ライフサイエンスコーパス: IAA

1 IAA accumulation does not require JA signaling and sprea

2 IAA accumulation starts 30 to 60 s after local induction

3 IAA induced their activity in galls while PEO-IAA treatm

4 IAA is elicited by herbivore oral secretions and fatty a

5 IAA is sequestered in reversible processes by adding ami

6 IAA levels are reduced in the cotyledon tissue but not m

7 IAA levels were also significantly lower in ecodormant b

8 IAA levels were positively correlated with markers of in

9 IAA redistribution occurred in maize roots, preceding hy

10 IAA removal rose from 16.8 +/- 0.3 to 34.5 +/- 0.7%.

11 IAA/DNP decreased ATP levels (p < 0.05) in cells.

12 IAA/DNP increased exosome secretion from mouse organ cul

13 IAA/DNP treatment (up to 10 uM each) was non-toxic and r

14 were foliar sprayed with water or 6 mg L(-1) IAA.

15 d the FAO recommended daily allowance (277mg IAA/g protein) and contributed on average 40% to total a

16 We found that indanyloxyacetic acid-94 (IAA-94), a blocker of CLICs, delays the growth of Escher

17 The digestible indispensable AA (IAA) score was 1.03 (histidine) for WPI and close to 0 f

18 duces postoperative intra-abdominal abscess (IAA) in children with perforated appendicitis.

19 The plant hormone indole-3-acetic acid (IAA or auxin) mediates the elongation growth of shoot ti

20 ol group and decreased indole-3-acetic acid (IAA) and abscisic acid (ABA) concentrations in the roots

21 indoxyl sulfate (IS), indole-3-acetic acid (IAA) and hippuric acid (HIPA) and their binding competit

22 urally occurring auxin indole 3-acetic acid (IAA) and is important for coordinating growth and patter

23 Indole-3-acetic acid (IAA) and other hormones were quantified using LC-MS/MS.

24 GH3.5) conjugates both indole-3-acetic acid (IAA) and salicylic acid (SA) to modulate auxin and patho

25 l conditions and after indole-3-acetic acid (IAA) application.

26 of genes encoding the indole-3-acetic acid (IAA) biosynthesis enzyme TRYPTOPHAN AMINOTRANSFERASE OF

27 y increased endogenous indole-3-acetic acid (IAA) content, whereas the combination of LCO and IBA loc

28 and leaves synthesize indole-3-acetic acid (IAA) from tryptophan through indole-3-pyruvic acid (3-IP

29 the role of the auxin indole-3-acetic acid (IAA) in this context is not well understood.

30 showed that levels of indole-3-acetic acid (IAA) increased and levels of abscisic acid (ABA) decreas

31 Whereas indole-3-acetic acid (IAA) levels were elevated in young phyB seedlings, there

32 Increasing indole-3-acetic acid (IAA) levels, either in stem tissues above a N-1-naphthyl

33 ogenous application of indole-3-acetic acid (IAA) or auxin analogues might effectively protect field

34 ther the uremic solute indole-3 acetic acid (IAA) predicts clinical outcomes in patients with CKD and

35 ination of auxin (aux)/indole-3-acetic acid (IAA) repressor proteins in the presence of auxin.

36 pyruvic acid (IPyA) to indole-3-acetic acid (IAA), acting downstream of CKRC1/TAA1 in the IPyA pathwa

37 for the production of indole-3-acetic acid (IAA), hydrogen cyanide (HCN), ammonia (NH(3)), and exopo

38 rm of auxin in plants, indole-3-acetic acid (IAA), remains unclear.

39 olism, mediated by the indole-3-acetic acid (IAA)-amido synthetase Gretchen Hagen 3 (GH3).17 [10].

40 reased auxin maxima in indole-3-acetic acid (IAA)-treated root apical meristems; hypergravitropic roo

41 the endogenous auxin, indole-3-acetic acid (IAA).

42 orts picloram, but not indole-3-acetic acid (IAA).

43 ntrations of the auxin indole-3-acetic acid (IAA).

44 curring in the form of indole-3-acetic acid (IAA).

