γ-neuropeptide K: A peptide isolated from rabbit gut that is derived from γ-preprotachykinin

Kage, R.; McGregor, GP; Thim, Lars; Conlon, J. Michael

doi:10.1016/0167-0115(87)90200-x

Cited by 7 publications

(6 citation statements)

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“…The finding that N‐terminally extended TKRPs are predominantly expressed only in the gut and not in the brain are in line with findings of enrichment of N‐terminally extended tachykinins, neuropeptide γ and neuropeptide K, in the mammalian intestine [29–31]. Another extended TKRP was isolated from the locust intestine [32].…”

Section: Discussionsupporting

confidence: 81%

Tachykinin‐related peptide precursors in two cockroach species

et al. 2005

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Tachykinins constitute a family of multifunctional neuropeptides whose signaling mechanisms seem to be partially conserved through evolution [1][2][3][4][5]. Although the tachykinin peptides display only limited sequence identities when comparing invertebrates and mammals, their G-protein-coupled receptors (GPCRs) display more striking similarities, suggesting ancestral relationships [4,5]. The three principal mammalian tachykinins, substance P, neurokinin A and neurokinin B, are processed from two precursors, preprotachykinin A and B and they act with preferential affinities on three different GPCRs, NK1-NK3 [5]. More recently, additional tachykinins, the hemokinins, were identified on a third precursor encoding gene, preprotachykinin C, expressed in hematopoietic cells of mouse, rat and humans [6,7].In invertebrates the tachykinins exist in two major forms: (a) the tachykinin-related peptides (TKRPs; previously termed TRPs) that differ from the mammalian tachykinins by having a C-terminus FXGXRamide (X ¼ variable residues), rather than FXGLMamide and (b) invertebrate tachykinins (Inv-TKs) with an

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Section: Discussionsupporting

confidence: 81%

Tachykinin‐related peptide precursors in two cockroach species

et al. 2005

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“…The observation that a significant amount of NKA-LI extractable from the guinea-pig colon co-elutes with authentic neuropeptide γ at reversephase HPLC, whilst no peak corresponding to neuropeptide K was detected, further suggests that γ-rather than β-PPT mRNA is expressed at this level. The presence of neuropeptide γ has been previously described in NKA-LI extracted from the rat duodenum and jejunum (Takeda et al 1990), while contrasting reports have been obtained about its presence in the guinea-pig intestine (Kage et al 1988;Too et al 1989;Shuttleworth et al 1991). The third component of NKA-LI has the same retention time of SP, but it is questionable whether it may represent SP itself since the cross-reactivity of the anti-NKA serum towards SP was <0.05%.…”

Section: Discussionmentioning

confidence: 85%

Depolarization evoked co-release of tachykinins from enteric nerves in the guinea-pig proximal colon

Lippi

Santicioli

Criscuoli

et al. 1998

Naunyn-Schmiedeberg's Arch Pharmacol

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The aim of this study was to assess at which extent an even co-release of the tachykinins, substance P (SP) and neurokinin A (NKA), occurs from enteric neurons/nerves of the guinea-pig proximal colon during graded depolarization. In this preparation, a sharply diverging NK1/NK2 receptor pattern of tachykininergic co-transmission has been observed in physiological studies. The experiments were performed in capsaicin-pretreated (10 microM for 15 min) mucosa-free smooth muscle of guinea-pig proximal colon, to exclude the mucosa and the peripheral endings of primary afferent nerves as possible sources of released tachykinins. The content of extractable tachykinins was measured as SP- and NKA-like immunoreactivities (-LI) by radioimmunoassay. Chromatographic characterization of aqueous acetic acid extracts showed one peak of SP-LI corresponding to authentic SP, whereas there were multiple peaks of NKA-LI, the major one co-eluting with authentic NKA. An increased outflow of both SP- and NKA-LI was evenly produced in a concentration-dependent manner when the preparations were superfused with a high potassium (K) medium in which NaCl had been replaced with equimolar amounts (20-100 mM) of KCl. The high K-evoked release of SP- and NKA-LI was dependent upon the presence of extracellular calcium and was inhibited by about 50% in the presence of the N-type voltage-dependent calcium channel blocker, omega-conotoxin GVIA (0.1 microM). Omega-conotoxin MVIIC (1 microM), a non-selective blocker of N-, P- and Q-type voltage-dependent calcium channels, likewise produced about 40% inhibition of evoked release of both peptides. No evidence for a role of L-type channels in tachykinin release was obtained, since the addition of nifedipine (1 microM) or Bay K8644 (1 microM) did not significantly affect the response to high K. Neither NK1 receptor agonist (septide, 0.1 microM) or antagonist (SR 140333, 10 nM) nor NK2 receptor agonists ([betaAla8]NKA(4-10) and GR 64349, 0.1 microM each) or antagonist (SR 48968, 10 nM) did affect the high K-evoked release of tachykinins. We conclude that SP and NKA are evenly co-released in response to graded depolarization of enteric nerves in the guinea-pig colon. Therefore, the specialization of tachykininergic transmission observed in functional studies does not originate at the prejunctional level. The co-release of tachykinins involves the influx of extracellular calcium via N-type but not L-type calcium channels. No evidence for the presence of NK1 or NK2 autoreceptors affecting tachykinin release from enteric neurons was obtained.

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“…[13] discovered an anionic tachykinin, which was named neuromedin K, now known as neurokinin B (NKB, also known as neurokinin β). Two more mammalian tachykinins are known such as neuropeptide γ (NP-γ) [14] and neuropeptide K (NPK) [15]. The non-mammalian tachykinins isolated from lower animals are eledoisin, physalemin, phyllomedusin, uperolein [16] and kassinin.…”

Section: History Of Tachykininsmentioning

confidence: 99%

Substance P: Structure, Function, and Therapeutics

Datar

Srivastava²,

Coutinho³

et al. 2004

CTMC

148

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Extensive efforts since 1931, on the structural determination of the mammalian tachykinin SP by NMR, CD and IR have turned out to be inconclusive. Studies are now being concentrated on the structural properties and characteristics of various NK receptors (NK(1), NK(2) and NK(3)) with the help of genetics, cloning, receptor engineering, mutagenesis and modeling. This knowledge is now being fruitfully used in the development of non-peptide NK(1) receptor antagonists that essentially block the pharmacological effects of SP. It is now being realized that the simultaneous blockade of two or more receptors gives promising results in emesis, depression and pulmonary obstructive diseases. In addition to the synthetic compounds, the discovery of antagonists from natural origin has added a great value to this field. In this review we have made an attempt to present the structural characteristics of SP, its analogs and antagonists, the structural characteristics of the NK receptor, and structure activity relationships that have helped to improve the therapeutic utilities of SP antagonists.

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γ-neuropeptide K: A peptide isolated from rabbit gut that is derived from γ-preprotachykinin

Cited by 7 publications

References 0 publications

Tachykinin‐related peptide precursors in two cockroach species

Tachykinin‐related peptide precursors in two cockroach species

Depolarization evoked co-release of tachykinins from enteric nerves in the guinea-pig proximal colon

Substance P: Structure, Function, and Therapeutics

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