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1 nes, beta-lipotropic hormone (beta LPH), and beta endorphin.
2 he amyloid fiber formed by the human hormone beta-endorphin.
3 an altered cleavage profile for the peptide beta-endorphin.
4 alpha-neoendorphin, but not endomorphins or beta-endorphin.
5 elanocyte-stimulating hormone (beta-MSH) and beta-endorphin.
6 n of beta-lipotropin to gamma-lipotropin and beta-endorphin.
7 ation in the level of C-terminally processed beta-endorphin.
8 ere used for dual immunocytochemistry of Fos/beta-endorphin.
9 through the post-translational processing of beta-endorphin.
10 n (POMC), or PVN levels of Met-Enkephalin or beta-Endorphin.
11 peptide Y, vasoactive intestinal peptide, or beta-endorphin.
12 are derived from pro-opiomelanocortin as is beta-endorphin.
13 -stimulating hormone, and the opioid peptide beta-endorphin.
14 amic acid decarboxylase 67 (GAD67), NPY, and beta-endorphin.
15 )O-induced increases in nitrite, nitrate and beta-endorphin.
16 timulate an NO-dependent neuronal release of beta-endorphin.
17 O metabolites nitrite and nitrate as well as beta-endorphin.
18 yzed for their content of NO metabolites and beta-endorphin.
19 tisera against the endogenous opioid peptide beta-endorphin.
20 ient or lacking either pre-pro-enkephalin or beta-endorphin.
22 a peptidase which converts beta-endorphin to beta-endorphin 1-17 (gamma-endorphin), beta-endorphin 1-
23 in to beta-endorphin 1-17 (gamma-endorphin), beta-endorphin 1-18, and their corresponding C-terminal
24 co-administration of morphine (1 microg) and beta-endorphin (1 microg) into either the amygdala alone
26 of morphine (1 microg) into the amygdala and beta-endorphin (1 microg) into the PAG failed to produce
27 he similar effects of intra-DVC injection of beta-endorphin (1 pmol) are inhibited by naloxone and no
28 psilon (epsilon)-opioid-receptor antagonist, beta-endorphin(1-27) prevents these effects of etorphine
29 ethadone (LAAM), morphine, meperidine, DADL, beta-endorphin(1-31), enkephalins, and dynorphin A(1-17)
30 ity to the suppressive actions of Gly-Gln or beta-endorphin-(1-27) injections that modulate voluntary
31 ficacy was shown to be comparable to central beta-endorphin-(1-27) or intraperitoneal (i.p.) naltrexo
32 In contrast, the opioid peptidergic agonist beta-endorphin (10 microgram/kg, i.p.) administered afte
34 rolysis of fluorogenic peptides based on the beta-endorphin 12-24 sequence, Abz-T-P-L-V-T-L-X(1)-X(2)
35 nto the rostral ventromedial medulla altered beta-endorphin (15 microg) analgesia elicited from the v
38 y, we investigated whether glycyl-glutamine (beta-endorphin(30-31)), an inhibitory dipeptide synthesi
39 ore effective in reducing morphine (60%) and beta-endorphin (79%) analgesia in the amygdala on the ju
40 essed pro-opiomelanocortin, the precursor of beta-endorphin (a known EOP), and constituted the majori
41 d in the DVC, whereas the similar effects of beta-endorphin, a peptide derived from the same precurso
45 sor proopiomelanocortin (POMC) gives rise to beta-endorphin, adrenocorticotropic hormone, beta-lipotr
48 point as well as more rapid dissociation of beta-endorphin amyloid fibrils at lower pH indicate the
52 ning exercise increases blood levels of both beta-endorphin (an opioid) and anandamide (an endocannab
53 However, the A118G variant receptor binds beta-endorphin, an endogenous opioid that activates the
55 e PAG significantly reduce both morphine and beta-endorphin analgesia elicited from the amygdala.
56 sary for the full expression of morphine and beta-endorphin analgesia elicited from the amygdala.