45 ncreases in the auxin [indole-3-acetic acid (IAA)] biosynthesis pathway.

46 he phytohormone auxin [indole-3-acetic acid (IAA)] is essential to plant growth.

47 n of the plant hormone indole-3-acetic acid (IAA, or auxin) is essential for plant development.

48 Indispensable amino acid (IAA) contents (mg IAA/g protein), found to be highest in

49 ed forms indole-3-acetic acid aspartic acid (IAA-Asp) and indole-3-acetic acid glutamic acid (IAA-Glu

50 Asp) and indole-3-acetic acid glutamic acid (IAA-Glu) of 438- and 240-fold, respectively, whereas aux

51 3.2 (ZmGH3.2, encoding indole-3-acetic acid [IAA] deactivating enzyme), and increased IAA in their em

52 main auxin in plants (indole-3-acetic acid [IAA]) has been elucidated recently and is thought to inv

53 he phytohormone auxin (indole-3-acetic acid, IAA) is a small organic molecule that coordinates many o

54 We showed that auxin (indole acetic acid, IAA) repressed the expression of key TIA pathway genes i

55 (IBA) to active auxin (indole-3-acetic acid; IAA) modulates lateral root formation.

56 digestibility of indispensable amino acids (IAAs) in children.

57 digestibility of indispensable amino acids (IAAs) of commonly consumed legumes is not known in human

58 This active IAA elicits shade- and high temperature-induced hypocoty

59 rporates the synthetic auxin derivative 5-Ad-IAA and its high-affinity-binding partner OsTIR1F74A.

60 Additionally, IAA increased production of endothelial reactive oxygen

61 ctin filaments became more 'organized' after IAA stopped elongation, refuting the hypothesis that 'mo

62 ing [U-13C] spirulina protein or a 13C-algal IAA mixture as the standard.

63 to [U-13C] spirulina protein or a 13C-algal IAA mixture did not differ significantly (63.2 +/- 1.5%

64 Co-overexpression of an IAA-conjugating enzyme reduces IAA levels but drought st

65 GADA but negatively with ZnT8WA, IA-2A, and IAA.

66 -pyruvic acid-dependent IAA biosynthesis and IAA conjugation and degradation pathways during ECM form

67 ibitions of IAA synthesis in apical buds and IAA transportation in roots, as well as the imbalance of

68 -D-specific mutants suggested that 2,4-D and IAA might also use distinct pathways to modulate root gr

69 trate that the distinct effects of 2,4-D and IAA on actin filament organization partly dictate the di

70 TRP infusion increased the removal of IS and IAA to 10.5 +/- 0.1% and 27.1 +/- 0.3%, respectively.

71 changes in steady-state levels of oxIAA and IAA conjugates but not IAA.

72 gh levels of ABA, the ABA metabolite PA, and IAA were found in paradormant buds.

73 SA and IAA are hormones known to control stress and defense res

74 ogenous auxin epitopes recognised by an anti-IAA antibody.

75 and reveal the molecular determinants of ARF-IAA interactions.

76 (ABA-GE) and low indole-3-acetate aspartate (IAA-Asp) and isopentenyladenine (iP) contents in BS berr

77 We observed that transcripts of AtDOA1 IAA oxidase and GH3 IAA-conjugating enzymes are auxin-in

78 developed persistent insulin autoantibodies (IAA), GAD autoantibodies (GADA), insulinoma-associated a

79 1 diabetes risk and to insulin autoantibody (IAA), GAD65 (GAD autoantibody [GADA]), IA-2 antigen (IA-

80 the cell cycle machinery and bud-autonomous IAA biosynthesis and transport.

81 There are 29 Aux/IAA genes in Arabidopsis that exhibit unique but partial

82 is thaliana) Auxin/indole-3-acetic acid (Aux/IAA) family member.

83 BIF4 encode AUXIN/INDOLE-3-ACETIC ACID (Aux/IAA) proteins, which are key components of the auxin hor

84 between the AUXIN/INDOLE-3-ACETIC ACID (Aux/IAA) repressor proteins and the AUXIN RESPONSE FACTOR (A

85 he interacting auxin/indole acetic acid (Aux/IAA) repressors.

