The Journal of Antibiotics
Online ISSN : 1881-1469
Print ISSN : 0021-8820
ISSN-L : 0021-8820
MITOGENIC POTENTIALS OF BESTATIN, AMASTATIN, ARPHAMENINES A AND B, FK-156 AND FK-565 ON SPLEEN LYMPHOCYTES
NORBERT WEIBMANNGABRIELE LEYHAUSENARMIN MAIDHOFWATARU TANAKAHAMAO UMEZAWAWERNER E. G. MÜLLER
著者情報
ジャーナル フリー

1985 年 38 巻 6 号 p. 772-778

詳細
抄録

The following aminopeptidase (AP) activities were found to be associated with the surface of mouse spleen cells: Leu-AP (138 pmol/105 cells×minute) and AP-B (16 pmol/105 cells×minute with Lys-β-naphthylamide as substrate and 21 pmol/105 cells×minute with Arg-β-naphthylamide substrate); AP-A activity was not detected by the assay system applied. The immunoactive peptide bestatin inhibited the Leu-AP, while AP-B activity decreased in the presence of both arphamenines A and B and bestatin. No effects on these enzymes were caused by amastatin (an AP-A inhibitor), FK-156, FK-565 and Bu-2743E; the latter peptide turned out to be not an inhibitor of cell surface associated microsomal Leu-AP but an inhibitor of cytosolic Leu-AP. The immunoactive peptides bestatin, arphamenines A and B, and amastatin increased [3H]thymidine incorporation into spleen cells containing lymphocytes and macrophages. These mitogenic actions were not observed when macrophages were removed from the cultures or the cells had been stimulated with ConA or LPS. The lactoyl- and heptanoyl peptides FK-156 and FK-565 caused a mitogenic action on lymphocytes independently of the presence of macrophages. The inhibitor of cytosolic Leu-AP did not change the incorporation into lymphocytes.

著者関連情報
© Japan Antibiotics Research Association
前の記事 次の記事
feedback
Top