57 PAG significantly reduced morphine, but not beta-endorphin analgesia in the amygdala on the tail-fli
58 the multiple modulatory mechanisms mediating beta-endorphin analgesia in the PAG, and in terms of whe
61 l (11%) and transient (30 min) reductions in beta-endorphin analgesia on the jump test, MK-801 produc
65 esidues in the helical address region of the beta-endorphin analogues without destroying mu-, delta-,
66 py showed colocalization of cathepsin L with beta-endorphin and alpha-MSH in the intermediate pituita
67 addiction, mediated by the hedonic action of beta-endorphin and anhedonic effects of withdrawal, may
70 the measurement of instrumental behavior of beta-endorphin and enkephalin knock-out mice that both o
72 y granules yet expresses endogenous opioids (beta-endorphin and Met-enkephalin) and uroguanylin in ap
73 eceptors (MOR, OPRM1) mediate the effects of beta-endorphin and modulate many biological functions in
76 hemistry and immunoelectron microscopy using beta-endorphin and mu-opiate receptor specific antibodie
78 udy reveals decreases in endogenous opioids, beta-endorphin and perhaps Met-enkephalin in the thalamu
79 (POMC) neurons release the endogenous opioid beta-endorphin and POMC neuron activity is inhibited by
80 f the infiltration of immunocytes containing beta-endorphin and the consequent decrease of the beta-e
81 y structural differences between melittin or beta-endorphin and their respective synthetic analogs.
82 Moreover, neurons triple-labeled with c-Fos, beta-endorphin and VGLUT3 were noted in this region foll
83 affinity for both endogenous opioids such as beta-endorphins and exogenous opioids such as fentanyl.
84 y completely prevented carboxy-shortening of beta-endorphins and greatly diminished conversion of bet
85 of neuroendocrine peptides (dynorphin A-17, beta-endorphin, and alpha- melanocyte-stimulating hormon
86 hormones adrenocorticotropic hormone (ACTH), beta-endorphin, and alpha-melanocyte stimulating hormone
87 e for cathepsin L in the production of ACTH, beta-endorphin, and alpha-MSH peptide hormones in the re
88 ock-out mice showed major decreases in ACTH, beta-endorphin, and alpha-MSH that were reduced to 23, 1
90 nadotropin-releasing hormone (GnRH), VP, OT, beta-endorphin, and dopamine neurons, are responsive to
91 proopiomelanocortin (POMC), the precursor to beta-endorphin, and endomorphin 1 and 2 on sectioned rat
92 mu-opioid receptor agonists (e.g., morphine, beta-endorphin, and enkephalin) inhibit luteinizing horm
93 gonadotropin-releasing hormone-I, dopamine, beta-endorphin, and gonadotropin-releasing hormone-II ne
94 analgesic responses induced by morphine and beta-endorphin, and indicate that the latter response is
95 prolactin, corticotropin-releasing hormone, beta-endorphin, and somatotropin release-inhibiting fact
96 tein as well as its derivatives beta LPH and beta-endorphin, and that this process is modulated by TP
97 ructures of EOP-OR-G(i) complexes, including beta-endorphin- and endomorphin-bound muOR, deltorphin-b
98 deprived feeding states but were reduced in beta-endorphin- and enkephalin-deficient mice only when
99 0-100 nmol) dose-dependently attenuates both beta-endorphin- and GRP-elicited robust scratching witho
101 selected for three different receptors: anti-beta-endorphin anti-body, streptavidin, and thrombin, an
102 nsulin, growth hormone releasing factor, and beta-endorphin are nearly equivalent substrates for the
105 Using a monoclonal antibody (3E-7) against beta-endorphin as a target, we selected a single peptide
107 fferential affinity to the endogenous ligand beta-endorphin as well as alterations in pain sensitivit
110 olved in pain modulation-metenkephalin (ME), beta-endorphin (BE), and substance P (SP)-in patients un
115 in-releasing hormone (CRH), urocortin (Ucn), beta-endorphin (beta-END), ACTH, and corticosterone (COR
120 cAMP system is involved in ethanol-regulated beta-endorphin (beta-EP) release from rat hypothalamic n
121 induced by the mu-sensitive opioid peptide, beta-endorphin (betaEND, 10 microg, i.c.v.) was signific
123 elanocyte-stimulating hormone (beta-MSH) and beta-endorphin but not alpha-MSH; humans, similar to dog
128 tion of cell bodies containing enkephalin or beta-endorphin, colchicine (90-100 microg/kg) was inject
129 A118G) may have higher receptor binding for beta-endorphin compared with AA homozygotes that may con
130 evels of oxidation products of NO as well as beta-endorphin, compared to levels in fractions collecte
131 fall in arterial pressure elicited by i.c.v. beta-endorphin, consistent with evidence that cyclic dip
133 bility, CB(2) immunolabeling was detected on beta-endorphin-containing keratinocytes in stratum granu
135 vital organs, we tested whether skin-derived beta-endorphin contributes to radiation-induced fatigue.
