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 as the first autoantibody showed a peak time of appe

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

5 IAA is elicited by herbivore oral secretions and fatty a

6 IAA is sequestered in reversible processes by adding ami

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

8 IAA levels were also significantly lower in ecodormant b

9 IAA levels were positively correlated with markers of in

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

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

12 he applied [13C1]IBA were converted to [13C1]IAA during transport, but [13C1]IBA transport was indepe

13 [13C1]IBA was dramatically lower than [13C6]IAA, and the IBA transport was not reduced by the auxin

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

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

16 indole-3-pyruvate (IPA) to indole-3-acetate (IAA).

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

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

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

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

21 synthesis of the auxin indole-3-acetic acid (IAA) and production of virulence factors that alter auxi

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

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

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

25 The bulk of indole-3-acetic acid (IAA) in plants is found in the form of conjugated molecu

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

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

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

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

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

31 ncrease in radioactive indole-3-acetic acid (IAA) transport and its accumulation in the hypocotyl abo

32 Indole-3-acetic acid (IAA), a major plant auxin, is produced in both tryptopha

33 and the production of indole-3-acetic acid (IAA), a ubiquitous plant hormone that signals bacterial

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

35 ion of the main auxin, indole-3-acetic acid (IAA), by sugars requires changes in the expression of mu

36 The native auxin, indole-3-acetic acid (IAA), is a major regulator of plant growth and developme

37 sistently regulated by indole-3-acetic acid (IAA), partitioning into 60 clusters with distinct respon

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

39 Levels of indole-3-acetic acid (IAA), the primary auxin, are tightly regulated through b

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

41 tion to amino acids by indole-3-acetic acid (IAA)-amido synthetases is an important part of auxin hom

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

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

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

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

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

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

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

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

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

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

52 ed to examine the role of indoleacetic acid (IAA) in regulating floral organ abscission in Arabidopsi

53 stress with a rank order of iodoacetic acid (IAA) > bromoacetic acid (BAA) >> chloroacetic acid (CAA)

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

55 he phytohormone auxin (indole-3-acetic acid [IAA]) plays a fundamental role in vegetative and reprodu

56 nactive form of auxin (indole-3-acetic acid [IAA]-alanine) and releases bioactive auxin (IAA), a cent

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

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

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

60 Additionally, IAA increased production of endothelial reactive oxygen

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

62 associations were found between HLA-A*24 and IAA or GADA.

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

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

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

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

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

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

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

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

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

72 The interaction between ARFs and IAAs is thus central to auxin signalling and occurs thro

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

74 Interrupted aortic arch (IAA) is a rare congenital malformation of the aortic arc

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

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

77 develops persistent insulin autoantibodies (IAA; almost always as the only islet autoantibody) witho

78 1 diabetes risk and to insulin autoantibody (IAA), GAD65 (GAD autoantibody [GADA]), IA-2 antigen (IA-

79 ive sample as insulin (insulin autoantibody [IAA]) in 180, as GAD (GAD antibody [GADA]) in 107, and a

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 raction with AUXIN/INDOLE 3-ACETIC ACID (Aux/IAA) proteins.

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

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

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

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

89 otein and an AUXIN/INDOLE-3-ACETIC ACID (Aux/IAA) transcriptional repressor.

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

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

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

93 ravitropic offset component via TIR1/AFB-Aux/IAA-ARF-dependent auxin signaling within the gravity-sen

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 We used an Aux/IAA-based reporter, domain II (DII)-VENUS, in conjunctio

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

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

99 etween AUXIN RESPONSE FACTORS (ARFs) and Aux/IAA repressors play a central role in auxin signal trans

100 However, of the 29 apparent Aux/IAA proteins in Arabidopsis thaliana, fewer than half ha

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

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

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

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

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

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

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

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

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

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

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

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

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

114 as AUXIN/INDOLE-3-ACETIC ACID INDUCIBLE (AUX/IAA) proteins that repress the activity of at least a su

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

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

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

118 ferent knockout mutants for the negative AUX/IAA regulators shy2-101 (iaa3), axr2-1 (iaa7) and slr-1

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

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

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

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

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

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

125 g of the IAA7/IAA14/IAA16/IAA17 clade of Aux/IAA proteins and the diverse roles of these repressors i

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

127 Similar detailed analyses of other Aux/IAA-ARF regulatory modules will be required to fully und

128 members of the TIR1/AFB auxin receptors, Aux/IAA repressors, and ARF transcription factors and/or mol

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

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

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

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

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

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

135 Expression of a stabilized Aux/IAA protein (i.e., IAA16) bearing PB1 mutations in Arabi

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

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

138 ctor (ARF) transcription factors and the Aux/IAA (IAA) transcriptional repressors.

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 transcription occurs exclusively through Aux/IAA function.

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

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

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

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

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

156 trella patens line that completely lacks Aux/IAAs.

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

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

159 ity between TIR1 and the degron motif of Aux/IAAs and enhance the activity of the SCF(TIR1) complex.

