Date: 10 Jul 2012
A “SUEL-type lectin domain”(IPR000922) was described by Yasuhiro Ozeki in 1991 as with a unique primary structure for animal lectins with specificity to D-galactosides in the eggs of the sea urchin Anthocidaris crassispina (http://en.wikipedia.org/wiki/Galactose_binding_lectin_domain). By 2012, over 1000 structural homologues with SUEL-type lectin domains have been registered in genome detabases such as in the cases of the receptor of spider neurotoxin in mammalian brain,fish egg lectins and β-galactosidase from plants. (http://www.ebi.ac.uk/interpro/IEntry?ac=IPR000922).
SAL is a Gb3 (Galα1-4Galβ1-4Glc)-binding lectin with three SUEL-type lectin domains which was purified from catfish eggs. The lectin depleted expression of mRNA coding multidrug resistant protein, MRP1, time- and dose-dependently through binding with Gb3 glycosphingolipid which is highly expressed on human Burkitt’s lymphoma Raji cells. This interaction inhibited the excretion of chemotherapy drugs. The administration of vincristine could effectively killed Raji cells even at l/10 lower concentration than the lethal-doses, if co-treatment with SAL was conducted. The Japanese Association for Marine Biology (JAMBIO) in MEXT Japan identified this research as a leading edge topic as part of their 2012 research activities reporting. These results were possible through the work of Assist. Profs. Yuki Fujii (Nagasaki International University and adjunct researcher of Yokonama City University) and Shigeki Sugawara (Tohoku Pharmaceutical University), Assoc. Prof. Sarkar M. Abe Kawsar (University of Chittagong, Bangladesh), Profs. Yasuhiro Ozeki, Hidetaro Yasumitsu and Robert A. Kanaly (Yokohama City University) and is published through the Canadian Web site Global Medical Discovery and The Protein Journal. They were carried out under the supervision of Profs. Kazuo Nitta, Masahiro Hosono, Motoaki Takayanagi (Tohoku Pharmaceutical University) and Prof. Sen-itiroh Hakomori (Membership of National Academy of Science USA and director of Pacific Northwest Diabetes Research Institute, Seattle Washington, USA). This work was supported by Grants-in-Aid from JAMBIO by MEXT and JSPS.