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   1 ortant role in the inactivation of mammalian tachykinins.                                            
     2 arge diameter nonnociceptive neurons express tachykinins.                                            
     3 arily conserved family of neuropeptides, the tachykinins.                                            
  
     5 peptide Y, neurotensin, preproenkephalin and tachykinin 1; this involved a critical period at the com
  
  
     8 lthough NK1R immunoreactivity was increased, tachykinin-1 receptor (Tacr1) mRNA was not increased in 
     9 ecently we determined that activation of the tachykinin 2 (Tac2) pathway in the central amygdala (CeA
    10 s been mounting for peripheral functions for tachykinins, a family of neuropeptides including substan
    11 motor neurons that release acetylcholine and tachykinins acting on muscarinic and NK1 receptors, resp
    12 tion in response to superfusion of different tachykinin agonists (neurokinins A (NKA) and B (NKB), SP
    13 revealed a similar profile of sensitivity to tachykinin agonists and antagonists for both receptors; 
  
  
    16 okinin receptor are homologous to vertebrate tachykinin and its receptor, and injection of tachykinin
  
    18 d genetic mutant analyses revealed that both Tachykinin and Tachykinin-like receptor (DTKR99D) are re
  
    20 sin C-terminal motifs to those of vertebrate tachykinins and of tachykinin-related peptides in arthro
  
    22 Furthermore, we examined the coexpression of tachykinins and two kisspeptin genes in the brain of zeb
  
  
  
  
  
    28 refore suitable pharmacological tools in the tachykinin area to elucidate further the pathophysiologi
    29 duce this effect (termed sub-threshold), the tachykinin attenuated AMG stimulation-evoked glutamaterg
    30 ive regulatory role of serotonin on striatal tachykinin biosynthesis, PPT and PPE gene regulation in 
    31  receptors) on microglia and shown that this tachykinin can significantly elevate bacterially induced
  
  
    34 tomy is mediated by sequential activation of tachykinin-containing spinal afferent and sympathetic ef
  
  
  
  
  
    40  lobe glomerulus wired for attraction, while tachykinin (DTK) suppresses activity of a glomerulus wir
    41 eness to inhaled CS, and that the endogenous tachykinins evoked by CS-induced activation of lung C fi
  
  
  
  
  
  
  
    49  for peripherally distributed members of the tachykinin family of peptides, namely substance P and th
  
    51  Tac1 gene encodes peptides belonging to the tachykinin family with substance P being the predominant
  
    53 ance P (SP), a neuropeptide belonging to the tachykinin family, is expressed in gastrointestinal trac
  
  
    56 dure which results in permanent depletion of tachykinins from the lungs and airways as well as degene
  
  
    59 tion of the location of neurons that express tachykinin gene transcripts in the human hypothalamus.  
    60    Two distinct but functionally overlapping tachykinins govern inflammation through NK-1R at sites o
  
    62 eripherally, adds support to the notion that tachykinins have physiologic/endocrine roles in the peri
  
    64 alysis has shown that during the first week, tachykinin-immunoreactive profiles appeared as round or 
    65 hypotension-induced release of an endogenous tachykinin in SON and evidence suggesting a role for NK3
  
    67 ublications have demonstrated a key role for tachykinins in the positive feedback regulation of plate
  
  
    70 igh affinities for other naturally occurring tachykinins including neurokinin A, neuropeptide K, neur
  
  
    73 he pattern of distribution and appearance of tachykinin-labelled fibers in the dorsal lateral genicul
    74 ypothesis, the binding affinities of natural tachykinin ligands may be largely determined by their co
  
    76 t analyses revealed that both Tachykinin and Tachykinin-like receptor (DTKR99D) are required for dama
  
  
  
  
  
  
    83 situ hybridization showed no coexpression of tachykinins mRNA with kisspeptins mRNA in hypothalamic n
  
    85 ng existing agents that have such properties-tachykinin neurokinin 3 receptor antagonists-is proposed
  
    87  senktide analogue, but not significantly by tachykinin neurokinin-1 or neurokinin-2 receptor-selecti
    88 ndogenous tachykinins or exogenous selective tachykinin neurokinin-3 receptor activation with senktid
    89 ide analogue were inhibited by the selective tachykinin neurokinin-3 receptor antagonists, SB 223412 
    90 is of lung disease, although the role of the tachykinin neurokinin-3 receptor has not been elucidated
    91 response was mimicked by exogenously applied tachykinin neurokinin-3 receptor-selective agonist, senk
    92     Using confocal microscopy, we identified tachykinin neurokinin-3 receptors on human bronchial par
  
  
  
    96 removal of extracellular calcium, but not by tachykinin neuropeptide, voltage-sensitive calcium chann
  
    98 ated peptides, including somatostatin (SST), tachykinin, neuropeptide Y (NPY) and cortistatin, in a p
  
  
  
  
   103 ated with apoptosis, 2) decreased macrophage tachykinin NK(1)-dependent phagocytosis, 3) substantiall
  
  
  
  
   108 the neuropeptide substance P (SP) acting via tachykinin NK1 receptor inhibition of GABA(A) currents. 
   109 e P release and activity because blockade of tachykinin NK1 receptors (66.3+/-13.7% inhibition, n=6; 
   110 role in emesis via the activation of central tachykinin NK1 receptors during the delayed phase of vom
   111 Phe8]-substance P (SENK; 25, 100, 200 ng), a tachykinin NK3 receptor agonist, and [Sar9, Met(O2)11]-s
   112 , and NK1-R and NK2-R mediate the effects of tachykinins on interstitial and smooth muscle cells, res
  