86 entrality of auxin/indole-3-acetic acid (Aux/IAA) transcriptional corepressors in controlling respons

87 hloem-specific auxin/indole acetic acid (Aux/IAA) transcriptional regulators was found to modulate vi

88 ce of auxin, AUXIN/INDOLE-3-ACETIC ACID (AUX/IAA) transcriptional repressors are targeted for degrada

89 ncluding (1) auxin/indole-3-acetic acid (AUX/IAA)-histone deacetylase (HDA) and (2) auxin response fa

90 ncluding (1) auxin/indole-3-acetic acid (AUX/IAA)-histone deacetylase (HDA) and (2) auxin response fa

91 c removal of auxin/indole-3-acetic acid (AUX/IAA)-inducible repressors, which directly bind to transc

92 ), transport (PIN), perception (TIR/AFB, Aux/IAA), and inactivation/conjugation (GH3, miR167, IAR3) t

93 cidification and growth require TIR1/AFB-Aux/IAA nuclear auxin perception.

94 ect regulation of nearly one-half of all Aux/IAA genes, and that these targets coincide with distinct

95 consisting of a TIR1/AFB protein and an Aux/IAA protein.

96 harged amino acids in conferring ARF and Aux/IAA interactions have confirmed the PB1 domain structure

97 Although the C termini of ARF and Aux/IAA proteins facilitate their homo- and heterooligomeriz

98 ed that members of the large Arabidopsis Aux/IAA family exhibit a range of degradation rates in synth

99 ture and significance of ARF-DNA and ARF-Aux/IAA interactions, we analyzed structure-guided variants

100 rs (ARFs) whose activity is repressed by Aux/IAA proteins under low auxin levels, but relieved from r

101 IAA33 is a non-canonical AUX/IAA protein lacking a TIR1-binding domain, and its role

102 the molecular functions of non-canonical AUX/IAA proteins in auxin signaling transduction.

103 auxin-dependent degradation of canonical AUX/IAA proteins, auxin stabilizes IAA33 protein via MITOGEN

104 pendent protein degradation of canonical AUX/IAA proteins, which normally repress the activity of aux

105 IAA33 competes with the canonical AUX/IAA repressor IAA5 for binding to ARF10/16 to protect th

106 Furthermore, CC Aux/IAA nuclear localization is disrupted upon infection wit

107 sequences flanking the highly conserved Aux/IAA W-P motif do not impact LRT2 catalysis, suggesting t

108 read shows that the inability to disrupt Aux/IAA CC nuclear localization correlates with a reduced ab

109 trate that a virus capable of disrupting Aux/IAA localization is significantly more competitive at mo

110 transcriptional regulation of the entire Aux/IAA family in Arabidopsis thaliana.

111 xpression studies demonstrate a role for Aux/IAA-interacting proteins in the regulation of salicylic

112 strong influence of natural variation in Aux/IAA degradation rates on circuit performance.

113 I/IV that is related to domain III/IV in Aux/IAA proteins).

114 unresolved issue whether differences in Aux/IAA turnover rates played a significant role in plant re

115 e studies have suggested that individual Aux/IAA genes have specialized function, genetic analyses of

116 ypothesis that the rate of auxin-induced Aux/IAA turnover sets the pace for auxin-regulated developme

117 Most AUX/IAA and ARF proteins share highly conserved C-termini me

118 Most Aux/IAA proteins function as negative regulators of auxin re

119 te that the protein products of multiple Aux/IAA targets negatively feed back onto ARF5/MP activity.

120 es between the homodimeric interfaces of AUX/IAA and ARF PB1 domains.

121 errogating auxin-mediated degradation of Aux/IAA by auxin receptors.

122 ling pathway initiated by degradation of Aux/IAA co-repressors.

123 underscoring the functional relevance of Aux/IAA degradation dynamics in regulating auxin responses.

124 hat contribute to tuning the dynamics of Aux/IAA degradation.

