GLYCAN MEDIATED REGULATION OF CD44 FUNCTION
聚糖介导的 CD44 功能调节
基本信息
- 批准号:2402752
- 负责人:
- 金额:$ 7.89万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:1997
- 资助国家:美国
- 起止时间:1997-09-30 至 2000-09-29
- 项目状态:已结题
- 来源:
- 关键词:CD44 molecule CHO cells capillary electrophoresis carbohydrate structure cell adhesion cell adhesion molecules cell type chemical binding chemical structure function enzyme activity enzyme substrate flow cytometry glycosylation glycosyltransferase hyaluronate laboratory mouse leukocyte activation /transformation messenger RNA metastasis neoplastic cell oligosaccharides phosphorylation sialyltransferases transfection
项目摘要
DESCRIPTION (Applicant's Description): The majority of human cancer deaths
are due to metastasis, a process that is poorly understood at the molecular
and cellular levels. In the multistep process of metastasis one expects
significant roles for cell adhesion molecules. CD44, a cell surface
receptor for hyaluronan (HA) that functions in cell adhesion, cell
migration, and cell activation, has been implicated in the process of
metastasis. CD44 has the property of regulated affinity for its ligand.
The role of glycosylation in regulating CD44-mediated hyaluronan binding
will therefore be examined. This study is consistent with the candidate's
long-term objective of elucidating enough detail of the mechanism by which
glycosylation regulates cell adhesion molecule function to enable modulation
of this mechanism as an intervention f o r metastasis. Preliminary studies
have identified oligosaccharide structures which impact the intrinsic
HA-binding properties of CD44. The present proposal aims to determine which
structures are biologically regulated and to elucidate the enzymatic basis
for regulation of the functionally i m portant glycan structure. After
identification of the key glycosyltransferase, the mechanism employed by the
cell to regulate CD44 glycosylation as part of an integrated cell behavior
will be defined. Mechanisms to be examined include synthetic
glycosyltransferase expression, glycosyltransferase phosphorylation, CD44
alternative RNA splicing, and interacting glycosyltransferases. CD44
oligosaccharide structure will be c h a n ged by glycosidase digestion and
glycosyltransferase modulation. I n t rinsic CD44 HA-affinity will be
determined by affinity capillary e l e ctrophoresis. Structure/function
correlations will be drawn. A physiologic change in CD44 glycosylation and
hyaluronan-affinity will be tested upon cellular activation. The effects on
metastasis of manipulating CD44 HA-affinity by glycosyltransferase
modulation will be determined using an in vivo model. This proposal will
serve as a basis to develop a general approach to defining the regulatory
role of glycosylation in cell-cell and cell-matrix adhesion.
描述(申请人描述):大多数人类癌症死亡
项目成果
期刊论文数量(0)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
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TIMOTHY P SKELTON其他文献
TIMOTHY P SKELTON的其他文献
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{{ truncateString('TIMOTHY P SKELTON', 18)}}的其他基金
DECODING CANCER SIGNATURE GLYCOFORMS OF SERUM TUMOR MARK
解码血清肿瘤标记的癌症特征糖型
- 批准号:
6287265 - 财政年份:2001
- 资助金额:
$ 7.89万 - 项目类别:
DECODING CANCER SIGNATURE GLYCOFORMS OF SERUM TUMOR MARK
解码血清肿瘤标记的癌症特征糖型
- 批准号:
6540881 - 财政年份:2001
- 资助金额:
$ 7.89万 - 项目类别:
DECODING CANCER SIGNATURE GLYCOFORMS OF SERUM TUMOR MARK
解码血清肿瘤标记的癌症特征糖型
- 批准号:
6489429 - 财政年份:2001
- 资助金额:
$ 7.89万 - 项目类别:
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