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1                                              SRIF action was blocked in cells pretreated with pertuss
2                                              SRIF amacrine cells, DA amacrine cells, and M1 ipRGCs fo
3                                              SRIF analog affinities were determined by membrane radio
4                                              SRIF analogs with selective affinity for this receptor m
5                                              SRIF and SMS increased the phosphorylation of the 71-kDa
6                                              SRIF immunostaining was observed in widely spaced amacri
7                                              SRIF increases K(+) currents, decreases Ca(2+) currents,
8                                              SRIF modulation of the microcircuit was investigated wit
9                                              SRIF reduced Ca(2+) current in rods by 33% but increased
10                                              SRIF, at concentrations of 100-500 nM, enhanced a delaye
11                                              SRIF-immunoreactive cells have two to five primary proce
12 1,2,5)-[d-Trp(8),(N(alpha)Me)IAmp(9),Tyr(11)]SRIF (34), and Des-AA(1,2,5)-[d-Agl(8)(N(beta)Me,2-napht
13 gl(8)(N(beta)Me,2-naphthoyl),IAmp(9),Tyr(11)]SRIF (42) (Agl = aminoglycine) are sst(1) agonists in th
14 es-AA(1,2,5)-[DTrp(8),IAmp(9),(125)ITyr(11)]-SRIF ((125)I-25) and des-AA(1,2,5)-[DTrp(8),IAmp(9), (12
15  and des-AA(1,2,5)-[DTrp(8),IAmp(9),Tyr(11)]-SRIF (25) are about (1)/(7), (1)/(4), (1)/(125), and (1)
16 3)-[DAgl(NMe,2naphthoyl)(8),IAmp(9),Tyr(11)]-SRIF-NH(2) (27) in DMSO.
17 5)-[Tyr(2),Glu(7),d-Trp(8),IAmp(9),hhLys(12)]SRIF (31) (sst(1) IC(50) = 16 nM) and cyclo(7-12) Des-AA
18 lu(7),d-Trp(8),IAmp(9),m-I-Tyr(11),hhLys(12)]SRIF (45) (sst(1) IC(50) = 6.1 nM) had equal or improved
19 1,2,5)-[d-Trp(8),IAmp(9),(N(alpha)Me)Ser(13)]SRIF (19), Des-AA(1,2,5)-[d-Trp(8),IAmp(9),(N(alpha)Me)C
20 1,2,5)-[d-Trp(8),IAmp(9),(N(alpha)Me)Cys(14)]SRIF (20), Des-AA(1,2,5)-[d-Trp(8),(N(alpha)Me)IAmp(9),T
21 Trp(8)-Lys(9)-Thr(10)-Cys(11)]Thr(12)-NH(2) (SRIF numbering), at the five known human somatostatin re
22 ls and acute and chronic pain in humans; (3) SRIF inhibits dorsal horn neuronal activity; and (4) SRI
23 ibits dorsal horn neuronal activity; and (4) SRIF reduces responses of joint mechanoreceptors to noxi
24 wis et al. on the effects on K(i)s of Ala(6)-SRIF-14-amide at the five receptor subtargets.
25 e the synthesis of two analogues of D-Trp(8)-SRIF in which Phe(6) and Phe(11) were replaced by the pr
26 also found that pyrazinylalanine(7)-D-Trp(8)-SRIF-14 does not bind, suggesting a repulsive interactio
27                   Des-AA(1,2,4,13)-[d-Trp(8)]SRIF (2) retained high binding affinity at all receptors
28 eptors but sst(1), Des-AA(1,2,4,5)-[d-Trp(8)]SRIF (3) at sst(4) and sst(5), and Des-AA(1,2,4,5,13)-[d
29 and sst(5), and Des-AA(1,2,4,5,13)-[d-Trp(8)]SRIF (4) at sst(2) and sst(4) (AA = amino acid).
