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1 ing before E75B, coincident with the rise of ecdysteroid.
2 s in insects and plants that have endogenous ecdysteroids.
3 espectively, two tissues known to synthesize ecdysteroids.
4 tial neuroprotective effect of nonconjugated ecdysteroids.
5              Here, we identify the signal as ecdysteroids.
6 nces in the sensitivity or responsiveness to ecdysteroids.
7 ts is regulated by juvenile hormone (JH) and ecdysteroids.
8 important roles in cross-talk between JH and ecdysteroids.
9 compounds include organic acids, hematin, or ecdysteroids.
10  the malaria mosquito Anopheles gambiae, the ecdysteroid 20-hydroxyecdysone (20E) appears to have evo
11  Two key hormones, juvenile hormone (JH) and ecdysteroids (20-hydroxyecdysone, 20E, is the most activ
12 gered hormonally by the prepupal peak of the ecdysteroid, 20-hydroxyecdysone (20-HE).
13 cessfully obtained and used to identify four ecdysteroids: 20-hydroxyecdysone-3-O-beta-D-glycopyranos
14 t not B. bassiana, has apparently evolved an ecdysteroid-22-oxidase (MrE22O) that inactivate ecdysone
15         We identify a male-specific oxidized ecdysteroid, 3-dehydro-20E (3D20E), which safeguards pat
16         With the evolution of metamorphosis, ecdysteroids acquired a metamorphic function that exploi
17                                              Ecdysteroids acting through multiple isoforms of the ecd
18 in both JH (methoprene-tolerant protein) and ecdysteroid action (ecdysone receptor and ultraspiracle)
19                                   JH directs ecdysteroid action, controlling Kr-h1 expression which i
20 c morphogenesis and does so independently of ecdysteroid action.
21  steroids through a sophisticated network of ecdysteroid-activating/inactivating enzymes.
22 orphosis reflect what would be predicted for ecdysteroid activation of the EcR/USP heterodimer.
23  field-use rates, a neurotoxic effect of the ecdysteroid agonist RH-5849 is observed that involves bl
24      Researchers have developed nonsteroidal ecdysteroid agonists for EcR that disrupt molting and ca
25  molting is known to be regulated largely by ecdysteroids and crustacean hyperglycemic hormone (CHH)
26 tasks, from the synthesis and degradation of ecdysteroids and juvenile hormones to the metabolism of
27                             The EcR binds to ecdysteroids and regulates transcription of genes that c
28 timately linked to two hormonal systems, the ecdysteroids and the juvenile hormones (JH), which funct
29 horacic glands are the predominate source of ecdysteroids, and the rate of synthesis of these polyhyd
30 correlated with changes in the titers of the ecdysteroids, and these events could be prevented by app
31                                              Ecdysteroids are multifunctional hormones in male and fe
32                                   MF and the ecdysteroids are respectively synthesised under the nega
33 However, little is known about the action of ecdysteroids at the level of gene transcription and regu
34 evidence for negative feedback regulation of ecdysteroids at the site of moult-inhibiting hormone (MI
35 gland, which results in an increased rate of ecdysteroid biosynthesis (upregulation); (b) how the con
36                                              Ecdysteroid biosynthesis and its hormonal regulation are
37 zonin (Crz)-producing neurons regulate basal ecdysteroid biosynthesis by affecting PTTH neurons.
38      This review summarizes the evidence for ecdysteroid biosynthesis by gonads and its metabolism in
39  25 hydroxylase and has an essential role in ecdysteroid biosynthesis during insect development.
40 )-producing neurons stimulate peak levels of ecdysteroid biosynthesis for maturation [3].
41 st that the Crz-PTTH neuronal axis modulates ecdysteroid biosynthesis in response to octopamine, unco
42 , designated Cyp306a1, that is essential for ecdysteroid biosynthesis in the PGs of the silkworm Bomb
43  physiological properties of the enzymes for ecdysteroid biosynthesis, most of the molecular identiti
44 h npc2b in regulating sterol homeostasis and ecdysteroid biosynthesis, probably by controlling the av
45 ts that the embryonic epidermis is a site of ecdysteroid biosynthesis.
46 ar how PTTH signaling is regulated for basal ecdysteroid biosynthesis.
47 t the ring gland and regulates expression of ecdysteroid biosynthetic genes.
48 ifferentiative and maturational responses to ecdysteroids by requiring tonic exposure to the hormone
49 on and off repeatedly simply by shifting the ecdysteroid concentration to above or below this thresho
50 sis of a standard of 20-hydroxyecdysone- and ecdysteroid-containing plant extracts.
