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1 or prodynorphin) with enkephalin (or Phe-Arg-Met-enkephalin).
2 ith morphine, but not opioid peptides (i.e., Met-enkephalin).
3 nosine, serotonin, or methionine enkephalin (met-enkephalin).
4 t-enk-Arg-Phe cleavage preferred (Met-enk is met-enkephalin).
5 ed amounts of nicotine-induced secretion of (Met)enkephalin.
6 the BD simulations for the global motions of met-enkephalin.
7  biological importance, the neurotransmitter met-enkephalin.
8 ay was demonstrated by its cosecretion with [Met]enkephalin.
9           In all neurons tested, methionine (Met)-enkephalin (0.003-30 microm) inhibited the peak amp
10 cordings with patch electrodes, bath-applied met-enkephalin, a nonselective opioid receptor agonist,
11         Thus, amnestic effects of [Leu]- or [Met]enkephalin administration are brain-region specific.
12 y formation produced by [Leu]enkephalin and [Met]enkephalin administration in 2 regions of the 2-day-
13 with localized amnestic effects produced by [Met]enkephalin administration.
14                   Previous studies show that Met-enkephalin, an endogenous opioid, down-regulates che
15 ry vesicle cathepsin L in the production of [Met]enkephalin, an endogenous peptide neurotransmitter.
16                                          The met-enkephalin analog D-Ala2-methionine enkephalinamide
17 nalization, and also enhanced the effects of Met-enkephalin and alpha-neoendorphin, but not endomorph
18                                              Met-Enkephalin and beta-Endorphin were not affected by d
19    PepE hydrolyzed internal peptide bonds in Met-enkephalin and bradykinin; however, hydrolysis of al
20 ecursor should contain the sequences of both Met-enkephalin and Leu-enkephalin as seen for mammalian
21                    The previous detection of Met-enkephalin and Leu-enkephalin in the CNS of the Aust
22                    Basal dialysate levels of Met-enkephalin and Leu-enkephalin were 60 +/- 30 and 70
23                    Computational studies for met-enkephalin and melittin, employing sequential and pa
24          Accordingly, immunofluorescence for met-enkephalin and neuropeptide tyrosine in these animal
25                                              Met-enkephalin and substance-P levels declined approxima
26                Here, we report that Leu- and Met-enkephalin and their des-tyrosyl derivatives potentl
27 ssing the D1 subtype were immunopositive for met-enkephalin and vesicular glutamate transporter VGLUT
28 dopin 1 with chromaffin granule components, [Met]enkephalin and a cysteine protease known as "prohorm
29 esses endogenous opioids (beta-endorphin and Met-enkephalin) and uroguanylin in apical compartments c
30 torphin II, [d-Pen(2), d-pen(5)]-enkephalin, met-enkephalin, and SNC-80 ((+)-4-[(alphaR)-alpha-((2S,5
31 ntagonists to attenuate the loss of striatal met-enkephalin are consistent with an excitotoxic lesion
32 for serotonin, dopamine-beta-hydroxylase and met-enkephalin are observed in the area and aid in the d
33 imilar to that of DAMGO, alpha-neoendorphin, Met-enkephalin-Arg-Phe, and the putatively endogenous pe
34                                              Met-enkephalin, as well as morphine, inhibited IL-8-indu
35                                              Met-enkephalin, but not the mu-selective (DAMGO) and del
36 alized with the secretory vesicle component (Met)enkephalin by confocal immunonfluorescence microscop
37 human SK-N-MC cells results in reduction of (Met)enkephalin by more than 80%, illustrating the promin
38 y 60 min after the last injection to measure met-enkephalin by radioimmunoassay.
39                               Production of [Met]enkephalin by cathepsin L occurred by proteolytic pr
40                          Training decreased [Met]enkephalin concentration in the LPO but not in the I
41 ) in dorsal horn homogenates and presynaptic met-enkephalin-containing boutons.
42 of the previously studied glycine oligomers; met-enkephalin contains the interesting motions of pheny
43                                              Met-enkephalin decreased the binding of 125I-Tyr-MIF-1 t
44 dependent secretion of KPI/APP with PTP and (Met)enkephalin demonstrated the colocalization of these
45             Regional activity of endogenous [Met]enkephalin during memory formation is consistent wit
46                                              Met-enkephalin (ENK) suppressed spontaneous and NMDA-ind
47 bition by gamma-aminobutyric acid (GABA) and met-enkephalin (ENK).
48 onal SK-N-MC cells results in production of (Met)enkephalin from proenkephalin.
49  neuropeptides (neuropeptide Y, substance P, met-enkephalin, galanin, dynorphin A and somatostatin) w
50 either the potency nor the efficacy of D-Ala-Met-enkephalin-Gly-ol (DAMGO) were changed; however, the
51 aining), and within given brain nuclei (more met-enkephalin immunoreactive cells).
52 mouse brains with a decrease in the level of Met-Enkephalin immunoreactivity (ir-Met-Enk) and an accu
53 ss (110 kDa), were colocalized with PTP and (Met)enkephalin in secretory vesicles of adrenal medulla
54    SNL led to increased immunoreactivity for met-enkephalin in dorsal horn homogenates, which was dos
55         Mass spectroscopy confirmed Leu- and Met-enkephalin in skin.
56 ociated with changes in the concentration of met-enkephalin in the brain.