30                Des-AA(1,2,4,12,13)-[d-Trp(8)]SRIF (6) was potent and sst(4)-selective (>25-fold); Des
31 ve (>25-fold); Des-AA(1,2,5,12,13)-[d-Trp(8)]SRIF (7) and Des-AA(1,2,4,5,12,13)-[d-Trp(8)]-SRIF (9, O
32 nalogues of des-AA(1,2,5)-[DTrp(8)/D2Nal(8)]-SRIF that contain a 4-(N-isopropyl)-aminomethylphenylala
33 RIF (7) and Des-AA(1,2,4,5,12,13)-[d-Trp(8)]-SRIF (9, ODT-8) were most potent at sst(4) and moderatel
34 Des-AA(1,2,5)-[d-Trp(8), (N(alpha)Me)IAmp(9)]SRIF (17), Des-AA(1,2,5)-[d-Trp(8),IAmp(9),(N(alpha)Me)S
35 ent compound Des-AA(1,2,5)-[d-Nal(8),IAmp(9)]SRIF (4).
36     Des-AA(1,2,5)-[d-Trp(8)/d-Nal(8),IAmp(9)]SRIF (AA = amino acid, Nal = 3-(2-naphthyl)-alanine, IAm
37 lective Des-AA(1,5)-[Tyr(2),d-Trp(8),IAmp(9)]SRIF, (14, sst(1) IC(50) = 14 nM) were prepared in which
38 o des-AA(1,5)-[(125)ITyr(2),DTrp(8),IAmp(9)]-SRIF ((125)I-16) for the detection of sst1 tumors in rec
39  7 to yield des-AA(1,2,5)-[D2Nal(8),IAmp(9)]-SRIF (13) and in 16 to yield des-AA(1,5)-[Tyr(2),D2Nal(8
40  yield des-AA(1,5)-[Tyr(2),D2Nal(8),IAmp(9)]-SRIF (17) was intended to increase chemical stability, s
41 (16), des-AA(1,2,5)-[Tyr(7),DTrp(8),IAmp(9)]-SRIF (23), and des-AA(1,2,5)-[DTrp(8),IAmp(9),Tyr(11)]-S
42 at des-AA(1,4,5,13)-[Tyr(2),DTrp(8),IAmp(9)]-SRIF (33) and des-AA(1,4,5,6,12,13)-[Tyr(2),DTrp(8),IAmp
43 s-AA(1,4,5,6,12,13)-[Tyr(2),DTrp(8),IAmp(9)]-SRIF (34) progressively lost affinity for all receptors.
44 ffinities of des-AA(1,2,5)-[DTrp(8),IAmp(9)]-SRIF (c[H-Cys-Lys-Phe-Phe-DTrp-IAmp-Thr-Phe-Thr-Ser-Cys-
45 5) (7), des-AA(1,5)-[Tyr(2),DTrp(8),IAmp(9)]-SRIF (CH-288) (16), des-AA(1,2,5)-[Tyr(7),DTrp(8),IAmp(9
46 AA(1,4-6,10,12,13)-[DPhe(2),DTrp(8),IAmp(9)]-SRIF-Thr-NH(2) (16), des-AA(1,2,4-6,10,12,13)-[DAgl(NMe,
47 ,10,12,13)-[DAgl(NMe,2naphthoyl)(8),IAmp(9)]-SRIF-Thr-NH(2) (23), and des-AA(1,2,4-6,10,12,13)-[DAgl(
48 3)-[DTyr(2),DAgl(NMe,2naphthoyl)(8),IAmp(9)]-SRIF-Thr-NH(2) (25) was radio-iodinated ((125)I-25) and
49                                            A SRIF-responsive yeast growth assay was used as a primary
50 h or without pretreatment with a long-acting SRIF agonist.
51 ess in vivo activity in the absence of added SRIF.
52                                 In addition, SRIF-immunoreactive cells often have a fine-caliber axon
53 nity of 75 nM and an IC50 of 15.1 nM against SRIF-14 in a rat in vitro antagonist bioassay.