51                                              Ecdysteroid control of proliferation is distinguished fr
52 urs throughout such animals, suggesting that ecdysteroids control development of other tissues in a m
53                  The insect steroid hormone, ecdysteroid, coordinates growth and maturation, represen
54                                   Subsequent ecdysteroid decline is required for peptide release, whi
55                           In contrast to the ecdysteroid-deficient, larval-lethal phenotype of npc1a
56 ping Drosophila eye is an early metamorphic, ecdysteroid-dependent event.
57 ptic lobe development to be divided into two ecdysteroid-dependent phases.
58 ows two different developmental responses to ecdysteroids depending on the concentration to which it
59                                    Pulses of ecdysteroids direct Drosophila through its life cycle by
60 tor E74 is one of the early genes induced by ecdysteroids during metamorphosis of Drosophila melanoga
61 ithin the optic lobe anlagen is dependent on ecdysteroids during metamorphosis of the moth Manduca se
62    Genetic analysis shows that DIOMs secrete ecdysteroids during mTOR-mediated muscle remodeling.
63 dysteroid receptor (EcR/USP) and products of ecdysteroid early responsive genes (E74, E75, and Broad)
64 t partially overlapping binding cavities for ecdysteroid (ECD) and diacylhydrazine (DAH) ligands, pro
65 ted from enhanced growth rate and a delay in ecdysteroid elevation during the mid-third instar larval
66 ponasterone A), identified through screening ecdysteroids from local plants, demonstrated sustained r
67                    The in vitro secretion of ecdysteroids from the prothoracic glands of last instar
68                  Here, we examine a putative ecdysteroid glycosyltransferase, Hba_07292 (Hb-ugt-1), w
69 amorphosis, a pulse of circulating steroids, ecdysteroids, governs the dramatic remodeling of larval
70 e fifth instar (after the commitment peak of ecdysteroids) had little effect on proliferation.
71 e gene regulation properties of one of these ecdysteroids have been examined in cell culture and in n
72                                  Fifty-eight ecdysteroids, herbal analogues of the insect molting hor
73                                          The ecdysteroid hormone 20-hydroxyecdysone (20E), transferre
74 emonstrates that molting is regulated by the ecdysteroid hormone in the tardigrade Hypsibius exemplar
75                    By removing the source of ecdysteroid hormone through ligation, and by subsequent
76 ods and considers the apparent uniqueness of ecdysteroid hormones in arthropods, given the predominan
77           The functional receptor for insect ecdysteroid hormones is a heterodimer consisting of two
78 od meal and stimulate the ovaries to secrete ecdysteroid hormones, which modulate yolk protein synthe
79 this complex responds to a distinct class of ecdysteroids in a manner that is independent of EcR.
80  integument of ticks are sources of secreted ecdysteroids in adults, as in earlier stages, but the ti
81                                  The role of ecdysteroids in modulating exoskeletal growth during the
82 nal) instar when the epidermis is exposed to ecdysteroids in the absence of juvenile hormone (JH) and
83 mplicating this tissue as a source of active ecdysteroids in the early embryo.
84             To better understand the role of ecdysteroids in the molt regulation, the full-length cDN
85 ttle is known about the relative activity of ecdysteroids in various arthropods.
86 o the changes in the levels of hemolymphatic ecdysteroids indicates that these tissues may have diffe
87                                          The ecdysteroids induce and direct molting through the ecdys
88                              We propose that ecdysteroid-induced E75A expression defines a feed-forwa
89                           The homolog of the ecdysteroid-induced transcription factor E75A in Drosoph
90 5A, E75B, and E75C, encoded by the E75 early ecdysteroid-inducible gene.
91                                              Ecdysteroids initiate molting and metamorphosis in insec
92  are elucidating the specificity of receptor-ecdysteroid interactions, the selectivity of some enviro
93 re viable and fertile with relatively normal ecdysteroid level.
94            Prior to behavioral onset, rising ecdysteroid levels induce expression of the ecdysone rec
95 proliferating and later degenerate with high ecdysteroids levels.
96                                              Ecdysteroids mediate a wide variety of developmental and
97  in regulating the cyclicity of vitellogenic ecdysteroid-mediated signaling through heterodimerizatio
98                                              Ecdysteroid metabolism occurs in several tissues of adul
99 eveloping epidermis when there is a surge of ecdysteroid midway through embryogenesis.
100 lateral cells of the ring gland that produce ecdysteroid molting hormone (EC).
101 eptor (EcR), functions as a receptor for the ecdysteroid molting hormones of insects.
