ライフサイエンスコーパス: astressin

1 icotropin releasing factor (CRF) antagonist, astressin.

2 blocked by the peptidergic CRF-R1 antagonist astressin.

3 9-41 and with the CRF-R1-specific antagonist astressin.

4 ndergoes conformational changes upon binding astressin.

5 ted bNT-CRFR1 does not bind [(125)I-D-Tyr(0)]astressin.

6 a radioreceptor assay using [(125)I-d-Tyr(0)]astressin.

7 )), which was found to be longer acting than astressin.

8 positions 14, 15, 19, 27, and 37 in [DHis32]astressin.

9 tment with the non-selective CRF antagonist, astressin (0.5-1 microM) or the selective CRF(2) recepto

10 Intracisternal (i.c.) injection of astressin (10 microg/rat) also completely prevented CRF

11 The peptide CRF-R1/R2 antagonist, astressin (10 microg/rat, i.c.v.) inhibited the colonic

12 i) values for binding to ECD1-CRFR2beta are: astressin = 10.7 (5.4-21.1) nm, urocortin I = 6.4 (4.7-8

13 The analogue [CalphaMe-Leu27,DHis32]astressin (16) was more potent (although not statistical

14 Ic-injection of a CRF antagonist, astressin (2.8 nmol), partially antagonized GLP-1-induce

15 The selective CRF(2) antagonist astressin(2)-B (i.c.v.), at a 20 : 1 antagonist: agonist

16 zero is antagonized by the administration of astressin(2)-B but not by antisauvagine-30 at times -3 a

17 s CRF(2) and CRF(1) in order to confirm that astressin(2)-B could indeed bind to established CRF(2) b

18 le + surgery), whereas the CRF(2) antagonist astressin(2)-B injected subcutaneously had no effect.

19 Extended duration of action of astressin(2)-B vs that of antisauvagine-30 is demonstrat

20 A selective antagonist of CRF(2) (astressin(2)-B) increased these responses.

21 e(17),Glu(31),Lys(34) ]Ac-sauvagine((8-40)) (astressin(2)-B) with CRF(2) selectivities greater than 1

22 rimidine)], but not of the CRF(2) antagonist astressin(2)-B, normalized jcBNST LTP-IE in animals with

23 selective antagonist of CRF(1) (NBI35965) or astressin(2)-B, respectively.

24 or the selective CRF(2) receptor antagonist, astressin 2B (500 nM) attenuated the CRF-induced increas

25 27914 (NBI), a CRF-sub-1 antagonist, but not Astressin 2B, a CRF-sub-2 antagonist.

26 ffect was recapitulated by administration of astressin 2B, a selective CRHR2 antagonist, before toxin

27 This effect was also suppressed by astressin 2B, implicating CRF(2) receptors.

28 endently inhibited by the CRF(2) antagonist, astressin 2B, with an IC(50) in the nanomolar range.

29 in 1 in toxin A-exposed mice pretreated with astressin 2B.

30 ted by pre-stress treatment with NBI but not Astressin 2B.

31 st antalarmin, but not the CRH-R2 antagonist astressin 2B.

32 (500 ng/side), but not the CRF-R2 antagonist astressin-2B (500 ng or 1 mug/side) or antisauvagine-30

33 In contrast, a CRF2 receptor antagonist (astressin-2B [cyclo(31-34) [d-Phe11,His12,C alphaMeLeu13

34 Astressin-2B had no significant behavioral effect.

35 Likewise, intra-VTA antalarmin, but not astressin-2B, blocked footshock-induced reinstatement in

36 , LS injections of CRF receptor 2 antagonist astressin-2B, but not a CRF receptor 1 antagonist, rever

37 of the relatively selective CRF2 antagonist astressin-2B, but not the CRF1-selective antagonist anta

38 Astressin (3 mug, ic) completely blocked the 2nd CRD- an

39 The CRF-R1/R2 antagonist astressin (33 microg/kg, IP) and the CRF-R1 antagonist C

40 Astressin (5 microg/5 microl, icv) exerted a similar eff

41 ucture of ECD1 of CRF-R2beta in complex with astressin, a peptide antagonist.

42 ential of a novel and potent CRF antagonist, astressin, against kainic acid-induced excitotoxic seizu

43 vage, the purified protein (bNT-CRFR1) binds astressin and the agonist urocortin with high affinity.