54 )]-Thr (15)-NH2 (1) (a somatostatin agonist, SRIF numbering) and H-Cpa (2)-c[DCys (3)-Tyr (7)-DTrp (8
55 RIF numbering) (ODT-8) that is potent at all SRIF receptor subtypes (sst's) but sst(1).
56  = 4-(N-isopropyl)-aminomethylphenylalanine, SRIF = somatostatin), with or without a tyrosine or mono
57                                     Here, an SRIF antagonist with no detectable agonist activity has
58 t modify the GH rise after termination of an SRIF infusion.
59 eatment of hepatocytes incubated with GH and SRIF, or with GH and octreotide, abrogated the inhibitor
60 0.09 nM) than Lanreotide (EC50, 2.30 nM) and SRIF (EC50, 0.19 nM).
61 RIF) receptors (SSTRs) 1 and 2 bind SRIF and SRIF 28 with high affinity, although a number of synthet
62                The SARs of the glycosides at SRIF receptors differ markedly from those at the NK-1 re
63 statin (SRIF) receptors (SSTRs) 1 and 2 bind SRIF and SRIF 28 with high affinity, although a number o
64 nity constant (Ki) of 172 +/- 12 nM, blocked SRIF inhibition of adenylate cyclase in vitro (IC50 = 5.
65                                         Both SRIF and its receptors were subsequently found widely di
66                     This D-hexapeptide bound SRIF receptor type 2 with an affinity constant (Ki) of 1
67 act the disinhibition of M1 ipRGCs caused by SRIF inhibition of DA amacrine cells.
68 ransfected cells was completely displaced by SRIF-28 or the sst(4)-selective L-803,087.
69 rods and cones were differently modulated by SRIF.
70 (1,2,5)-[DTrp(8),IAmp(9), (125)ITyr(11)]-Cbm-SRIF ((125)I-27), used them as in vitro tracers, and fou
71  des-AA(1,2,5)-[DTrp(8),IAmp(9),Tyr(11)]-Cbm-SRIF (27) and des-AA(1,2,5)-[DCys(3),DTrp(8),IAmp(9),Tyr
72  des-AA(1,2,5)-[DTrp(8),IAmp(9),Tyr(11)]-Cbm-SRIF (27) increased affinity slightly as well as improve
73 1,2,5)-[DCys(3),DTrp(8),IAmp(9),Tyr(11)]-Cbm-SRIF (29) show agonistic activity in a cAMP assay; there
74 eraction of M1 ipRGCs and DA amacrine cells, SRIF amacrine cells would provide inhibitory modulation
75  is important for the selectivity of certain SRIF agonists for binding to SSTR1.
76 ere used to confirm and further characterize SRIF antagonist activity.
77                     In conclusion, cytotoxic SRIF analogue AN-238 inhibits the growth of experimental
78 nomas, the treatment with targeted cytotoxic SRIF analogue AN-238, consisting of 2-pyrrolinodoxorubic
79                                     Dicyclic SRIF agonists of the sst(1)-selective Des-AA(1,5)-[Tyr(2
80   Recently, five pharmacologically different SRIF receptors (sst1-5) were cloned.
81 when c-SOM is coapplied with three different SRIF agonists.
82   Replacement of basal insulin levels during SRIF resulted in a fall of FFA levels from 545+/-47 to 2
83         A 30-min exposure of cells to either SRIF or the analog SMS 201-995 (SMS) reduced both the po
84 ifficult to establish the role of endogenous SRIF release in the absence of pure SRIF antagonists.
85 n-14 somatotropin-release inhibiting factor (SRIF) and 2 of its analogs, (125)I-WOC 4a and (111)In-pe
86 tin [somatotropin release inhibiting factor (SRIF)] also inhibits the intrinsic light response of M1
87 tin [somatotropin release-inhibiting factor (SRIF)] is widely distributed in the body and exerts a va
88  [or somatotropin release-inhibiting factor (SRIF)] receptors, sst(2A), and studied the modulatory ac
89 in (somatotrophin release-inhibiting factor, SRIF) were determined in cultured locus coeruleus neuron
90 ary (somatotropin release inhibitory factor, SRIF).
