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1 ated by mechanisms other than the identified CRF receptors.
2 factor (CRF) and CRF-related peptides on two CRF receptors.
3 sidered to be a second endogenous ligand for CRF receptors.
4 s to neurodegeneration through activation of CRF receptors.
5 sing factor (hCRF) C-terminal 33 residues to CRF receptors.
6 inding of the CRF C-terminus 30 residues, to CRF receptors.
7 a-helical conformation when interacting with CRF receptors.
8 elatively independently of the activation of CRF receptors.
9 nificantly blocking both brain and pituitary CRF receptors.
10 slightly altered by blockade of hypothalamic CRF receptors.
11 rats and at determining the role of central CRF receptors.
12 ceptor activation and, to a lesser extent on CRF receptors.
13 receptors (GPCRs) known as type-1 and type-2 CRF receptors.
14 st of corticotropin (ACTH) releasing factor (CRF) receptors.
16 endent and requires the downstream action of CRF receptor 1 (CRF-R1), suggesting that dopamine induce
18 ctions are mediated through their receptors, CRF receptor 1 (CRFR1) and CRFR2, found throughout the C
19 ment increases Abeta production and triggers CRF receptor 1 (CRFR1) and gamma-secretase internalizati
20 y, pharmacological experiments revealed that CRF receptor 1 and protein kinase A pathways were newly
21 to (1) determine the effect of the selective CRF receptor 1 antagonist (CRF(1)) GW876008 relative to
23 eceptor 2 antagonist astressin-2B, but not a CRF receptor 1 antagonist, reversed the inhibitory effec
26 -protein-coupled receptors of the B1 family, CRF receptors 1 and 2 (CRF-R1 and CRF-R2alpha,beta).
28 dependent on corticotropin-releasing factor (CRF) receptor 1 signaling and an intact hypothalamic-pit
29 ng, which was prevented by antagonism of the CRF receptor-1 (CRF-R1), and was mimicked by CRF-R1 agon
30 relapse, a subsequent experiment found that CRF receptor-1 (CRF1) blockade in the AId similarly redu
33 g elevations in tryptophan hydroxylase-2 and CRF receptor-1 expression and concordant increases in be
34 by increased corticotropin releasing factor (CRF) receptor-1 expression and signalling, which modulat
37 ides similarly modulate maternal defense via CRF receptor 2, and that LS is a critical site for the n
41 of the first extracellular domain (ECD1) of CRF receptor 2beta (CRF-R2beta), free and complexed with
42 nal extracellular domain (ECD1) of the mouse CRF receptor 2beta, which is the major ligand recognitio
45 hese results support a propinquity effect in CRF receptor activation, in which the amino-terminal por
48 e effects of corticotropin-releasing factor (CRF) receptor activation and antagonism on intracranial
53 n of anorexia is a well documented effect of CRF receptor agonist administration, the central sites a
54 d for the effects on ICSS of the competitive CRF receptor agonist h/rCRF (0-5.0 microg, i.c.v.), the
55 r agonist h/rCRF (0-5.0 microg, i.c.v.), the CRF receptor agonist urocortin (0-5.0 microg, i.c.v.), a
59 components of the HPA axis, such as CRF and CRF receptors, along with POMC gene and gene products.
62 blastoma cell line for functional studies on CRF receptors and suggest that CRF may play a regulatory
63 lting in down-regulation of adenohypophyseal CRF receptors and symptoms of depression and anxiety.
