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1                                              LH-RH receptor-positive (MCF-7) and -negative (UCI-107)
2                    The components of AN-207 (LH-RH analogue carrier and cytotoxic radical AN-201 as s
3       We stably transfected COS cells with a LH-RH receptor (LH-RH-Rc) mammalian expression vector an
4 152 can be regulated by the number of active LH-RH receptors on cancer cells.
5 sing hormone (LH-RH), is more potent against LH-RH receptor-bearing cancers and produces less periphe
6  increase in medium concentrations of AA and LH-RH induced by high [K(+)], suggesting that NO mediate
7 creased medium concentrations of both AA and LH-RH.
8 ting that NO mediates release of both AA and LH-RH.
9 tagonists suppress gonadotroph functions and LH-RH receptor (LH-RH-R) production are incompletely und
10 reas CP hydrolysis gives rise to CCK5-GR and LH-RH-GK, both of which are susceptible to the dipeptidy
11 no acids from the C-terminus of CCK5-GRR and LH-RH-GKR, but only CP is responsible for converting dia
12  (10(-5) to 10(-3) M) had no effect on basal LH-RH release but completely blocked high [K(+)]- and ni
13 reated with AN-207 was partially restored by LH-RH antagonist.
14  effects on the gonadotroph cells containing LH-RH receptors and is less toxic for other cells.
15                    From these DOX containing LH-RH hybrids, intensely potent analogs with daunosamine
16   This study demonstrates that the cytotoxic LH-RH analog AN-207 exerts highly selective effects on t
17                              Thus, cytotoxic LH-RH agonist containing DOX (AN-152) can be converted i
18  we applied an in vitro method to desaturate LH-RH receptors by chaotropic agents such as manganous c
19 racting the stimulatory effect of endogenous LH-RH.
20 , was increased in stable cells that express LH-RH-Rc compared with parental cells.
21 lent concentrations, in COS cells expressing LH-RH-Rc but not in parental COS cells.
22 d down-regulation of pituitary receptors for LH-RH and not merely an occupancy of binding sites.
23 ecreased the level of membrane receptors for LH-RH by 83% (P < 0.01) after 7 days, and 86% (P < 0.01)
24 e number of pituitary membrane receptors for LH-RH in a time-dependent manner with the nadir occurrin
25 the binding characteristics of receptors for LH-RH in membrane fractions from rat anterior pituitarie
26 nd subcellular localization of receptors for LH-RH in rat pituitaries.
27 eatment of tumors that possess receptors for LH-RH such as prostatic, mammary, ovarian, and endometri
28 NA expression of the pituitary receptors for LH-RH.
29 e mRNA expression of pituitary receptors for LH-RH.
30 he conjugates to rat pituitary receptors for LH-RH.
31 ment, the concentration of binding sites for LH-RH in the nuclei of rat pituitaries was significantly
32                                       Higher LH-RH receptor concentrations coincided with elevated se
33 Lys6] luteinizing hormone-releasing hormone (LH-RH) (AN-207), was demonstrated to be less toxic than
34 og of luteinizing hormone-releasing hormone (LH-RH) containing DOX, at 0.3 mg/ml is 19.49 +/- 0.74 mi
35 ts of luteinizing hormone-releasing hormone (LH-RH) leads to down-regulation of pituitary LH-RH recep
36 on of luteinizing hormone-releasing hormone (LH-RH) release from medial basal hypothalamic explants b
37 07 of luteinizing hormone-releasing hormone (LH-RH), consisting of an intensely potent derivative of
38 Lys6]-luteinizing hormone-releasing hormone (LH-RH), is more potent against LH-RH receptor-bearing ca
39 ts of luteinizing hormone-releasing hormone (LH-RH), unlike the LH-RH agonists, suppress gonadotropin
40 gs of luteinizing hormone-releasing hormone (LH-RH).
41 tion in cycling rats with normal hypophysial LH-RH environment.
42 RH, did not cause any significant changes in LH-RH-R mRNA level.
43 ocked high [K(+)]- and nitroprusside-induced LH-RH release.
