Robinson H C, Lindahl U
Biochem J. 1981 Feb 15;194(2):575-86. doi: 10.1042/bj1940575.
Heparin biosynthesis has been investigated with mouse mastocytoma in vitro. Minced tumour tissue catalysed the incorporation of [35S]sulphate and [3H]glucosamine into heparin and to a smaller extent into chondroitin sulphate. Addition of cycloheximide caused an inhibition (greater than 80%) of incorporation of each labelled precursor into both polysaccharides. Addition of benzyl beta-D-xyloside relieved the inhibition of incorporation into chondroitin sulphate and restored it to more than threefold that of the control incubation. The effect of beta-D-xyloside on incorporation into heparin was less marked although a consistent small increase of incorporation into this polysaccharide was observed. beta-D-Xyloside did, however, cause a marked incorporation of 35S and 3H labels into material of low molecular weight, which appeared to comprise heparin-like fragments. It is proposed that these fragments arise through a breakdown of the usual process of heparin biosynthesis.
已在体外利用小鼠肥大细胞瘤对肝素生物合成进行了研究。切碎的肿瘤组织催化将[35S]硫酸盐和[3H]葡糖胺掺入肝素，并在较小程度上掺入硫酸软骨素。加入环己酰亚胺会导致每种标记前体掺入两种多糖的过程受到抑制（超过80%）。加入苄基β-D-木糖苷可减轻对硫酸软骨素掺入的抑制，并使其恢复到对照孵育的三倍以上。β-D-木糖苷对肝素掺入的影响不太明显，尽管观察到该多糖的掺入量持续小幅增加。然而，β-D-木糖苷确实导致35S和3H标记大量掺入低分子量物质中，这些物质似乎由类肝素片段组成。有人提出，这些片段是通过肝素生物合成的正常过程的分解产生的。