57         Furthermore, labeling for the opioid met-enkephalin in the medial preoptic nucleus (POM) corr
58 owed the colocalization of cathepsin L with [Met]enkephalin in secretory vesicles of neuroendocrine c
59                        The endogenous opioid met-enkephalin induced monocyte chemotaxis in a pertussi
60      Our data showed that preincubation with Met-enkephalin inhibited both MIP-1 alpha-mediated chemo
61 a(2), N-Me-Phe(4), Gly-ol(5)]-enkephalin and met-enkephalin inhibited both ST-stimulated EPSCs and th
62                  Neuropeptides dynorphin and met-enkephalin inhibited dopamine neurons, whereas oxyto
63               These results demonstrate that met-enkephalin inhibition of cholinergic secretion is me
64 O to determine the role of the G proteins in met-enkephalin inhibition of cholinergic stimulation of
65     The SCN did not contain cell bodies with met-enkephalin-IR and substance P-IR, but did contain fi
66                              The dynamics of met-enkephalin is considerably more complicated than tha
67                                              Met-enkephalin is one of the smallest opiate peptides.
68 dy, which recognized Leu-, Met-, and Phe-Arg-Met-enkephalin, labeled the dorsolateral funiculus and n
69 enkephalin, which did not recognize Leu- and Met-enkephalin, labeled the same puncta.
70 MS2 scans enabled simultaneous monitoring of Met-enkephalin, Leu-enkephalin, and unknown peptides.
71             The method was used to determine met-enkephalin, leu-enkephalin, dynorphin A(1-8), and be
72 rtex and midbrain region and the decrease in met-enkephalin level in the medulla region observed in m
73  by reversing some of the changes induced in met-enkephalin levels in brain by morphine in morphine t
74 ether, midazolam antagonized the increase in met-enkephalin levels in cortex and midbrain region and
75                                              Met-enkephalin levels in neuronal projections from the e
76 ant animals showed a significant increase in met-enkephalin levels in the cortex (137%) and midbrain
77 ted animals showed a significant decrease in met-enkephalin levels in the pituitary (63%), cortex (39
78 idbrain (89%), and a significant decrease in met-enkephalin levels in the pituitary (74%), cerebellum
79 of midazolam, morphine, and both together on met-enkephalin levels in the rat.
80 drenals (43%), and a significant increase in met-enkephalin levels in the striatum (54%) and pons (51
81 Y 274614 ameliorated the decline in striatal met-enkephalin levels observed in mice after 8 weeks of
82                                  Hippocampal met-enkephalin levels were reduced to 50% only at 12 wee
83 Finally, in cathepsin L gene knockout mice, [Met]enkephalin levels in brain were reduced significantl
84                              YAP3p generated Met-enkephalin-Lys-Lys from amidorphin showing that clea
85 amphetamine (METH) significantly altered the met-enkephalin (M-Enk) systems associated with some, but
86                                In contrast, [Met]enkephalin may be amnestic when administered in the
87 Cs (eIPSCs) was unaffected by perfusion with met-enkephalin (ME) or by mu-, delta-, or kappa-opioid r
88                                             [Met]Enkephalin (ME), [D-Ser2,Leu5,Thr6]-enkephalin, etor
89                                     Numerous met-enkephalin (mENK) and dynorphin-immunoreactive bouto
90                                              Met-enkephalin (mENK), an endogenous opioid, and exogeno
91  vasopressin (AVP), angiotensin II (AII) and met-enkephalin (mENK), and receive input from galanin (G
92 ut was combined with local microinjection of met-enkephalin (Met-ENK) and naltrexone (NLTX) to determ
93 presumed synthesis/enhanced accumulation) of met-enkephalin (Met-Enk) in dorsal and ventral striatum
94 nvestigate the effects of the opioid peptide Met-enkephalin (met-enk) on the release of substance P-l
95 proOpiomelanocortin (POMC), or PVN levels of Met-Enkephalin or beta-Endorphin.
96 de of evoked IPSCs was not altered either by Met-enkephalin or by any of the opioid receptor-selectiv
97 ochemistry for either methionine enkephalin (met-enkephalin) or leucine enkephalin (leu-enkephalin),
98 eine protease cathepsin L for producing the (Met)enkephalin peptide neurotransmitter from proenkephal
99 flux induced by chemokines was unaffected by met-enkephalin pretreatment.
100 lation of enkephalin precursor Penk mRNA and met-enkephalin protein in sensory neurons.
101 subtype regulates MOR function by modulating met-enkephalin release.
102 lted in highly increased cellular levels of (Met)enkephalin, resulting from the conversion of PE to e
103                 There are five copies of the Met-enkephalin sequence flanked by sets of paired basic
104          Tyr-MIF-1 (Tyr-Pro-Leu-Gly-NH2) and Met-enkephalin share a saturable transport system (pepti
105                         Our initial study on met-enkephalin strongly suggests that even fairly long t
106 ressing immunoreactivity for calbindin D28k, met-enkephalin, substance P, tyrosine hydroxylase, and p
107 ussis toxin-sensitive G proteins that couple met-enkephalin to the inhibition of cholinergically stim
108 nal nerve ligation is accompanied by D1R and met-enkephalin upregulation, acquired D1LR-mediated anti
109 sensory cells that coexpress beta-endorphin, Met-enkephalin, uroguanylin, and Trpm5 exist in mouse du
110 tch those of mammals (i.e., distributions of met-enkephalin, vasotocin, galanin, calcitonin gene-rela
111 ranslational processing of preproenkephalin, met-enkephalin was more abundant than leu-enkephalin bot
112 lin, and the main olfactory bulb, where only met-enkephalin was observed.
113                               All effects of met-enkephalin were mimicked by a mu receptor agonist, b
114 ntrations of endogenous [Leu]enkephalin and [Met]enkephalin were determined for 5 brain regions, and
115                  An antibody against Phe-Arg-Met-enkephalin, which did not recognize Leu- and Met-enk
116  These results indicate increased levels of (Met)enkephalin within secretory vesicles of the regulate
117 sites and two C-terminally extended forms of Met-enkephalin: YGGFMRSL and YGGFMGY.

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