125 othesize that transcriptional control of Aux/IAA genes plays a central role in the establishment of t

126 on between TIR1 and a specific subset of AUX/IAA proteins, stimulating the degradation of particular

127 ndirectly by facilitating degradation of Aux/IAA repressors, direct ETTIN-auxin interactions allow sw

128 Characterization of other Aux/IAA proteins showed that they have diverse degradation r

129 timulating the degradation of particular AUX/IAA combinations.

130 r knowledge of the factors that regulate Aux/IAA expression is limited [1, 5].

131 raccumulation of a degradation-resistant Aux/IAA-interacting protein was found to inhibit TMV accumul

132 E/IAA9, a member of the auxin-responsive Aux/IAA protein family of transcriptional repressors, partia

133 nce of the hormonal cue, auxin sensitive Aux/IAA proteins bound to MONOPTEROS block recruitment of th

134 els are regulated by the auxin-sensitive Aux/IAA repressors IAA5, IAA6, and IAA19.

135 oordinated action of the auxin-sensitive Aux/IAA transcriptional repressors and ARF transcription fac

136 ed a minimal complex-comprising a single Aux/IAA repressing a pair of dimerized ARFs-sufficient for a

137 f the Arabidopsis (Arabidopsis thaliana) Aux/IAA family, as well as in their putative Brassica rapa o

138 Altogether, these data indicate that Aux/IAA family members have protein-specific degradation rat

139 is partly due to increased levels of the Aux/IAA and DELLA proteins.

140 duced degradation vary widely within the Aux/IAA family, and sequences outside of the characterized d

141 broadly influences the expression of the Aux/IAA gene family, and suggests that such regulation invol

142 We propose that the Aux/IAA genes function as hubs that integrate genetic and en

143 cription factors (TFs) that regulate the Aux/IAA genes.

144 twork (GRN) through transcription of the Aux/IAA genes.

145 of C-terminal domains III and IV of the AUX/IAA protein PsIAA4 from pea (Pisum sativum) revealed a g

146 The Aux/IAA proteins are auxin-sensitive repressors that mediate

147 associated with increased levels of the Aux/IAA proteins as well as the DELLA repressors, substrate

148 ting of the TIR1/AFB F-box proteins, the Aux/IAA transcriptional repressors, and the ARF transcriptio

149 igase responsible for degradation of the Aux/IAA transcriptional repressors.

150 In particular, the AUX/IAA, ERFs, WRKY, NAC, and MADS TF family members were up

151 highly conserved cyclophilins and their Aux/IAA targets.

152 transcription occurs exclusively through Aux/IAA function.

153 quitin ligase, allowing interaction with Aux/IAA transcriptional repressor proteins.

154 e (TIR1) with auxin/3-indoleacetic acid (Aux/IAAs) proteins, further supporting the possibility that

155 Recent structural analyses of ARFs and Aux/IAAs have raised questions about the functional complexe

156 inance relationships between coexpressed Aux/IAAs were sufficient to generate distinct response modul

157 ture tissues TMV 126/183-kDa-interacting Aux/IAAs predominantly express and accumulate within the nuc

158 trella patens line that completely lacks Aux/IAAs.

159 In addition, monomeric Aux/IAAs were able to repress ARF activity in both yeast and

160 circuit was expanded to include multiple Aux/IAAs, we found that dominance relationships between coex

161 adation rates and that ubiquitination of Aux/IAAs can occur on multiple types of amino residues to pr

162 gnaling and demonstrates the key role of Aux/IAAs in tuning auxin response dynamics.

163 turnover, leading to the conclusion that Aux/IAAs are auxin-initiated timers that synchronize develop

164 coreceptor results in degradation of the Aux/IAAs and derepression of ARF-based transcription.

165 d on analysis of stabilized forms of the Aux/IAAs, and studies of a subgroup of ARFs that function as

166 ion jointly with activating ARFs and the Aux/IAAs.

167 ithin the cell by applying the natural auxin IAA.

168 hormones such as abscisic acid (ABA), auxin (IAA), and gibberellic acid (GA).

169 ses (FMOs), with an important role in auxin (IAA) biosynthesis.

