ライフサイエンスコーパス: GH-RH

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1 inhibited by GH-RH antagonist JV-1-38 and a GH-RH antiserum.

2 tro was stimulated by IGF-I and inhibited by GH-RH antagonist JV-1-38 and a GH-RH antiserum.

3 gonists indicate an improvement over earlier GH-RH analogs.

4 tion-PCR revealed the expression of mRNA for GH-RH and splice variant 1 (SV(1)) of GH-RH receptor in

5 42, specific high-affinity binding sites for GH-RH were found on tumor membranes.

6 es tested, analog JV-1-36 showed the highest GH-RH antagonistic activity in vitro and also induced a

7 n (TSH), stimulated by GH-releasing hormone (GH-RH) and TSH-releasing hormone (TRH), respectively, wa

8 effects of growth hormone-releasing hormone (GH-RH) antagonist MZ-4-71 on the proliferation of the hu

9 gonists of growth hormone-releasing hormone (GH-RH) inhibit proliferation of various cancers indirect

10 gonists of growth hormone-releasing hormone (GH-RH) inhibit the growth of various tumors through mech

11 gonists of growth hormone-releasing hormone (GH-RH) produces a reduction in IGF-I and -II, concomitan

12 ion of GH-RH antagonists and may explain how GH-RH antagonists inhibit tumor growth.

13 igand competition assays with (125)I-labeled GH-RH antagonist JV-1-42, specific high-affinity binding

14 The finding of GH-RH and SV(1) of GH-RH receptors in NSCLC provides a new approach to the

15 NA for GH-RH and splice variant 1 (SV(1)) of GH-RH receptor in H838 tumors.

16 r observations on the mechanism of action of GH-RH antagonists and may explain how GH-RH antagonists

17 The antitumorigenic action of GH-RH antagonists could be partly direct and mediated by

18 ased on the use of antagonistic analogues of GH-RH.

19 The finding of GH-RH and SV(1) of GH-RH receptors in NSCLC provides a n

20 ion of autocrine/paracrine IGF-I, IGF-II, or GH-RH.

21 dent prostate cancer for 8 weeks with potent GH-RH antagonist MZ-5-156 at a dose of 20 microg/animal

22 itro studies showed that H838 cells secreted GH-RH and IGF-I into the medium.

23 Our findings demonstrate that GH-RH antagonist MZ-4-71 can significantly inhibit the g

24 volvement of IGF-I in NSCLC and suggest that GH-RH may be an autocrine growth factor for H838 NSCLC.

25 Our work suggests that GH-RH antagonist MZ-5-156 may inhibit the growth of DU-1

26 suggest that tumor inhibition induced by the GH-RH antagonists in U-87MG glioblastomas is associated

27 be very long-acting in vivo, suppressing the GH-RH-induced GH release even after 60 min.

28 The binding affinity of the peptides to GH-RH receptors also was determined.

29 rtly direct and mediated by SV(1) of tumoral GH-RH receptors.

30 ther studies are needed to establish whether GH-RH antagonists produce telomerase inhibition in other

31 responses to receptor-mediated stimuli with GH-RH and TRH were normal at 2 weeks in both treated gro

32 The effectiveness of therapy with GH-RH antagonist JV-1-38 and its mechanisms of action we

33 U-87MG human glioblastomas were treated with GH-RH antagonist MZ-5-156.

34 Treatment with GH-RH antagonist also significantly reduced tumor weight

35 Treatment with GH-RH antagonist JV-1-38 significantly (P < 0.05-0.001)

36 Treatment with GH-RH antagonist MZ-5-156 decreased the expression of IG

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