91 ter the functional expression of human fetal SRIF neurons in culture and if so, is this effect fetal-
92 xis, providing a mechanistic explanation for SRIF analog action in treating patients with GH-secretin
93 mple a 4-benzyl substituent is important for SRIF receptor binding, but the 4-desbenzyl analogue 27 w
94  rings to bind the Trp(8) binding pocket for SRIF-14 and the inability of pyrazine to do so was expla
95 of sst mRNAs suggests a significant role for SRIF in the regulation of GI function.
96                               During the 2-h SRIF infusion, insulin levels fell, and FFA levels rose
97 a-turn such as the potent cyclic hexapeptide SRIF agonist L-363,301 (6a), but not substance P.
98 ng receptor autoradiography; those with high SRIF receptor subtype 1 (sst(1)) affinity and selectivit
99        In a proportion of patients, however, SRIF analogs may lead to discordant growth hormone (GH)
100 of a glucose-based peptidomimetic at a human SRIF receptor to date (K(i) 53 +/- 23 nM, n = 6 at sst4)
101 atostatin (SRIF) analogues at the five human SRIF receptors (sst) was determined to identify sterical
102 lubility and enhanced affinity for the human SRIF subtype receptor 4 (sst4).
103 1)/(1000) that of 1 to the other three human SRIF receptor subtypes.
104 potent and highly selective binding to human SRIF subtype 1 receptors (sst(1)).
105 potent and highly selective binding to human SRIF type 2 (sst2) receptors.
106 potent and highly selective binding to human SRIF type 4 (sst(4)) receptors.
107 r from GHRH release or from acute decline in SRIF secretion.
108  We first tested whether an acute decline in SRIF, independent of GHRH action, would release GH.
109  BDNF alone led to a significant increase in SRIF production (p=0.014), whereas exposure to gp120 alo
110                       After 24-h incubation, SRIF was degraded or recycled, whereas its protease-resi
111 and gp120 led to an increase in BDNF-induced SRIF production which was significantly greater than tha
112  with 100 nm SRIF for 30 min reduced maximal SRIF inhibition of adenylyl cyclase from 40 to 10%.
113 or internalization, the mechanisms mediating SRIF receptor (sst) desensitization are unknown.
114                        One hundred nanomolar SRIF-28 activated an inwardly rectifying K+ current (ISR
115 e numbering refers to the position in native SRIF), with Xxx(7) being Phe/Ala/Tyr, Yyy(8) being Trp/D
116 e numbering refers to the position in native SRIF), with Xxx7 being Ala/Aph, exhibit potent and highl
117 brane, they also potentiate the neuropeptide SRIF inhibitory effects on seizure activity.
118               Treatment of cells with 100 nm SRIF for 30 min reduced maximal SRIF inhibition of adeny
119             In cell-attached patches, 100 nM SRIF-14 activated two types of single-channel currents w
120            The activation of ISRIF by 100 nM SRIF-28 was, however, inhibited 93 % by BIM-23056; CYN-1
121 pported these results by showing that 500 nM SRIF reduced a K(+)-induced increase in intracellular Ca
122 s do not stain for GAD-67, parvalbumin, NPY, SRIF, or NOS.
123 nodoxorubicin (AN-201) linked to octapeptide SRIF carrier RC-121, may overcome this resistance by pro
124 ic binding pocket such as that for Trp(8) of SRIF-14.
125 st(2A), and studied the modulatory action of SRIF on voltage-gated K(+) and Ca(2+) currents in rod an
126                    These parallel actions of SRIF may serve to counteract the disinhibition of M1 ipR
127                   This allows the actions of SRIF on DA amacrine cells to proceed with adjusting reti
128 orsal root ganglion cells; (2) activation of SRIF receptors results in inhibition of both nociceptive
129 hetic hexapeptide and octapeptide analogs of SRIF bind selectively to SSTR2.