170 r lines, MIR172A-E::GUS, treated with auxin (IAA) and an auxin-inhibitor (a-(phenyl ethyl-2-one)-indo

171 ion of AUXIN SIGNALING F-BOX PROTEIN5, AUXIN/IAA, and AUXIN RESPONSE FACTOR expression in ECM roots s

172 ABA was found to suppress bud IAA accumulation, thus confirming this aspect of its act

173 In cultured human endothelial cells, IAA activated an inflammatory nongenomic aryl hydrocarbo

174 no evidence that Pinus spp. synthesize 4-Cl-IAA in seeds, contrary to a previous report.

175 the first time, to our knowledge, that 4-Cl-IAA is found in the seeds of Medicago truncatula, Melilo

176 dicates a single evolutionary origin of 4-Cl-IAA synthesis in the Fabaceae, which may provide an idea

177 ed auxin, 4-chloroindole-3-acetic acid (4-Cl-IAA), greatly exceeds that of IAA.

178 s produce halogenated compounds such as 4-Cl-IAA.

179 At low auxin concentrations, IAA repressors associate with ARF proteins and recruit c

180 primary endpoint was 30-day image-confirmed IAA.

181 In contrast, IAA does not affect the accumulation of nicotine or 7-hy

182 nd inflorescence stems, thus supporting DAO1 IAA oxidase function in vivo.

183 hanges in the indol-3-pyruvic acid-dependent IAA biosynthesis and IAA conjugation and degradation pat

184 Residues that determine IAA versus BA substrate preference were identified.

185 in life (median age <2 years) and developed IAA and IA-2A that were stable-positive on follow-up had

186 ggests that AtGH3.5 conjugates auxins (i.e., IAA and PAA) and benzoates (i.e., SA and BA) to mediate

187 ly onset of each initial autoantibody, i.e., IAA-first by 12 months and GADA-first by 21 months, cons

188 plants overexpressing YUC6 display enhanced IAA-related phenotypes and exhibit improved drought stre

189 hthylphthalamic acid treatment and exogenous IAA application depends on a known auxin signaling pathw

190 pyl9 double mutant was reversed by exogenous IAA.

191 ma ascorbic acid and cholesterol experienced IAA-first earlier, while early onset of GADA-first was p

192 5-F-IAA selectively activated the TIR1/AFB pathway but did n

193 -IAA), and 5-fluoroindole-3-acetic acid (5-F-IAA) to discriminate between ABP1- and TIR1/AFB-mediated

194 olyol or simple alcohols, or sugars, forming IAA conjugates, or through a two-carbon elongation formi

195 A auto-inserts into lipid bilayers and forms IAA-94-sensitive ion channels.

196 Hagen 3 (GH3).17) leads to increases in free IAA at the expense of IAA-Glu (IAA-glutamate) in the hyp

197 Exosomes from IAA/DNP-treated or untreated cells had similar biologica

198 Further, IAA-94 delayed the growth of wild-type but not sspA null

199 itivity for at least one autoantibody (GADA, IAA, or IA-2A) on two or more visits.

200 During SD induction, auxin genes IAA, ARF and SAURs were down-regulated and circadian gen

201 at transcripts of AtDOA1 IAA oxidase and GH3 IAA-conjugating enzymes are auxin-inducible, providing a

202 eases in free IAA at the expense of IAA-Glu (IAA-glutamate) in the hypocotyl epidermis.

203 ignificantly higher in the higher IAA group (IAA>3.73 microM) than in the lower IAA group (IAA<3.73 m

204 AA>3.73 microM) than in the lower IAA group (IAA<3.73 microM).

205 Hence, IAA conjugation and catabolism seem to regulate auxin le

206 cing a hydrostimulant, resulting in a higher IAA content on the dry side.

207 ents were significantly higher in the higher IAA group (IAA>3.73 microM) than in the lower IAA group

208 s concentration of a conjugated form of IAA (IAA-Ala).