66 Using the corticotropin-releasing factor (CRF) receptor and the thrombin receptor as a model, we p
68 ut relatively impotent in blocking pituitary CRF receptors; and (2) astressin, inverted question mark
69 Therefore, we investigated the effects of CRF receptor antagonism within the dRN on social anxiety
70 particular, administration of a competitive CRF receptor antagonist [0.2, 1 or 5 microg intracerebro
71 st urocortin (0-5.0 microg, i.c.v.), and the CRF receptor antagonist [D-Phe(12), Nle(21,38), C(alpha)
74 to the BLA either alone or together with the CRF receptor antagonist alpha-helical CRF(9-41) immediat
75 as blocked by treatment with the competitive CRF receptor antagonist alpha-helical CRF9-41 and with t
77 ntral tegmental area (VTA), a site where the CRF receptor antagonist antalarmin prevents the reinstat
78 nificantly reduced following infusion of the CRF receptor antagonist D-Phe CRF((12-41)) into the BNST
79 arena, rats were infused with vehicle or the CRF receptor antagonist d-Phe-CRF((12-41)) (50 or 500 ng
80 lar (1000 ng) injections of the nonselective CRF receptor antagonist D-Phe-CRF(12-41) decreased frust
83 i.c.v.) was blocked by pretreatment with the CRF receptor antagonist d-PheCRF(12-41) (3.0 microg, i.c
85 ely absent after exposure to the competitive CRF receptor antagonists alpha-helical CRF(9-41) or rat/
88 Furthermore, these results imply a role for CRF receptor antagonists in the prevention and treatment
89 ned the effects of two different competitive CRF receptor antagonists on the expression of conditione
92 of the amygdala (CeA), despite the fact that CRF receptors are more densely distributed in BLA than i
93 saicin-sensitive primary afferents and brain CRF receptors are part of the pathways and biochemical c
94 hat corticotropin-releasing factor (CRF) and CRF receptors are prominent in the PFC, the cognitive ef
97 ists for the corticotropin releasing factor (CRF) receptors are new tools to investigate stress-relat
98 nding peptide binding and specificity by the CRF receptors as well as a template for designing potent
99 dent and provides important insight into the CRF receptor-associated circuitry that likely underpins
101 agonists of corticotrophin-releasing factor (CRF) receptors bind to the receptor by a two-site mechan
106 tor (CRF)-immunoreactive fibers and contains CRF receptor-binding sites, suggesting that endogenous C
107 with biological responses mediated by brain CRF receptors, but relatively impotent in blocking pitui
108 ing protein (CRF-BP), a moiety distinct from CRF receptors, but which is nonetheless capable of bindi
109 irect endogenous mechanism for activation of CRF receptors by new mammalian members of the CRF family
110 These results suggest that the pituitary CRF receptor can discriminate between slightly different
111 d urocortin 1 (Ucn1), which bind to both the CRF receptors CRF-R1 and CRF-R2, and the urocortins 2 (U
116 factor (CRF) activates neurons that express CRF receptors (CRF-Rs), we followed the kinetics and dis
118 ow sex differences in the association of the CRF receptor (CRF1) with the Gs protein and beta-arresti
120 mpared the telencephalic distribution of the CRF receptors, CRF1 and CRF2 , and two of their ligands,
121 wo different corticotropin-releasing factor (CRF) receptors, CRF1 and CRF2, have been identified in r
124 ral nucleus of the amygdala (CeA), where the CRF receptor (CRFr) plays an important role in anxiety-
125 d -III signal by activating their receptors, CRF receptors (CRFR)1 and -2, to maintain homeostasis th
127 factor (CRF) family, and its cognate type 2 CRF receptor (CRFR2) are highly expressed in skeletal mu
129 cologic blockade of its receptor, the type 2 CRF receptor (CRFR2), attenuated high but not low glucos
130 ) family, binds with high affinity to type 2 CRF receptors (CRFR2) on cardiomyocytes and confers prot
132 routinely used for the study of transfected CRF receptors do express endogenous CRF1 mRNA with splic
136 Both of the characterized members of the CRF receptor family (CRF1 and CRF2), are found in the am
138 data reinforce the importance of the ECD1 of CRF receptors for ligand recognition and raise the inter
140 nergic, serotonergic, histamine, opiate, and CRF receptors had no effect, but those for adrenergic an
145 activation of pituitary and/or hypothalamic CRF receptors in mediating the stimulatory effect of EtO
146 ctural evidence for a primary involvement of CRF receptors in modulation of the postsynaptic excitabi
147 downregulation and desensitization of cloned CRF receptors in murine fibroblast cells (Ltk-) stably t
152 stems and may also support an involvement of CRF receptors in the development of depression such that
153 9, 12-15, 18, 19, 22-26, 28, 31) had k(i) to CRF receptors in the high picomolar and low nanomole ran
155 in, a novel peptide activating both types of CRF receptors in vitro, but with preferential affinity f
158 xpression of corticotropin-releasing factor (CRF) receptors in the guinea pig enteric nervous system.