137 Although conversion of beta-lipotropin to beta-endorphin decreased, the lack of PC2 activity cause
141 th the aggressive conspecific several of the beta-endorphin deficient mice showed clear signs of coun
145 tion in proenkephalin knockout (PENK KO) and beta-endorphin-deficient (BEND KO) mice, and how the bod
146 Herein we demonstrate that morphine and beta-endorphin disrupt this long-range synchrony of gamm
147 so challenge the dogma that shorter forms of beta-endorphin do not exhibit receptor activity; we show
149 at mu and kappa opioid receptors as well as beta-endorphin each produce analgesia elicited from the
150 studies have demonstrated that morphine and beta-endorphin employ different anatomical and neurochem
152 ls and neurons double-labeled with c-Fos and beta-endorphin, enkephalin or VGLUT3 in the ARC were sig
153 however, growth hormone releasing factor and beta-endorphin exhibit a 40-fold higher kcat, but a 10-f
154 ansgenic mice with a selective deficiency of beta-endorphin exhibit normal analgesia in response to m
156 king beta-endorphin), heterozygous mice (50% beta-endorphin expression) and sibling wildtype mice fro
157 ule has an acidic pH but, on exocytosis, the beta-endorphin fibril would encounter neutral pH conditi
160 ) receptor activation induces the release of beta-endorphin from keratinocytes and the activation of
162 s with the rank order of etorphine > DAMGO = beta-endorphin > morphine > butorphanol, and the affinit
165 imulating hormone; and the endogenous opioid beta-endorphin) have a diverse array of biological activ
166 Homozygous knockout mice (entirely lacking beta-endorphin), heterozygous mice (50% beta-endorphin e
167 that hemorrhage increased Fos expression by beta-endorphin immunoreactive neurons significantly.
169 e for beta-endorphin immunostaining, whereas beta-endorphin-immunoreactive neurons were absent in ret
170 ell extracts, coinciding with an increase of beta-endorphin-immunoreactive protein in the culture med
171 aused significant increases in POMC mRNA and beta-endorphin immunoreactivity in both ipsilateral and
172 d-expressing amacrine cells was positive for beta-endorphin immunostaining, whereas beta-endorphin-im
175 gulated secretion of both chromogranin A and beta-endorphin in response to the usual secretagogue, co
177 s and/or dendrites) containing enkephalin or beta-endorphin in specific regions of the brain stem.
179 oid analgesia elicited by either morphine or beta-endorphin in the amygdala could be altered by eithe
180 roopiomelanocortin (POMC) neurons to release beta-endorphin in the arcuate nucleus (ARC) of the hypot
182 own that enhancement of endogenous levels of beta-endorphin in the hypothalamus via beta-endorphin ne
183 tration of AAS also increased the content of beta-endorphin in the midline thalamus, suggesting a pos
184 est, but decreased the potency of the opioid beta-endorphin in the periaqueductal gray region of the
186 let radiation, to date a functional role for beta-endorphin in the regulation of human epidermal mela
187 ta-melanocyte-stimulating hormone (MSH), and beta-endorphin in the regulation of skin pigmentation, a
188 but the data do not support a major role for beta-endorphin in the regulation of sleep or social stre
189 s activates neurons containing enkephalin or beta-endorphin in the rVLM as well as in the periaqueduc
190 -endorphin were used to study the release of beta-endorphin in the urethane anaesthetized rat followi
192 oxidation of epidermal ACTH, alpha-MSH, and beta-endorphin in vitiligo owing to oxidation of methion
194 Over a 6-week radiation regimen, plasma beta-endorphin increased in rats, paralleled by opiate p
196 tion produced a dose-dependent inhibition of beta-endorphin-induced hypotension, but not bradycardia,
198 ere active toward the physiological peptides beta-endorphin, insulin, and amyloid beta peptide 1-40.
