LR, MC-LL, MC

218 ctive compounds including the harmful toxins microcystins (MC).

219 and analogues), cylindrospermopsin (CYN) and microcystins (MC, and analogues).

220 eric noncompetitive assay for cyanobacterial microcystins (MCs) and nodularins (Nod), a group of stru

221 Microcystins (MCs) are a group of biotoxins (>150) produ

222 Microcystins (MCs) are a group of hepatotoxins produced

223 Microcystins (MCs) are a growing problem in drinking wat

224 Microcystins (MCs) are hepatotoxins produced by cyanobac

225 Microcystins (MCs) are highly toxic natural products whi

226 Microcystins (MCs) are primarily hepatotoxins produced b

227 ication and highly sensitive quantitation of microcystins (MCs) as model targets.

228 tion has been developed for the detection of microcystins (MCs) in freshwater samples.

229 To evaluate ecotoxicological effect of microcystins (MCs) on earthworms, filter paper acute tox

230 Microcystins (MCs) were the most abundant toxins measure

231 yanobacteria producing hepatotoxins, such as microcystins (MCs), together with other bioactive compou

232 of Planktothrix rubescens, which can produce microcystins (MCs), was observed in early 2009 in the Oc

233 iorecognition molecules for the detection of microcystins (MCs).

234 serine-threonine protein phosphatases (PP), microcystin (MCYST) and okadaic acid (OKA) as probes to

235 scovery of three new cyclic peptides, namely microcystin-MhtyR (6), which comprised about half of the

236 ining raw test data from regularly scheduled microcystin monitoring program or (2) the manufacturer o

237 Here, we explored the effect of microcystin/nonmicrocystin (MC/non-MC) producing cyanoba

238 Compounds (calyculin A, microcystin, okadaic acid, and cantharidin) that inhibit

239 und either the biosynthetic genes for making microcystins or the toxin itself in 12% of all analyzed

240 -1C by inhibitor-2, but not by okadaic acid, microcystin, or calyculin A, was also attentuated by the

241 thiophosphorylation at Ser(19), followed by microcystin (phosphatase inhibitor) in the absence of Ca

242 Modeling of microcystin photodegradation along this transect indicat

243 ies (RHS)) could significantly contribute to microcystin photodegradation during transport within est

244 dicated that the time scale for RHS-mediated microcystin photodegradation is comparable to the time s

245 nobacterial cells, and the immobilization of microcystins, preventing their release into the water co

246 Microcystins produced by cyanobacteria were detected in

247 rotein-serine/threonine phosphatase from the microcystin-producing cyanobacterium Microcystis aerugin

248 The microcystin-producing Microcystis aeruginosa PCC 7806 an

249 trains of Microcystis, including 6 different microcystin-producing strains.

250 encoding the enzyme complex responsible for microcystin production and detecting toxins directly fro

251 n differences in global metabolism, cellular microcystin quotas and congener composition.

252 t phenylephrine-induced contractions but not microcystin-racemic mixture-induced contractions.

253 ay disc and applied for the determination of microcystin residues and pathogenic microorganisms.

254 simulation data suggest a wind event caused microcystin-rich water from Maumee Bay to be transported

255 challenges, a numerical index for screening microcystin risks above the World Health Organization's

256 oss-reactivity to other related MCs, such as microcystin-RR (MCRR, 90%), microcystin-RR desmethylated

257 ted MCs, such as microcystin-RR (MCRR, 90%), microcystin-RR desmethylated (dm-MCRR, 95%) and microcys

258 enrichment of hydrophilic microcystin (e.g., microcystin-RR) was lower.

259 obacteria toxins anatoxin-a, microcystin-LR, microcystin-RR, microcystin-YR, and nodularin were separ

260 nously applied protein phosphatase 1 or by a microcystin-sensitive phosphatase also endogenous to exc

261 fied with PP1c by affinity chromatography on microcystin sepharos Immunocytochemical analysis demonst

262 PP2A; and 3) PAK3 and p70 S6 kinase bound to microcystin-Sepharose (an affinity resin for PP2A-PP1).

263 rotein, termed PP4R1, and PP4C also bound to microcystin-Sepharose.

264 fusion of the antigen-binding regions of the microcystin-specific single-chain antibody, 3A8, with co

265 ition of protein phosphatases with 10 microM microcystin stimulated both ICa and ICl, but the stimula

266 n-replete conditions, while the nonproducing microcystin strain is not able to grow.

267 the mcyE gene and the chemical diversity of microcystins suggest that lichen symbioses may have been

268 ular dialysis with the phosphatase inhibitor microcystin, suggesting involvement of endogenous phosph

269 nobacterium and the role of N in controlling microcystin synthesis.

270 time quantitative PCR (qPCR) measurements of microcystin synthetase E (mcyE) gene equivalents (Adj. R

271 ificant decrease in the transcription of the microcystin synthetase gene set under low N and a signif

272 tease inhibitors (aer and mcn gene sets) and microcystin synthetase genes (mcy), with urea enrichment

273 Here, we report the development of novel microcystin-targeting molecules and their application in

274 ocess that gives valuable sequence ions from microcystins that do not contain arginine.

275 reshwater environments produce toxins (e.g., microcystin) that are harmful to human and animal health

276 lters, and water-treatment columns contained microcystins, the highly toxic low-molecular-weight hepa

277 measured by ELISA that exceeded the 4 mug/L microcystin threshold.

278 gger changes (for example, in the binding of microcystin to proteins).

279 n immunogen made by conjugating a mixture of microcystins to cationised bovine serum albumin, and the

280 xicity estimation in terms of cyanobacterial microcystin toxins (MCs) detection.

281 The cyclic heptapeptide microcystin toxins produced by a strain of Microcystis a

282 Microcystin toxins were identified in freshwater, as wel

283 (microcystin-leucine-arginine (MC-LR) 100%, microcystin-tyrosine-arginine (MC-YR) 79.7%, microcystin

284 0.83, p < 0.0001) was equally predicative of microcystin variance across the lake as fluorescence bas

285 dominated by Microcystis sp. and associated microcystin variants, have been implicated in illnesses

286 Organization's (WHO) low-risk threshold for microcystin was developed for eutrophic Midwestern U.S.

287 The effect of microcystin was inhibited by staurosporine (Ki = 171.5 a

288 A plethora of different microcystins was found with over 50 chemical variants, a

289 alpha,beta-unsaturated amide present in most microcystins was shown to simplify analysis of LC-MS chr

290 ark (2.9 x 10(1) mug/L), where low levels of microcystin were found (2.1 x 10 degrees mug/L).

291 The microcystins were separated by reversed-phase microbore

292 d and very reliable identifications of known microcystins when standards are not available and of mos

293 members of a few genera produce hepatotoxic microcystins, whereas production of hepatotoxic nodulari

294 ng mice to the hepatotoxins, griseofulvin or microcystin, which are associated with K18 ser52 and oth

295 t blocking was inhibited by okadaic acid and microcystin with IC50 values of 70 nM and 0.15 nM, respe

296 ll-known of biosensor types for detection of microcystins with a summary of their analytical performa

297 rocystin-RR desmethylated (dm-MCRR, 95%) and microcystin-YR (MCYR, 91%), was also evaluated.

298 es that nodularin was preferred over [15N]10-microcystin-YR or angiotensin I.

299 anatoxin-a, microcystin-LR, microcystin-RR, microcystin-YR, and nodularin were separated in less tha

300 ctivity to okadaic acid, microcystin-LA, and microcystin-YR.