Disease relevance of neo-kyotorphin

• No neo-kyotorphin could be isolated from normal lung tissue using the same procedures as those used for carcinomas [1].
• It is shown that neokyotorphin (the alpha-globin fragment 137-141) stimulates proliferation of normal cells (murine embryonic fibroblasts, red bone marrow and spleen cells) and tumor cells (murine melanoma and transformed fibroblasts L929) in the absence or in the presence of fetal bovine serum [2].

High impact information on neo-kyotorphin

• The effects of neuropeptides identified in the brain tissue of hibernators (Thr-Ser-Lys-Tyr, Thr-Ser-Lys-Tyr-Arg and Asp-Tyr) on the background activity and responses to electrical stimulation of the median forebrain bundle were analysed [3].
• Human erythrocytes release neokyotorphin, the 137-141 fragment of hemoglobin alpha-chain into the supernatant of red blood cells primary culture [4].
• Neokyotorphin and neokyotorphin (1-4): secretion by erythrocytes and regulation of tumor cell growth [4].
• Hydrolysis of neo-kyotorphin (Thr-Ser-Lys-Tyr-Arg) and [Met]enkephalin-Arg6-Phe7 by angiotensin-converting enzyme from monkey brain [5].
• The amino acid sequence of the peptide has been revealed to be H-Thr-Ser-Lys-Tyr-Arg-OH, which is exactly the same as that of neo-kyotorphin, an analgesic peptide originally isolated from bovine brain [(1982) Life Sci. 31, 1733] [1].

Biological context of neo-kyotorphin

• The results of flow cytometry analysis suggest that the effect of neokyotorphin on survival of L929 cells in serum-free culture medium is due to maintenance of cell proliferation in the absence of growth factors [2].
• Neo-kyotorphin inhibited AP, DPP, and ACE with IC50 values of 131, 306, and 200 microM, respectively, but the inhibition of the enzyme activities were not effective [6].
• PKC suppression (downregulation with PMA or inhibition with bisindolylmaleimide XI) did not affect neokyotorphin action [7].
• Neokyotorphin [TSKYR, hemoglobin alpha-chain fragment (137-141)] has previously been shown to enhance fibroblast proliferation, its effect depending on cell density and serum level [7].

Anatomical context of neo-kyotorphin

• Lipidic membranes are potential "catalysts" in the ligand activity of the multifunctional pentapeptide neokyotorphin [8].
• The interaction of neokyotorphin with cell membranes is potentially important to all these multiple biological processes since receptor-mediated processes are thought to be involved in neokyotorphin action [8].
• Neo-kyotorphin inhibited the Ca2+-dependent and depolarization-evoked release of 3H-GABA, from crude synaptosomes of the lower brain stem of rats [9].
• When injected into the substantia nigra reticulata, the 10 nmol dose of NKT and d-ser-2-NKT displayed equal seizure-protecting effect, which was higher than that for KT [10].

Associations of neo-kyotorphin with other chemical compounds

• Isolation from bovine brain of a novel analgesic pentapeptide, neo-kyotorphin, containing the Tyr-Arg (kyotorphin) unit [11].
• These findings suggest that inhibition of GABA in the brain may in part be involved in neo-kyotorphin-induced analgesia [9].
• The best conditions for preparing neokyotorphin and VV-haemorphin-4 were to achieve the peptic reaction in the buffer alone or in the presence of urea at a high degree of hydrolysis [12].

Gene context of neo-kyotorphin

• Stimulation of fibroblast proliferation by neokyotorphin requires Ca influx and activation of PKA, CaMK II and MAPK/ERK [7].

Analytical, diagnostic and therapeutic context of neo-kyotorphin

• The novel neuropeptide, neo-kyotorphin, produced a naloxone-resistant analgesia in the tail pinch test when given (IC) to mice [9].
• The quantitative evolution of neokyotorphin following the hydrolysis was determined by high-performance liquid chromatography coupled with a photodiode array detector [13].
• Proliferative activity of neokyotorphin-related hemoglobin fragments in cell cultures [14].

References