COMPARING GLYCANS OF HER-2 MOUSE MAMMARY TUMORS TO NON-DISEASED MAMMARY TISSUE

这个子项目是许多利用资源的研究子项目之一 由NIH/NCRR资助的中心拨款提供。子项目的主要支持 而子项目的主要调查员可能是由其他来源提供的， 包括其它NIH来源。 列出的子项目总成本可能 代表子项目使用的中心基础设施的估计数量， 而不是由NCRR赠款提供给子项目或子项目工作人员的直接资金。 我们最近表明，GnT-V表达水平调节小鼠乳腺癌干细胞隔室导致HER-2过表达。 此外，我们已经表明，当GnT-V的活性被调节时，作为GnT-V产物的聚糖在HER-2受体上以不同水平存在。 我们现在正在确定由HER-2诱导的乳腺肿瘤上N-连接聚糖的精确结构，并将其与非患病乳腺中表达的结构进行定量比较。

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. Primary support for the subproject and the subproject's principal investigator may have been provided by other sources, including other NIH sources. The Total Cost listed for the subproject likely represents the estimated amount of Center infrastructure utilized by the subproject, not direct funding provided by the NCRR grant to the subproject or subproject staff. We have recently shown that GnT-V expression levels regulate the mouse mammary cancer stem cell compartment resulting from her-2 over-expression. In addition, we have shown that glycans that are products of GnT-V are found in different levels on the her-2 receptor when the activity of GnT-V is modulated. We are now determining the precise structures of the N-linked glycans on the mammary tumors induced by her-2 and comparing those quantitatively with the structures expressed in the non-diseased mammary gland.