ライフサイエンスコーパス: GHRP

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1 [azaTyr(4)]-GHRP-6 (15), [Ala(1), azaPhe(2)]-GHRP-6 (16), and [azaLeu(3), Ala(6)]-GHRP-6 (33) all exh

2 ect blocked by the GHSR1 antagonist, d-Lys-3-GHRP-6.

3 g assay using a choroid explant, [azaTyr(4)]-GHRP-6 (15), [Ala(1), azaPhe(2)]-GHRP-6 (16), and [azaLe

4 For example, [A(1), azaF(4)]- and [azaY(4)]-GHRP-6 (1a and 2b) were previously shown to bind selecti

5 MK-677), growth hormone-releasing peptide 6 (GHRP-6), and the 2(R)-hydroxypropyl derivative of 3-amin

6 ogues of growth hormone releasing peptide-6 (GHRP-6) exhibit promising affinity, selectivity, and mod

7 apeptide growth hormone releasing peptide-6 (GHRP-6) exhibits dual affinity for the growth hormone se

8 Phe(2)]-GHRP-6 (16), and [azaLeu(3), Ala(6)]-GHRP-6 (33) all exhibited antiangiogenic activity.

9 trations of ghrelin on the action of MK-677, GHRP-6, and L-692,585 was analyzed globally according to

10 owed that fibrinogen-like acyl-GPRP and acyl-GHRP could inhibit D.

11 To explain acyl-GPRP and acyl-GHRP inhibition of D.E association, it is proposed that

12 acy compared with the GHSR1a peptide agonist GHRP-6, and high nanomolar to low micromolar potency, de

13 -Pro-amide (GPRP) and Gly-His-Arg-Pro-amide (GHRP), respectively.

14 sequence starts with Gly-His-Arg-Pro-amide (GHRP).

15 rnal standards (triply deuterated GHRP-4 and GHRP-2 metabolite) were used to optimize the extraction

16 iation kinetics of (125)I-[His]-ghrelin, and GHRP-6 and MK-677 were able to fully displace (125)I-[Hi

17 e polymerization inhibitor peptides GPRP and GHRP.

18 nthetic peptides GPRP (knob 'A' mimetic) and GHRP (knob 'B' mimetic).

19 eritoneal injections of the GHS-R antagonist GHRP-6 [D-Lys3] prior to subsequent transfer and sucrose

20 ced the same local conformational changes as GHRP to this site.

21 atorial split-and-mix approach furnished aza-GHRP-6 leads, which were further examined by alanine sca

22 -Trp(2), Ala(3), or Trp(4) position gave aza-GHRP-6 analogues with reduced affinity toward the GHS-R1

23 Azapeptide GHRP-6 analogues have been synthesized, exhibiting micro

24 abeled internal standards (triply deuterated GHRP-4 and GHRP-2 metabolite) were used to optimize the

25 all, 28 metabolites (at least three for each GHRP) were identified from the in vivo samples and main

26 s is available and merely one metabolite for GHRP-2 is established.

27 LHRH), growth hormone releasing hexapeptide (GHRP-6), and TrpCage (sequence NLYIQWLKDGGPSSGRPPPS) yie

28 hereas the ghrelin receptor antagonist D-Lys GHRP-6 reduced plasma levels of GLP-1 and insulin and di

29 D-Lys3-GHRP-6 and JMV 3002 also blocked ghrelin-induced increas

30 uperfusion of the GHS-R1A antagonists D-Lys3-GHRP-6 and JMV 3002 decreased evoked IPSP and mIPSC freq

31 Furthermore, D-Lys3-GHRP-6 did not affect ethanol-induced increases in IPSP

32 With the exemption of GHRP-2, the entity of these peptides represents nonappro

33 onferred to rEC by the peptides GPRPamide or GHRP, nor did rEC bind to a GPR peptide column.

34 cture (rfD-BbetaD432A+GH) showed the peptide GHRP was not bound to hole "b." We then re-evaluated the

35 es are the growth hormone releasing peptide (GHRP)-1, -2, -4, -5, -6, hexarelin, alexamorelin, and ip

36 ns begin with the sequence Gly-His-Arg-Pro- (GHRP-), but the homologous sequence in chicken fibrin be

37 Similarly, the lateral-association-promoting GHRP (IC30 of 1.25-1.43 mM) gave a high turbidity vs clo

38 natal rats, although to a lesser degree than GHRP-6.

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