209 elongation zone prior to bending identified IAA response and lignin synthesis/wall cross-linking as

210 The true mean ileal IAA digestibility of legumes in healthy Indian adults wa

211 The true mean ileal IAA digestibility of mung bean when referenced to [U-13C

212 The true ileal IAA digestibilities (mean +/- SD) of chickpea, yellow pe

213 In this study we measured the true ileal IAA digestibility of 2H-intrinsically labeled chickpea,

214 of this study was to measure the true ileal IAA digestibility of 4 (rice, finger millet, mung bean,

215 The true ileal IAA digestibility of 4 foods commonly consumed in comple

216 The true ileal IAA digestibility of mung bean improved to 70.9 +/- 2.1%

217 True ileal IAA digestibility was determined by the dual-isotope tra

218 True ileal IAA digestibility was lowest in mung bean (65.2% +/- 7.1

219 hy Indian adults to measure their true ileal IAA digestibility with the dual-isotope tracer technique

220 llows the plant to compensate for changes in IAA input pathways and maintain cellular homeostasis.

221 hat overlaps with the FMO domain involved in IAA biosynthesis.

222 id [IAA] deactivating enzyme), and increased IAA in their embryo, produced longer seedling shoots and

223 vitropic root growth and response; increased IAA levels in shoot apices; and reduced auxin accumulati

224 uced inhibition of root growth by increasing IAA accumulation and recovering the damaged cell structu

225 this study was to investigate Al(3+)-induced IAA transport, distribution, and the relation of these t

226 isk and with autoantibodies against insulin (IAA), GAD65 (GADA), IA-2 (IA-2A), and ZnT8 (ZnT8A).

227 n initial autoantibody only against insulin (IAA-first) or GAD (GADA-first) by unsupervised clusterin

228 against GAD (GADA-first) or against insulin (IAA-first).

229 with the first autoantibody against insulin (IAA-first).

230 were treated or not with sodium iodoacetate (IAA; glycolysis inhibitor) plus 2,4-dinitrophenol (DNP;

231 Stable isotope-labeled IAA feeding studies of loss and gain of function AtDAO1

232 ated in young phyB seedlings, there was less IAA in mature stems compared with the wild type.

233 ly root-expressed, cytoplasmically localized IAA oxidase.

234 ic process in Arabidopsis and that localized IAA oxidation plays a role in plant morphogenesis.

235 AA group (IAA>3.73 microM) than in the lower IAA group (IAA<3.73 microM).

236 tion largely independently of 3-IPA-mediated IAA biosynthesis in cotyledons.

237 Indispensable amino acid (IAA) contents (mg IAA/g protein), found to be highest in pangas (430) and

238 5 is unique to this enzyme although multiple IAA-conjugating GH3 proteins share nearly identical acyl

239 when based on the relative amounts of native IAA in the stems.

240 2,4-D but not IAA altered the actin structure in long-term and short-t

241 e levels of oxIAA and IAA conjugates but not IAA.

242 Notably, IAA level remained predictive of mortality when adjusted

243 etabolic profiling showed an accumulation of IAA and changes in the indol-3-pyruvic acid-dependent IA

244 In planta analysis of IAA, PAA, SA, and BA and their respective aspartyl conju

245 Exogenous application of IAA markedly alleviated the Al(3+)-induced inhibition of

246 The distribution of IAA fluorescence signals in root tips was disturbed, and

247 2',3'-cAMP into 2'- and 3'-AMP), effects of IAA/DNP on exosome secretion were enhanced.

248 3'-AMP mimicked the potentiating effects of IAA/DNP on exosome secretion.

249 s to increases in free IAA at the expense of IAA-Glu (IAA-glutamate) in the hypocotyl epidermis.

250 genous concentration of a conjugated form of IAA (IAA-Ala).

251 tation in roots, as well as the imbalance of IAA distribution in root tips.

252 could be associated with the inhibitions of IAA synthesis in apical buds and IAA transportation in r

253 ydrostimulant sensing and the involvement of IAA redistribution.