160 This resulted in faster degradation of Aux/IAAs and increased transcription of auxin-responsive gen

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 entified that increased interaction with Aux/IAAs.

168 [IAA]-alanine) and releases bioactive auxin (IAA), a central phytohormone for root development.

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 ed a nonradioactive IAA assay where bivalent IAA cross-link two insulin moieties in a fluid phase.

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

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

175 ontrast, 100% (32 of 32) high-risk children (IAA plus other islet autoantibodies) were positive with

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

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

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

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

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

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

182 At higher auxin concentrations, IAAs are degraded and ARFs become free to regulate auxin

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

184 bine disruptions in the pathways, converting IAA conjugates and indole-3-butyric acid to free IAA.

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

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

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

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

189 Elevated IAA levels did not interfere significantly with host def

190 We demonstrated that elevated IAA biosynthesis in transgenic plants overexpressing the

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

192 n after hypocotyl excision leads to enhanced IAA transport and local IAA accumulation driving adventi

193 pyl9 double mutant was reversed by exogenous IAA.

194 5-F-IAA selectively activated the TIR1/AFB pathway but did n

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

196 These observations support a key role for IAA in the regulation of abscission in planta and reveal

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

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

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

200 conjugates and indole-3-butyric acid to free IAA.

201 and the transport mechanism is distinct from IAA transport.

202 e first time, a requirement for a functional IAA signaling pathway in AZ cells for organ shedding to

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

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

205 or pathway in Arabidopsis thaliana generates IAA in two reactions from tryptophan.

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

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

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

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

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

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

212 (ARF) transcription factors and the Aux/IAA (IAA) transcriptional repressors.

213 lysis of petal breakstrength reveals that if IAA AZ levels are reduced, shedding takes place prematur

214 ng function were examined for alterations in IAA-regulated root growth and development.

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

216 ctive endosperm18 (de18) that is impaired in IAA biosynthesis.

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

218 Thus, in IAA overproducing plants, the promotion of pathogen grow

219 nt extracts for indolic compounds, including IAA conjugates.

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

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

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

223 Autoantibodies to insulin (IAA), GAD (GADA), islet antigen-2 (IA-2A), and zinc tran

224 otype and autoantibody responses to insulin (IAA), glutamate decarboxylase (GADA), IA-2, IA-2beta, an

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

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

227 on leads to enhanced IAA transport and local IAA accumulation driving adventitious root formation.

228 is temporally and spatially linked to local IAA accumulation leading to adventitious root formation.

229 ly root-expressed, cytoplasmically localized IAA oxidase.

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

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

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

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

234 bset of IAA with current radioassay (not MSD-IAA) represents biologic false positives in terms of aut

235 islet autoantibodies) were positive with MSD-IAA.

236 5 is unique to this enzyme although multiple IAA-conjugating GH3 proteins share nearly identical acyl

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

238 We developed a nonradioactive IAA assay where bivalent IAA cross-link two insulin moie

239 2,4-D but not IAA altered the actin structure in long-term and short-t

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

241 Notably, IAA level remained predictive of mortality when adjusted

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

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

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

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

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

247 These sequestered forms of IAA alter hormone activity.

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

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

250 Modeling of IAA and two synthetic auxins, benzothiazole-2-oxyacetic

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

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

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

254 These data suggest that a subset of IAA with current radioassay (not MSD-IAA) represents bio

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

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

257 s, we conducted site-directed mutagenesis on IAA-CONJUGATE-RESISTANT4 (IAR4), a protein putatively fu

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

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

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

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

262 4 nondiabetic subjects who were persistently IAA(+) were analyzed.

263 ole-3-acetic acid (oxIAA) is a major primary IAA catabolite formed in Arabidopsis thaliana root tissu

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

265 of the C4a-intermediate with IPA to produce IAA.

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

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

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

269 iple genes and metabolites linked to several IAA biosynthetic pathways.

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

271 he polar transport of IBA is much lower than IAA in Arabidopsis hypocotyls, and the transport mechani

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

273 We found that IAA degradation dynamics vary widely, depending on which

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

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

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

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

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

279 analyses of membrane potential revealed that IAA-induced hyperpolarization of the plasma membrane is

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

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

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

283 Disrupting this IAA-sensing ability induces morphological aberrations wi

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

285 ed by a rate-limiting step converting IPA to IAA catalyzed by YUCCA proteins.

286 YUC6 uses NADPH and oxygen to convert IPA to IAA.

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

288 The two-step conversion of Trp to IAA is the main auxin biosynthesis pathway that plays an

289 13C1]IBA transport was independent of IBA-to-IAA conversion.

290 transport was measured by tracing tritiated IAA in excised shoots.

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

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

293 In vitro, IAA induces endothelial inflammation and oxidative stres

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

295 Many cases with IAA are diagnosed at their neonatal and newborn period b

296 enotypes were more frequent in children with IAA as the first autoantibody compared with the other ch

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 Here we report a 20-year-old young man with IAA associated with sinus venosus atrial septal defect (

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