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

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