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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.                                         
  
    10 cordings with patch electrodes, bath-applied met-enkephalin, a nonselective opioid receptor agonist, 
  
    12 y formation produced by [Leu]enkephalin and [Met]enkephalin administration in 2 regions of the 2-day-
  
  
    15 ry vesicle cathepsin L in the production of [Met]enkephalin, an endogenous peptide neurotransmitter. 
  
    17 nalization, and also enhanced the effects of Met-enkephalin and alpha-neoendorphin, but not endomorph
  
    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 
  
  
  
  
  
  
    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
  
  
    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
  
  
  
  
    42 of the previously studied glycine oligomers; met-enkephalin contains the interesting motions of pheny
  
    44 dependent secretion of KPI/APP with PTP and (Met)enkephalin demonstrated the colocalization of these 
  
  
  
  
    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
  
    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
  
  
  
    58 owed the colocalization of cathepsin L with [Met]enkephalin in secretory vesicles of neuroendocrine c
  
  
    61 a(2), N-Me-Phe(4), Gly-ol(5)]-enkephalin and met-enkephalin inhibited both ST-stimulated EPSCs and th
  
  
    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
  
  
    68 dy, which recognized Leu-, Met-, and Phe-Arg-Met-enkephalin, labeled the dorsolateral funiculus and n
  
    70 MS2 scans enabled simultaneous monitoring of Met-enkephalin, Leu-enkephalin, and unknown peptides.   
  
    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 
  
    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
  
    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 
  
    83 Finally, in cathepsin L gene knockout mice, [Met]enkephalin levels in brain were reduced significantl
  
    85 amphetamine (METH) significantly altered the met-enkephalin (M-Enk) systems associated with some, but
  
    87 Cs (eIPSCs) was unaffected by perfusion with met-enkephalin (ME) or by mu-, delta-, or kappa-opioid r
  
  
  
    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
  
    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
  
  
  
   102 lted in highly increased cellular levels of (Met)enkephalin, resulting from the conversion of PE to e
  
  
  
   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
  
  
   114 ntrations of endogenous [Leu]enkephalin and [Met]enkephalin were determined for 5 brain regions, and 
  
   116  These results indicate increased levels of (Met)enkephalin within secretory vesicles of the regulate
  
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