159 he levels of corticotropin-releasing factor (CRF) receptors in the serotonergic dorsal raphe nucleus
160 himera in which the N-terminal domain of the CRF receptor is replaced by the amino-terminal 16 residu
163 ion that contains both CRF-ergic neurons and CRF receptors is the midbrain periaqueductal gray (PAG).
165 ists of the corticotrophin releasing factor (CRF) receptor markedly inhibit experimentally induced ex
167 calcium activated by postsynaptic Gs-coupled CRF receptors may represent a fundamental mechanism by w
171 )) and sauvagine showed some selectivity for CRF receptors other than that responsible for ACTH secre
172 dentify several brain regions with conserved CRF receptor patterns across rodent and primate species,
174 brain regions with phylogenetically plastic CRF receptor patterns, and have interesting implications
175 a large group of selective and nonselective CRF receptor peptide agonists will facilitate the develo
176 rn blot analysis of cultured BMEC identified CRF receptor protein; stimulation with CRF, or it struct
177 in 1 and 3, anxiogenic peptides that bind to CRF receptors, reduce maternal aggression in lactating m
179 These data support a new model of respective CRF receptor roles in stress-related behavior such that,
180 the first extracellular domain (ECD1) of the CRF receptor(s) comprises the major ligand binding site
182 havioral effects may be mediated by enhanced CRF receptor signaling or compensatory changes in CRF re
186 stigated the functional significance of this CRF receptor subtype in anxiety-like and memory processe
188 antagonists, administered systemically, and CRF receptor subtype nonspecific antagonists, administer
189 f the present study were to characterize the CRF receptor subtypes (CRF-R1 and -R2) and cellular mech
190 biochemically and pharmacologically distinct CRF receptor subtypes (CRFR1 and CRFR2) have been descri
191 ults indicate a differential role of central CRF receptor subtypes in the colonic stimulatory and gas
193 v.) on gastric and colonic motility, and the CRF receptor subtypes involved and their role in colonic
199 fibers and also contained immunolabeling for CRF receptor, suggesting that c-fos-expressing neurons i
200 administration, the function of DA(1/5) and CRF receptors switched from inhibitory to excitatory.
201 esults show that sex differences pervade the CRF receptor system in juvenile and adult rats, and the
203 for the immediate early gene NGFI-B and for CRF receptor type 1 (CRF-R(1)) in the parvocellular port
206 nal through the activation of two receptors, CRF receptor type 1 (CRFR1) and type 2 (CRFR2), both of
209 rsy, however, concerning the contribution of CRF receptor type 1 (CRFR1) to this effect and whether C
211 erging evidence also links the activation of CRF receptors type 1 and type 2 with stress-related alte
212 (NT) of the corticotropin releasing factor (CRF) receptor type 1 (R1) were studied by use of murine
213 atement was blocked by administration of the CRF-receptor type 1 (CRF-R1) antagonist antalarmin (500
214 vation of the serotonergic dorsal raphe, (2) CRF-Receptor type 1 (CRF-R1) in the dorsal raphe, (3) Ur
215 al hydrate-anesthetized rats and the role of CRF receptors using the nonselective CRF(1)/CRF(2) antag
220 omized rats, suggesting that a proportion of CRF receptors were occupied before CRF administration, a
222 light recent advances in the interactions of CRF receptors with other GPCRs and non-GPCR proteins and
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