102 urs at a characteristic concentration of the ecdysteroid molting hormones that regulate metamorphosis
103                                 Synthesis of ecdysteroids (molting hormones) by crustacean Y-organs i
104                         The prepupal peak of ecdysteroids (molting hormones) triggers the regression
105 d by a combination of neuropeptide hormones, ecdysteroids (moulting hormones) and the isoprenoid, met
106         We use cultured tissues to show that ecdysteroids must be maintained above a sharp threshold
107 TTH signaling indicated that basal levels of ecdysteroid negatively affect systemic growth prior to m
108                When exposed to low levels of ecdysteroid, NO production is stimulated and proliferati
109 ulture experiments indicate that the peak of ecdysteroids occurring at pupariation is required for th
110               Our results show the effect of ecdysteroids on MDR cancer cells for the first time.
111  signaling pathway, and the juvenile hormone/ecdysteroid pathway.
112 gulated CYP307A1 in the juvenile hormone and ecdysteroid pathways, respectively, were linked to accel
113 r cascade', which translates features of the ecdysteroid peak into the different phases of the molt.
114 result from some cells 'misinterpreting' the ecdysteroid peaks that drive metamorphosis.
115    The results suggest that both neurons and ecdysteroids play an important regulatory role in adult
116 100-400 microg on column) but also the major ecdysteroids present in crude extracts of Silene otites,
117 ease in intracellular free Ca(2+) stimulates ecdysteroid production by crustacean molting glands (Y-o
118 dently stimulated yolk uptake by oocytes and ecdysteroid production by the ovaries at lower concentra
119                                 In contrast, ecdysteroids promote metamorphosis by inducing the E93 t
120                            In contrast, free ecdysteroids protected both cell lines from tBHP-induced
121                                              Ecdysteroid pulses trigger the major developmental trans
122  responses are thought to be mediated by the ecdysteroid receptor (EcR) and its heterodimeric partner
123 consisting of two nuclear hormone receptors, ecdysteroid receptor (EcR) and the retinoid X receptor h
124 traspiracle (USP), the obligatory functional ecdysteroid receptor (EcR) partner.
125 erived from the Drosophila melanogaster (Dm) ecdysteroid receptor (EcR)- and retinoid X receptor (RXR
126 s an obligatory dimerization partner for the ecdysteroid receptor (EcR).
127 yecdysone (20E) are dually controlled by the ecdysteroid receptor (EcR/USP) and products of ecdystero
128 ow that a transcriptional coactivator of the ecdysteroid receptor complex, FISC, acts as a functional
129 operative interaction between AaE74B and the ecdysteroid receptor is required for high-level expressi
130 secticidal activity via interaction with the ecdysteroid receptor proteins.
131                               AaE74B and the ecdysteroid receptor synergistically enhanced 20E-induce
132               AHR38 also disrupts binding of ecdysteroid receptor to ecdysone response elements.
133 h is an obligatory partner in the functional ecdysteroid receptor, exists at the state-of-arrest as a
134       DHR78, which encodes another candidate ecdysteroid receptor, is also not required.
135 pendent activation of a reporter gene by the ecdysteroid receptor.
136 nuclear receptor isoforms are the only known ecdysteroid receptors, we show that the Ecdysone recepto
137                                              Ecdysteroids regulate a wide variety of cellular process
138                                              Ecdysteroids regulate many key developmental events in a
139 n the ecdysone biosynthetic pathway and that ecdysteroids regulate many late embryonic morphogenetic
140                                              Ecdysteroids regulate the remodeling of the dorsal exter
141               DHR78 protein is bound to many ecdysteroid-regulated puff loci, suggesting that DHR78 d
142 receptor, DHR78, functions at the top of the ecdysteroid regulatory hierarchies.
143 n rather than binding competition for the Vg ecdysteroid response element accounts for the inhibition
144 idermal growth factor signaling pathways, an ecdysteroid-response gene, cabut, and an ubiquitin-speci
145    Our results provide novel evidence for an ecdysteroid responsive gene in a crustacean that has man
146         This paper reports the cloning of an ecdysteroid responsive gene, HHR3, a potential Manduca s
147 the question of whether a similar cascade of ecdysteroid responsive genes exist in other members of A
148       Although EcR.USP-A recognizes the same ecdysteroid-responsive elements, EcR.USP-B binds them wi
149 lude that EcR/USP activation by the systemic ecdysteroid signal may be spatially restricted in vivo.
150                             However, whether ecdysteroid signaling can bypass transcriptional hierarc
151  gene mediates the transcriptional output of ecdysteroid signaling in Drosophila myoblast fusion, a c
152                                              Ecdysteroid signaling in insects is transduced by a hete
153 monitor the temporal and spatial patterns of ecdysteroid signaling in vivo we established transgenic
154                  Furthermore, we showed that ecdysteroid signaling is essential for the proper activa
155          In this study, we demonstrated that ecdysteroid signaling is operating in mature follicle ce
156             We provide evidence for a second ecdysteroid signaling pathway mediated by DHR38, the Dro
157 sis, providing a new tool for characterizing ecdysteroid signaling pathways during development.