44 -pyrrolinodoxorubicin conjugated to [D-Lys6] LH-RH, exerted through induction of apoptosis and modula
45 p of the D-Lys side chain of agonist [D-Lys6]LH-RH or antagonistic analog AC-D-Nal(2)-D-Phe(4Cl)-D-Pa
46 nd on the cellular uptake of AN-152, [D-Lys6]LH-RH, or doxorubicin was assessed by the 3-(4,5-dimethy
47 N-201) conjugated to carrier agonist [D-Lys6]LH-RH.
48 x can affect the concentration of measurable LH-RH binding sites, we applied an in vitro method to de
49 time intervals, we could not detect occupied LH-RH binding sites.
50 esults show that the percentages of occupied LH-RH receptors at 1, 3, and 6 h after administration of
51  Our results indicate that administration of LH-RH antagonist Cetrorelix produces a marked down-regul
52 ) is a modern, potent antagonistic analog of LH-RH.
53     These highly potent cytotoxic analogs of LH-RH were designed as targeted anti-cancer agents for t
54 tive group to yield cytotoxic derivatives of LH-RH analogs containing DOX.
55 n the superfusion system, which is devoid of LH-RH, did not cause any significant changes in LH-RH-R
56                          Thus, the effect of LH-RH antagonists is similar to that of the LH-RH agonis
57 this study was to investigate the effects of LH-RH antagonist cetrorelix on the binding characteristi
58                                The number of LH-RH binding sites in the nuclear pellet was increased
59                       The down-regulation of LH-RH binding sites induced by Cetrorelix was accompanie
60 ults demonstrate that the down-regulation of LH-RH receptors on the cell membranes of rat pituitaries
61  in AA in the medium but also the release of LH-RH.
62 ansmitter that blocks NOergic stimulation of LH-RH release by chemically reducing the NO released by
63                     In addition, survival of LH-RH-Rc positive cells treated with AN-207 was partiall
64 rnalization and subcellular translocation of LH-RH receptors.
65 xperimental systems with different pituitary LH-RH environments.
66 ased the concentration of mRNA for pituitary LH-RH-R by 72.6% in OVX rats, but only by 32.9% in norma
67 LH-RH) leads to down-regulation of pituitary LH-RH receptors.
68 trorelix on the mRNA expression of pituitary LH-RH-R and luteinizing hormone (LH) secretion in three
69  effects on the gene expression of pituitary LH-RH-R by counteracting the stimulatory effect of endog
70 ase occurred in the mRNA levels of pituitary LH-RH-R in ovariectomized (OVX) rats with high pituitary
71 ncreases in the mRNA expression of pituitary LH-RH-R in rats after 11 and 21 days, respectively.
72 esaturation, demonstrated that rat pituitary LH-RH receptors were significantly (P < 0.01) down-regul
73 ss gonadotroph functions and LH-RH receptor (LH-RH-R) production are incompletely understood.
74 transfected COS cells with a LH-RH receptor (LH-RH-Rc) mammalian expression vector and examined the e
75 C-160 have been shown previously to regulate LH-RH receptors through phosphorylation.
76 cid neurotransmitter glutamic acid, releases LH-RH by releasing NO.
77 nitroprusside, which releases NO, stimulated LH-RH release and decreased the concentration of AA in t
78                   Our findings indicate that LH-RH antagonists exert their inhibitory effects on the
79          Two weeks after administration, the LH-RH-stimulated LH release in vivo entirely normalized
80 N-207, as evidenced by a 63% decrease in the LH-RH-stimulated release of LH in vitro.
81        AA (10(-5) to 10(-3) M) inhibited the LH-RH-releasing action of NMDA.
82  LH-RH antagonists is similar to that of the LH-RH agonists, but the mode of action of antagonists is
83 ormone-releasing hormone (LH-RH), unlike the LH-RH agonists, suppress gonadotropins and sex steroid s
84 d (OVX) rats with high pituitary exposure to LH-RH, but there was a significant 23.2% reduction in cy
85                              Clinically used LH-RH antagonists partially inhibited apoptotic Bax expr
86                 The mechanisms through which LH-RH antagonists suppress gonadotroph functions and LH-
87 conjugate was: (a) specific for cancers with LH-RH receptors; (b) up-regulated by EGF; (c) down-regul
88                  The conjugation of DOX with LH-RH analogs was performed by using N-(9-fluorenylmetho
89 single injection or prolonged treatment with LH-RH antagonist also decreased the mRNA expression of p

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