254 ever, the enzyme that catalyzes oxidation of IAA to its primary catabolite 2-oxindole-3-acetic acid (

255 d manipulated the spatiotemporal patterns of IAA accumulation in herbivore-attacked Nicotiana attenua

256 e redistribution is caused by a reduction of IAA content on the side facing a hydrostimulant, resulti

257 This method enables quick screening of IAA conjugates in both previously characterized as well

258 Exogenous supplementation of IAA to the unaged, germinating NS seeds increased subseq

259 3-phosphate dehydrogenase as a key target of IAA, specifically attacking the catalytic Cys 152.

260 tic acid (4-Cl-IAA), greatly exceeds that of IAA.

261 the stress-related phenotype is not based on IAA overproduction.

262 henyl ethyl-2-one)-indole-3-acetic acid (PEO-IAA)), together with the MIR172C AuxRE::GUS line with tw

263 phenylethyl-2-oxo)-indole-3-acetic acid (PEO-IAA), and 5-fluoroindole-3-acetic acid (5-F-IAA) to disc

264 In contrast, PEO-IAA induced an auxin-like swelling response but no hypoc

265 AA induced their activity in galls while PEO-IAA treatment and mutations in AuxRe motifs abolished it

266 Plasma IAA concentration significantly increased after WPI inta

267 The PVI arm had 12% postoperative IAA versus 16% in the NI arm (relative risk 0.72, 95% cr

268 ng probability of reduction in postoperative IAA with a high probability of decreased LOS.

269 levels, indicating that DAO1 is the primary IAA oxidase in seedlings.

270 ression of an IAA-conjugating enzyme reduces IAA levels but drought stress tolerance is unaffected, i

271 s estimates 89% probability that PVI reduces IAA.

272 In conclusion, serum IAA may be an independent predictor of mortality and car

273 regression analysis demonstrated that serum IAA was a significant predictor of mortality and cardiov

274 for the facile characterization of the small IAA conjugate profile of plants.

275 on and dynamics in control roots; short-term IAA treatments stimulated denser and more parallel, long

276 Together, these data confirm that IAA oxidation by DAO1 is the principal auxin catabolic p

277 We found that IAA is strongly, rapidly, and specifically induced by he

278 We found that IAA-targeted gene activity is frequently increased in hy

279 ts in pea and maize (Zea mays) indicate that IAA biosynthetic enzymes are not the main enzymes for PA

280 transport inhibition experiments reveal that IAA is required for the herbivore-specific, JA-dependent

281 of the auxin response pathway revealed that IAA and 2,4-D share a common mode of action to elicit do

282 Our findings suggest that IAA-first and GADA-first are heralded by different patte

283 The IAA/DNP combination is a powerful stimulator of exosome

284 signals in root tips was disturbed, and the IAA transportation from shoot base to root tip was inhib

285 reversible auxin conjugation mediated by the IAA-amino synthase GRETCHEN HAGEN 3.17 (GH3.17).

286 Aluminium stress significantly decreased the IAA concentration in apical buds and root tips.

287 Recessive mutations in these IAA genes result in decreased tolerance to stress condit

288 Disrupting this IAA-sensing ability induces morphological aberrations wi

289 onversion of Trp to indole-3-pyruvic acid to IAA However, the pathway leading to a less well studied

290 similarities between the pathways leading to IAA and PAA, evidence from mutants in pea and maize (Zea

291 aux1 mutant actin organization responses to IAA and the membrane-permeable auxin 1-naphthylacetic ac

292 However, mechanisms governing IBA-to-IAA conversion have yet to be elucidated.

293 Taken together, our results uncover IAA as a rapid and specific signal that regulates a subs

294 Here we show that loss of function of VAS2 (IAA-amido synthetase Gretchen Hagen 3 (GH3).17) leads to

295 In vitro, IAA induces endothelial inflammation and oxidative stres

296 rmancy, ABA and PA levels decreased, whereas IAA levels were maintained.

297 w enhanced resistance to 2,4-D compared with IAA for inhibition of root growth, were also found to ha

298 stal structure of the enzyme in complex with IAA and AMP.

299 ed region or in plants directly sprayed with IAA, inhibits fiber wall thickening.

300 rent growth conditions, after treatment with IAA, and in different developmental stages.