130 (11) stabilize the bioactive conformation of SRIF-14.
131 rs are under the tonic inhibitory control of SRIF.
132      Furthermore, the sparse distribution of SRIF-immunoreactive somata, the wide-ranging, asymmetric
133                     The inhibitory effect of SRIF was not apparent without added GH and in the presen
134                               The effects of SRIF-14 were mimicked by 100 nM L-362,855 (a partial ago
135 onal significance of transient expression of SRIF and its receptors in the development of the cerebel
136 lling pathway(s) mediating BDNF induction of SRIF production; an effect expressed by fetal brains thr
137       Furthermore, intraplantar injection of SRIF antiserum also results in nociceptive behaviors.
138                   In addition, the number of SRIF-immunoreactive somata remains unchanged following t
139 NF or BDNF+gp120; BDNF induced production of SRIF during the subsequent 24-48 h was assessed.
140 dy of the structure-activity relationship of SRIF.
141 dy of the structure-activity relationship of SRIF.
142 H3 cells demonstrate that basal secretion of SRIF-related material is largely calcium-dependent and t
143 (7), (1)/(4), (1)/(125), and (1)/(4) that of SRIF-28 (1) to sst1, respectively, about (1)/(65), (1)/(
144 gands at the hSSTRs is compared with that of SRIF.
145 -DTrp(8)-Lys(9)-Thr(10)-Phe(11)-Cys(14)]-OH (SRIF numbering) (ODT-8) by one of the four conformationa
146 -dTrp(8)-Lys(9)-Thr(10)-Phe(11)-Cys(14)]-OH (SRIF numbering) (ODT-8) that is potent at all SRIF recep
147 oid receptor antagonism influence peripheral SRIF effects on nociceptors.
148 ium is absolutely required for efficient pro-SRIF cleavage, even at the optimal pH of 6.1.
149 3187 to determine the role of calcium in pro-SRIF cleavage and nascent vesicle formation from the tra
150 ry GH3 cells expressing prosomatostatin (pro-SRIF) to study prohormone processing and nascent secreto
151                 Here we demonstrate that pro-SRIF cleavage was markedly inhibited when lumenal free c
152 her, these observations demonstrate that pro-SRIF processing and budding of nascent secretory vesicle
153 ative fashion to identify AC-178,335, a pure SRIF antagonist of the sequence Ac-hfirwf-NH2.
154 dogenous SRIF release in the absence of pure SRIF antagonists.
155 show that prolonged exposure to radiolabeled SRIF analogs significantly increases their cellular inte
156 ors, the SRIF receptors (SSTR 1-5) recognize SRIF and related peptides which retain its beta-turn suc
157                        In the rabbit retina, SRIF immunoreactivity is present in a sparse population
158  as shown to be the case in 18-membered ring SRIF octapeptides.
159                             Although several SRIF antagonists have recently been described, none have
160                                Somatostatin (SRIF) analogs provide safe and effective therapy for acr
161                                Somatostatin (SRIF) is a neuroactive peptide that is distributed throu
162                                Somatostatin (SRIF) is the main inhibitory peptide regulating growth h
163                                Somatostatin (SRIF), a hypothalamic inhibitor of pituitary growth horm
164                        Because somatostatin (SRIF) receptors (ssts) are present in colorectal carcino
165 7) and irreversibly reduced by somatostatin (SRIF-14); this was associated with hyperpolarization of
166 inding affinity of short chain somatostatin (SRIF) analogues at the five human SRIF receptors (sst) w
167 inity (IC(50) = 2-4 nM) cyclic somatostatin (SRIF) octapeptides.
168 binding properties to all five somatostatin (SRIF) receptors using receptor autoradiography; those wi
169 that structural constraints in somatostatin (SRIF) analogues may result in receptor selectivity, and
170 hin the hippocampus, the major somatostatin (SRIF) receptor subtype, the sst2A receptor, is localized
171 albumin, neuropeptide Y (NPY), somatostatin (SRIF), or nitric oxide synthase (NOS).