  
  
  
  
  
  
  
   121 rimary effector of this pathway, co-released tachykinin peptides and their respective nigral tachykin
  
   123 esent and previous findings, we suggest that tachykinin peptides not only play a role as putative neu
  
   125 and the structure of two naturally occurring tachykinin peptides, substance P (SP, RPKPQQFFGLM-NH2) a
   126 e piscine Tac3 gene encodes for two putative tachykinin peptides, the mammalian ortholog encodes for 
  
   128 mice lacking SP signaling by deletion of the tachykinin precursor 1 (Tac1) gene or coadministration o
  
  
   131 d analysis of sialyltransferase 4A (SIAT4A), tachykinin receptor 1 (TACR1), and gamma-aminobutyric ac
   132 rotein-coupled receptor, previously known as tachykinin receptor 86C (also known as the neurokinin K 
   133 ulphonic acid (PPADS; 10 microM) or an NK(3) tachykinin receptor antagonist (Neurokinin A 4-10; 100 n
  
   135 tamate receptor antagonist; L733,060, an NK1 tachykinin receptor antagonist, and chelerythrine, a pro
  
  
  
  
   140 15 and CG7887 by showing these two suspected tachykinin receptor family members respond specifically 
  
   142 rpolarization or current was mimicked by the tachykinin receptor NK1 agonist Ac-[Arg6, Sar9, Met(O2)1
   143 ith DOCA once daily for 11 days and analyzed tachykinin receptor subtype, neurokinin 3 (NK3r)-immunor
   144 ent studies determined to what extent nigral tachykinin receptor subtypes contribute to striatal D1-m
  
   146 we have attempted to: (1) define the type of tachykinin receptor which mediates the negative chronotr
  
   148  been implicated in RSV pathophysiology, and tachykinin receptor-null mice were similarly protected f
  
  
   151 GIR shares 31-34% amino acid identity to the tachykinin receptors (substance P receptor, neurokinin A
   152  human ileum, we examined a possible role of tachykinin receptors and neurokinin (NK) A in neurally i
   153 hykinin peptides and their respective nigral tachykinin receptors are also in position to influence m
  
  
  
  
  
  
  
  
  
   163 ro(5)-Asp(6)-Asn(7)-Pro(8)-Gly(9)-NH2) and a tachykinin-related peptide (CabTRP Ia, Ala(1)-Pro(2)-Ser
   164 entrating hormone (RPCH) and Cancer borealis tachykinin-related peptide (CabTRP) are colocalized in a
   165 wo closely related neuropeptidergic systems, tachykinin-related peptide (TRP) and natalisin (NTL), an
   166  show by immunocytochemistry that GABA and a tachykinin-related peptide (TRP) are localized in the am
  
   168  and five additional modulators [C. borealis tachykinin-related peptide Ia (CabTRP Ia), crustacean ca
  
  
   171  neuromodulators [proctolin, Cancer borealis tachykinin-related peptide Ia, crustacean cardioactive p
  
   173    This endopeptidase cleaved another insect tachykinin-related peptide, CavTK-II, in a predictable m
   174 in, allatostatin, serotonin, Cancer borealis tachykinin-related peptide, cholecystokinin, and crustac
   175 fs to those of vertebrate tachykinins and of tachykinin-related peptides in arthropods led us to iden
   176 bound NEP is involved in the inactivation of tachykinin-related peptides in the brain of the cockroac
  
   178 t neuropeptide F, myoinhibitory peptide, and tachykinin-related peptides were found to be expressed i
   179  suggesting that the peptidase can hydrolyse tachykinin-related peptides with different structures.  
  
  
   182 ke significant action potential discharge or tachykinin release from bronchopulmonary C-fibre termina
   183 d substantial action potential discharge and tachykinin release from bronchopulmonary C-fibre termina
  
   185 nfection where initial C3a production causes tachykinin release, followed by activation of the IL-17A
   186      Understanding the physiological role of tachykinins requires precise cellular and subcellular lo
  
   188 ociceptive signaling pathways we examined SP/Tachykinin signaling in a Drosophila model of tissue dam
   189   Our results highlight a conserved role for Tachykinin signaling in regulating nociception and the p
  
  
  
  
  
  
  
   197 tion on enkephalin (Met5-enkephalin; ME) and tachykinin (substance P; SP) systems of basal ganglia of
  
  
  
   201    Our results suggest that the roles of the tachykinin system in regulating food intake might be evo
   202 nctions of neurokinin B (NKB), we identified tachykinin (tac) and tac receptor (NKBR) genes from many
  
  
  
   206 st that natalisin is an ancestral sibling of tachykinin that evolved only in the arthropod lineage.  
  
  
  
   210 evertheless, the ability of pro-inflammatory tachykinins to affect the immune functions of DCs remain
   211 traction since leukotriene C4, histamine and tachykinins, which all caused a similar contraction to a
  
   213 NK1-R and NK3-R mediate neurotransmission by tachykinins within enteric nerve plexuses, and NK1-R and
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