Detail of "54827-14-4"

Reference

Sialoglycoconjugate changes during 2-acetylaminofluorene-induced hepatocarcinogenesis in the rat

Sialoglycoconjugate changes during 2-acetylaminofluorene-induced hepatocarcinogenesis in the rat. Creek, Kim E.; Walter, Vivian P.; Evers, David; Yeo, Emily; Elliott, William L.; Heinstein, Peter F.; Morre, Dorothy M.; Morre, D. James (Dep. Biol. Sci., Purdue Univ., West Lafayette, IN 47907, USA). Biochim. Biophys. Acta, 793(2), 133-40 (English) 1984. CODEN: BBACAQ. ISSN: 0006-3002. DOCUMENT TYPE: Journal CA Section: 4 (Toxicology) The early events of glycolipid biosynthesis during the 1st 11 wk of 2-acetylaminofluorene (I) [53-96-3] administration were obsd. Transient elevations in CMP-sialic acid synthetase [9067-82-7] and elevations in neutral glycosphingolipid precursors to gangliosides preceded the major elevations in CMP-sialic acid:lactosylceramide sialyltransferase (GM3 synthetase) [12575-29-0]. Two cycles of response were obsd. prior to the initiation of the sustained enhancement of biosynthesis of precursor ganglioside, GM3 [54827-14-4], and(or) a significant increase in total or lipid-sol. sialic acid. In vitro rates of sialyl transfer from CMP-sialic to endogenous protein acceptors were not altered. Thus, the previous observations of altered ganglioside biosynthesis following I administration are not an isolated occurrence but may represent late events in a sequence or cascade of biochem. change involving, as well. biosynthesis of ganglioside precurssors, CMP-sialic acid and neutral glycosphingolipids.

Binding of tetanus toxin to somatic neural hybrid cells with varying ganglioside composition

Binding of tetanus toxin to somatic neural hybrid cells with varying ganglioside composition. Yavin, Ephraim; Habig, William H. (Dep. Neurobiol., Weizmann Inst. Sci., Rehovot 76100, Israel). J. Neurochem., 42(5), 1313-20 (English) 1984. CODEN: JONRA9. ISSN: 0022-3042. DOCUMENT TYPE: Journal CA Section: 4 (Toxicology) 125I-labeled tetanus toxin interaction with several somatic hybrid cell lines was investigated. Binding of toxin is most effective in NCB-20, followed by NBr-10A, NG108-C15, and SB21-B1 cells. Specific binding of toxin to NCB-20 and SB21-B1 cells is 7- and 60-fold lower, relatively, in comparison to enriched rat cerebral neuron cultures. The NCB-20, NBr-10A, and NG108-C15 clones display a complex ganglioside pattern, including the presence of GD1a [12707-58-3] and 2 unidentified [14C]galactose-labeled lipid-sol. compds., while the SB21-B1 is most abundant in GM3 [54827-14-4] and GM2 [19600-01-2]. None of the cells tested contain measurable levels of [14C]galactose-labeled or resorcinol-pos. bands of GD1b [19553-76-5] and GT1b [59247-13-1]. After 2 h at 37°, a near plateau of toxin assocn. with NCB-20 cells is seen. Binding in low-ionic-strength medium is 1.35-fold higher at 37° than at 4°, but is reduced by 21 and 51% at 4° and 37°, resp., in physiol. medium. Treatment of NCB-20 cells with neuraminidase causes a partial loss (29%) of toxin-binding sites. Binding to the hybrid cells is significantly different from that of cerebral cultures with respect to temp., salt effect, and sensitivity to neuraminidase, suggesting perhaps a different class of receptors for the toxin. Unlike dibutyryl cyclic AMP or prostaglandin, long-term serum removal causes a significant increase in toxin binding to NCB-20 and NG108-C15 cells. Binding of toxin to ganglioside-supplemented SB21-B1 cells is 5-fold higher compared to untreated cells; it is impaired by neuraminidase added before but not after cell interaction with toxin at 37°.