44 pressed by the CRF1/CRF2 receptor antagonist astressin and the selective CRF1 receptor antagonist NBI

45 in several families of antagonists (such as Astressin) and in a number of CRF agonists and investiga

46 g the nonselective CRF(1)/CRF(2) antagonist, astressin, and the water-soluble CRF(1) receptor antagon

47 effects of the CRF(1) and CRF(2) antagonist Astressin (Asn) on the anxiety-like responses produced d

48 We examined the influence of CRF and astressin (AST), a non-specific CRF antagonist, on sleep

49 We examined the effects of CRH and astressin (AST), a non-specific CRH antagonist, on wakef

50 alogues 22 and 23 were also more potent than astressin at reversing intracisternal CRF- and abdominal

51 rs was shown by the ability of i.v. injected astressin, at doses shown to completely block CRF-induce

52 is and chemical and biological properties of astressin B analogues {cyclo(30-33)[D-Phe(12),Nle(21,38)

53 six ligands of this family (the antagonists astressin B and astressin2-B, the agonists stressin1, an

54 le(38), CalphaMeLeu(40)]Ac-hCRF((9)(-)(41)) (astressin B, 19) was one of the most efficacious analogu

55 and DMP-696 only partially inhibited (125)I-astressin binding (22-32% maximal inhibition).

56 ne, CRF, and urocortin for displacing (125)I-astressin binding (by 4.0-7.1-fold).

57 being unable to activate the CRF1 receptor, astressin binding results in the internalization of the

58 Similar effects were seen on astressin binding to the ECD1.

59 RF1 receptors are utilized following CRF and astressin binding.

60 Astressin binds with 6-fold higher affinity to full-leng

61 The nonselective CRH antagonist astressin blocked these agonist-induced increases in luc

62 uch as alpha-helical CRF (alpha-hel-CRF) and Astressin both in vitro and in vivo.

63 ssume a conformation very similar to that of astressin bound to the ECD1 of CRF-R2 recently reported

64 When Astressin C 2 was administered to adrenalectomized rats

65 2beta (CRF-R2beta), free and complexed with astressin, comprises a Sushi domain.

66 members, and competitive antagonists such as astressin [cyclo(30-33)[DPhe(12),Nle(21),Glu(30),Lys(33)

67 NBI 35965 accelerated (125)I-astressin dissociation and only partially increased the

68 ve conformation similar to that shown in the Astressin family of CRF antagonists and that residue 8 (

69 ure of the complex the C-terminal segment of astressin forms an amphipathic helix, whose entire hydro

70 (6) or acetylation of the N-terminus (7) of astressin had a minor deleterious or a favorable influen

71 IIB receptor, yet two 12-residue analogs of astressin have similar affinities for both proteins but

72 Astressin, however, fails to induce receptor phosphoryla

73 minus of 16 (i.e., 18) or of [CalphaMe-Leu27]astressin (i.e., 19) did not have a significant effect o

74 nclude epitope tags, binds a CRF antagonist, astressin, in a radioreceptor assay using [(125)I-d-Tyr(

75 Neither ic vehicle nor astressin influenced basal LC neuronal activity.

76 ed duration of action as compared to that of astressin inverted question markcyclo(30-33)[DPhe(12),Nl

77 (residues 8-14) produced antagonists such as astressin inverted question markcyclo(30-33)[DPhe12,Nle2

78 e12,Glu20,Lys23,Nle21,38]hCRF (12-41) and of astressin inverted question markcyclo(30-33)[DPhe12,Nle2

79 in blocking pituitary CRF receptors; and (2) astressin, inverted question markcyclo(30-33)[DPhe12,Nle

80 In vivo, astressin is also significantly more potent than earlier

81 Astressin is an amino-terminal truncated analog of CRF t

82 )[DPhe12,-Nle21,38,Glu30, Lys33]hCRF(12-41) (astressin) is 32 times more potent than the assay standa

83 nd 6 and 8 to be slightly longer-acting than astressin or [DHis32]astressin, while their potencies in

84 (9-41) were ca. twice and 1/100 as potent as astressin, respectively, suggesting a putative turn that

85 Furthermore, we present evidence that for astressin to induce internalization it must interact wit

86 Administration of astressin was done against both local microinfusion (0.0

87 htly longer-acting than astressin or [DHis32]astressin, while their potencies in vitro were not signi

88 R was detected with the antagonist (125)I-astressin with 30 microM guanosine 5'-O-(3-thiotriphosph