158                                     Although ecdysteroid signaling regulates multiple steps in oogene
159 pamycin (TOR) pathways, juvenile hormone and ecdysteroid signaling, and epigenetic regulation.
160 llicle cells in late stages of oogenesis via ecdysteroid signaling.
161                     However, at pupariation, ecdysteroid signalling stimulates Ab expression, which c
162                                        Eight ecdysteroid-squalene conjugates were semi-synthesized an
163                Initially, moderate levels of ecdysteroid stimulate proliferation.
164 f NO repression though, but also requires an ecdysteroid stimulatory pathway.
165 ervous systems (CNS) cultured with low or no ecdysteroids survive and continue to divide, whereas the
166 mol and testosterone (reported inhibitors of ecdysteroid synthesis and an EcR antagonist, respectivel
167 th decreased expression of genes involved in ecdysteroid synthesis and signaling.
168 mic hormone (CHH), which not only influences ecdysteroid synthesis but also water uptake during moult
169 ined hyperglycemia in vivo and repression of ecdysteroid synthesis in vitro.
170 stacean hyperglycaemic hormone (CHH) repress ecdysteroid synthesis of the target tissue (Y-organ) onl
171 nd cellular level by bioassay (inhibition of ecdysteroid synthesis), radioligand (receptor) binding a
172  molting to adulthood due to a deficiency in ecdysteroid synthesis.
173 lt-inhibiting hormone (MIH), which represses ecdysteroid synthesis; crustacean hyperglycaemic hormone
174   Molting is elicited by a critical titer of ecdysteroids that includes the principal molting hormone
175 lowed by betaFTZ-F1 mRNA expression when the ecdysteroid titer becomes low.
176 tly during the larval and pupal molts as the ecdysteroid titer begins to decline and again just befor
177 low levels and in the adult molt just as the ecdysteroid titer begins to decline.
178 sion patterns are correlated with changes in ecdysteroid titer during development.
179 ward pathway that amplifies or maintains the ecdysteroid titer during larval development, ensuring pr
180     In contrast, E75A mutants have a reduced ecdysteroid titer during larval development, resulting i
181 s transiently at the onset of the decline of ecdysteroid titer followed by betaFTZ-F1 mRNA expression
182 e in the larval and the pupal molts when the ecdysteroid titer has declined to low levels and in the
183 A and MHR3, whose mRNAs are induced when the ecdysteroid titer increases, the expression of MHR4 mRNA
184 s observed at the end of the instar when the ecdysteroid titer is high.
185  is seen in mid-third instar larvae when the ecdysteroid titer is low, and strong widespread activati
186 ng the development of the adult wings as the ecdysteroid titer is rising, and this increase was preve
187 s from a failure to induce the large rise in ecdysteroid titer that triggers metamorphosis.
188  were not well correlated with the hemolymph ecdysteroid titer, developmental expression and phosphor
189 nic stages, corresponding to a period of low ecdysteroid titer, while USP-B mRNA exhibits its highest
190 , about the time of the premolt peaks in the ecdysteroid titer.
191 vitellogenic period, correlating with a high ecdysteroid titer.
192 rrelated with PTTH release and the hemolymph ecdysteroid titer.
193 nearly disappears in mid-vitellogenesis when ecdysteroid titers are high.
194 uring pre- and postvitellogenic periods when ecdysteroid titers are low.
195 he spook (spo) locus result in low embryonic ecdysteroid titers, severe late embryonic morphological
196 d by interactions between rising and falling ecdysteroid titers, the pattern of expression of EcR iso
197 s the overgrowth and is a consequence of low ecdysteroid titers.
198 ds to the period of the moult cycle when the ecdysteroid titre is high.
199 reach a peak prior to that of the haemolymph ecdysteroid titre, supporting a role for the enzyme in d
200 ured primordia simply by adjusting levels of ecdysteroid to be above or below a critical threshold co
201 nile hormone, which acts in conjunction with ecdysteroids to control gene expression in insects.
202 n that it does not involve direct binding of ecdysteroids to either DHR38 or USP.
203  In insects, the principal steroid hormones, ecdysteroids, trigger the expression of thousands of gen
204 ring the third larval instar with defects in ecdysteroid-triggered developmental responses.
205                                          The ecdysteroids unequivocally identified in these extracts
206 , we have analyzed the activities of various ecdysteroids using gel mobility shift assays and transfe
207 nvolvement of hormone signaling by measuring ecdysteroids, which increase following cocaine exposure,
208 anoconjugates of naturally derived antitumor ecdysteroids, which were designed to interfere with oxid
209  The observed bioactivity and composition of ecdysteroids will contribute to the future development o
210 gism or antagonism was observed by combining ecdysteroids with doxorubicin, and specific structure-ac
211 l-derived animal steroid hormones and insect ecdysteroids, with no known function in mammals.

 
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