172 structures of six analogues of somatostatin (SRIF) are described.
173 yclic octapeptide analogues of somatostatin (SRIF) are described.
174   Changes in the expression of somatostatin (SRIF) have been observed in the brains of HIV encephalit
175 eleasing hormone (GHRH) and of somatostatin (SRIF) in pharmacologically stimulated growth hormone (GH
176 tapeptide agonist analogues of somatostatin (SRIF) in the free form are described.
177 endogenously by an infusion of somatostatin (SRIF) to produce insulinopenia in groups of lean healthy
178 rch for synthetic analogues of somatostatin (SRIF) which exhibit selective affinities for the five kn
179 rch for synthetic analogues of somatostatin (SRIF) which exhibit selective affinities for the five kn
180 synthetic peptide analogues of somatostatin (SRIF) which exhibit selective affinities for the five kn
181 s a major source and target of somatostatin (SRIF).
182 opments, unusual properties of somatostatin (SRIF, 1) analogues are still being uncovered.
183 ucose-based peptidomimetics of somatostatin (SRIF-14), we sought to improve the water solubility of o
184 re required for the binding of somatostatin (SRIF-14).
185 ness to the inhibitory peptide somatostatin (SRIF) or its clinically used analogs can desensitize wit
186        The endogenous peptides somatostatin (SRIF) and substance P comprise very different structures
187                       The sst1 somatostatin (SRIF) receptor subtype is widely expressed in the endocr
188                            The somatostatin (SRIF) receptors (SSTRs) 1 and 2 bind SRIF and SRIF 28 wi
189    We therefore tested SSTR subtype-specific SRIF analogs in primary human fetal pituitary cultures (
190                 The results demonstrate that SRIF acts both centrally and peripherally to control the
191              These findings demonstrate that SRIF receptors maintain a tonic inhibitory control over
192      Several lines of evidence indicate that SRIF is important in nociceptive processing: (1) it is l
193     Taken together, these data indicate that SRIF-immunoreactive neurons of the rabbit retina are dis
194                     Our results suggest that SRIF may play a role in the regulation of glutamate tran
195                                          The SRIF-induced activation of the inward rectifier was supp
196 he nature of the ligand binding sites at the SRIF receptor.
197  to synthesize peptidomimetics that bind the SRIF receptors on AtT-20 mouse pituitary cells, five clo
198                         In AtT-20 cells, the SRIF-induced activation of inward rectifier K+ currents
199  DA amacrine cells and M1 ipRGCs express the SRIF receptor subtypes sst(2A) and sst4 respectively.
200  above results indicate that Gi mediates the SRIF effects on inward rectifier K+ currents.
201             In locus coeruleus neurones, the SRIF-induced activation of inward rectifier K+ currents
202 endent manner, intraplantar injection of the SRIF receptor antagonist cyclo-somatostatin (c-SOM) resu
203 h both bind G-protein-coupled receptors, the SRIF receptors (SSTR 1-5) recognize SRIF and related pep
204 a i3 antibody injection, suggesting that the SRIF response is mediated through G alpha i1 and/or G al
205  suggest that G alpha i2 is involved in this SRIF response.
206 d this increase is blocked by the same three SRIF agonists.
207                                        Thus, SRIF regulation of GH and TSH in primary human fetal pit
208  HEK 293 cells (sst2)] utilizing [125I]Tyr11-SRIF as the radioligand.
209 wth hormone in vitro antagonist assay versus SRIF (1 nM).
210 d by approximately 20% (P < 0.02, saline vs. SRIF, ANOVA).
211                         To elucidate whether SRIF acts peripherally on the GH-IGF-I axis, we showed t
212                     Incubation of cells with SRIF also caused a rapid (t(12) < 2 min) increase in sst
213 irment of Mch-induced vasodilation seen with SRIF alone.
214                               Treatment with SRIF and GH increased protein tyrosine phosphatase (PTP)

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