199 Co-administration of subthreshold doses of beta-endorphin into both structures also results in a pr
200 hold doses of morphine into both structures, beta-endorphin into both structures, morphine into one s
203 structures, morphine into one structure and beta-endorphin into the other structure, or morphine and
208 hermal stimulus was applied, suggesting that beta-endorphin is necessary for CB(2) receptor-mediated
211 t, in rodents, another POMC-derived peptide, beta-endorphin, is coordinately synthesized in skin, ele
212 eptive and behavioral effects were absent in beta-endorphin knockout mice and in mice lacking p53-med
213 nist treatment and were undetected in either beta-endorphin knockout mice or mice lacking keratinocyt
214 An antibody that selectively recognized beta-endorphin labeled fibers and neurons in the ventral
215 ty caused an increase in beta-lipotropin and beta-endorphin levels in the mutant animals, but no incr
218 fe-threatening episodes implicates increased beta-endorphin levels resulting from acid-mediated esoph
220 r women, dyadic satisfaction correlated with beta-endorphin levels, depression, and perception of ill
223 Solitary chemosensory cells that coexpress beta-endorphin, Met-enkephalin, uroguanylin, and Trpm5 e
224 In conclusion, the results suggest that beta-endorphin modulates the acute endocrine, thermoregu
226 e causal links for itch-eliciting effects by beta-endorphin-MOP receptor and GRP-BB2 receptor systems
227 0 microM concentrations of etorphine, DAMGO, beta-endorphin, morphine, and butorphanol, DAMGO-stimula
228 s designed to examine the involvement of the beta-endorphin/mu-opiate receptor system in human epider
229 elanocortin-1 receptor, we conclude that the beta-endorphin/mu-opiate receptor system participates in
231 ls of beta-endorphin in the hypothalamus via beta-endorphin neuron transplantation suppresses stress
233 deposition of the complement protein C1q in beta-endorphin neuronal cells in both in vitro and in vi
234 regulates exosome-mediated, ethanol-induced beta-endorphin neuronal death.SIGNIFICANCE STATEMENT Neu
235 anol treatments increased the number and the beta-endorphin neuronal killing activity of microglial e
236 0 +/- 2.6%, depending on neuronal location), beta-endorphin neurons (68.3.0 +/- 4.4%), and VP neurons
239 rast to traditional mu and kappa opioids and beta-endorphin, none of the OFQ/N fragments in the amygd
244 CD+CID can improve the sequence coverage for beta-endorphin over performing ECD alone (i.e., from 72
245 networks) to show that three neuropeptides (beta-endorphin, oxytocin, and dopamine) play particularl
248 proopiomelanocortin (POMC) neuron-producing beta-endorphin peptides in the hypothalamus in a postnat
250 )), an inhibitory dipeptide synthesized from beta-endorphin post-translationally, inhibits IL-1beta a
251 c-rAAV8 expressing the analgesic gene prepro-beta-endorphin (ppbetaEP) led to significant (P < 0.0001
252 role for insulin-degrading enzyme as both a beta-endorphin-processing and -inactivating enzyme is im
253 et of experiments tested the hypothesis that beta-endorphin-producing neurons, that is, proopiomelano
254 mes when introduced into primary cultures of beta-endorphin-producing POMC neurons, increased cellula
255 utyric acid (GABA), neuropeptide Y (NPY), or beta-endorphin receptor blockade in the ipsilateral hypo
256 rdiovascular reflexes through enkephalin- or beta-endorphin-related opioid receptors in the rostral v
257 emperature, at least in part, by stimulating beta-endorphin release from pro-opiomelanocortin neurons
259 u-opioid receptors (MORs) and an increase in beta-endorphins released into the VTA and the plasma.
262 tone, sensation, plasma levels of cortisol, beta-endorphin, selected gut neuropeptides, norepinephri
263 ng in keratinocytes, subsequently increasing beta-endorphin signaling at opioid receptors, and produc
265 phine (tail-flick: 70-75%; jump: 60-81%) and beta-endorphin (tail-flick: 100%; jump: 93%) analgesia e
266 des alpha-melanocyte-stimulating hormone and beta-endorphin, the glucocorticoids; and the catecholami
267 ting hormone (alpha-Msh) and carboxy-cleaved beta-endorphin, the products of Cpe-dependent processing
268 have shown the distribution of dynorphin and beta-endorphin throughout social behavior circuits withi
269 ell line contains a peptidase which converts beta-endorphin to beta-endorphin 1-17 (gamma-endorphin),
270 cial attachment, binding of the neuropeptide beta-endorphin to mu-opioid receptors in the central ner
271 al tone regulating feeding behavior, whereas beta-endorphin underlies orosensory reward in high need
278 of the sum of CSF alpha- and beta-MSH to CSF beta-endorphin was highest, intermediate, and lowest in
279 vented in rats when naloxone or antiserum to beta-endorphin was injected in the hindpaw where the nox
281 proximity to fibers containing enkephalin or beta-endorphin, was observed in the rVLM and ventrolater
282 timulate an NO-dependent neuronal release of beta-endorphin, we conducted a ventricular-cisternal per
283 Given the powerful analgesic properties of beta-endorphin, we tested this hypothesis using pain tol
284 n Western blot analysis, POMC, beta LPH, and beta-endorphin were detected in cell extracts under base
288 ilized antibodies to the carboxy-terminus of beta-endorphin were used to study the release of beta-en
289 is mechanism allows for the local release of beta-endorphin, where CB(2) receptors are present, leadi
290 tially to inflamed sites, where they release beta-endorphin which activates peripheral opioid recepto
291 ion stimulates release from keratinocytes of beta-endorphin, which acts at local neuronal mu-opioid r
292 emia and exercise both induce the release of beta-endorphin, which plays an important role in the mod
294 from keratinocytes of the endogenous opioid beta-endorphin, which then acts at opioid receptors on p