GLYCOPROTEINS EXPRESSING POLYSIALIC ACID AS MARKERS OF LOSS OF PLURIPOTENCY

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。 干细胞计划（道尔顿）已经证明，小鼠ESC和人ESC，当分化成迄今为止测试的所有途径时，开始在其表面上表达聚唾液酸（PSA），如通过抗PSA抗体结合所证明的。 PSA合成糖基转移酶转录上调的变化表明了这一发现。 该子项目的重点是确定PSA在分化过程中的表达机制及其功能。 该子项目的范围包括糖基因转录调控、受体蛋白表达和鉴定调控机制的技术开发。 总之，该项目证明了糖转录组学核心在指导后续实验以鉴定ESC分化期间聚糖变化方面的实用性。 有趣的是，小鼠和人的分化途径都显示出相似的聚糖变化。 这与SSEA-1和SSEA-3形成对比，SSEA-1和SSEA-3是在小鼠ESC分化期间发现的两种分化阶段特异性聚糖，其在人ESC分化中未发现。

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. The Stem Cell Program (Dalton) has demonstrated that both mouse ESC and human ESC, when differentiated into all pathways tested thus far, begin to express polysialic acid (PSA) on their surfaces, as evidenced by anti-PSA antibody binding. This finding was suggested by changes in PSA synthetic glycosyltransferase transcript upregulation. The Subproject focuses on determining the mechanisms of expression of PSA during differentiation and its function. The scope of the subproject encompasses glycogene transcription regulation, acceptor protein expression, and development of technologies to identify the mechanism of regulation. In sum, this project demonstrates the utility of the Glycotranscriptomics Core in directing subsequent experiments to identify glycan changes during ESC differentiation. Intriguingly, both mouse and human differentiation pathways show similar glycan changes. This is by contrast to SSEA-1 and SSEA-3, two differentiation stage-specific glycans found during mouse ESC differentiation which are not found in human ESC differentiation.