CSHL Conference on PTEN Pathways

CSHL PTEN 途径会议

基本信息

批准号：
7577341
负责人：
DAVID J. STEWART
金额：
$ 0.7万
依托单位：
COLD SPRING HARBOR LABORATORY
依托单位国家：
美国
项目类别：
财政年份：
2006
资助国家：
美国
起止时间：
2006-03-01 至 2011-02-28
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/7577341
关键词：
1-Phosphatidylinositol 3-Kinase Address Affect Alleles Apoptosis Attenuated Autistic Disorder Basic Science Binding Proteins Biochemical Bladder Brain Breast Breast Carcinoma Cancer cell line Candidate Disease Gene Cell Cycle Regulation Cell Surface Receptors Cells Child Childhood Chromosomes Colon Colorectal DNA Methylation Development Diabetes Mellitus Disease Disease model Epigenetic Process Family Family member Female Focal Adhesions Genes Genetic Germ-Line Mutation Growth Hamartoma Human Inositol Inositol Phosphates Insulin Insulin Receptor Link Location Lung Lymphoma Macrocephaly Malignant Neoplasms Malignant neoplasm of prostate Mammalian Cell Mediator of activation protein Metabolism Molecular Molecular Genetics Multiple Hamartoma Syndrome Mutate Mutation Names Organ PDPK1 gene PTEN gene PTEN protein Parkinson Disease Pathogenesis Pathway interactions Patient Care Patients Phosphatidylinositols Phosphoric Monoester Hydrolases Phosphotransferases Physiological Processes Prostate Proteins Proteus Syndrome Proto-Oncogene Proteins c-akt Research Research Personnel Risk Scientist Second Messenger Systems Signal Pathway Signal Transduction Skin Skin Neoplasms Suppressor Genes Syndrome Therapeutic Intervention Thyroid carcinoma Tumor Suppressor Genes Tumor Suppressor Proteins Woman base cell growth human PTEN protein improved malignant breast neoplasm meetings melanoma migration nervous system disorder oxidation promoter protein expression second messenger symposium tensin tripolyphosphate tumor

1-Phosphatidylinositol 3-Kinase Address Affect Alleles Apoptosis Attenuated Autistic Disorder Basic Science Binding Proteins Biochemical Bladder Brain Breast Breast Carcinoma Cancer cell line Candidate Disease Gene Cell Cycle Regulation Cell Surface Receptors Cells Child Childhood Chromosomes Colon Colorectal DNA Methylation Development Diabetes Mellitus Disease Disease model Epigenetic Process Family Family member Female Focal Adhesions Genes Genetic Germ-Line Mutation Growth Hamartoma Human Inositol Inositol Phosphates Insulin Insulin Receptor Link Location Lung Lymphoma Macrocephaly Malignant Neoplasms Malignant neoplasm of prostate Mammalian Cell Mediator of activation protein Metabolism Molecular Molecular Genetics Multiple Hamartoma Syndrome Mutate Mutation Names Organ PDPK1 gene PTEN gene PTEN protein Parkinson Disease Pathogenesis Pathway interactions Patient Care Patients Phosphatidylinositols Phosphoric Monoester Hydrolases Phosphotransferases Physiological Processes Prostate Proteins Proteus Syndrome Proto-Oncogene Proteins c-akt Research Research Personnel Risk Scientist Second Messenger Systems Signal Pathway Signal Transduction Skin Skin Neoplasms Suppressor Genes Syndrome Therapeutic Intervention Thyroid carcinoma Tumor Suppressor Genes Tumor Suppressor Proteins Woman base cell growth human PTEN protein improved malignant breast neoplasm meetings melanoma migration nervous system disorder oxidation promoter protein expression second messenger symposium tensin tripolyphosphate tumor

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项目摘要

DESCRIPTION (provided by applicant): PTEN protein negatively regulates cellular signals used in a wide variety of physiological processes. At the molecular level, PTEN is a phosphatase that destroys the second messenger phosphatidylinositol-3,4,5-triphosphate (Pl- 3,4,5-P) by removing a phosphate from the inositol ring. When PTEN is mutated, PI-3,4,5-P levels rise in the cell. PI-3 kinase proteins generate PI-3,4,5-P. PTEN and PI-3 kinase are key mediators of many cell surface receptors. Insulin is perhaps the best understood signal that utilizes PTEN and PI-3 kinase. T his highly conserved pathway employs the insulin receptor to stimulate PI-3 kinase. Elevated PI-3,4,5-P levels activate AKT kinase, which can phosphorylate the FOXO family members to attenuate their transcriptional activity. PTEN also regulates many other proteins in the cell and has been implicated in the control of the cell cycle, metabolism, cell growth, apoptosis, oxidation, and migration. Aberrant PTEN pathway signaling is associated with cancer, diabetes, and Parkinson's disease. Genetic alteration of the PTEN/PI-3 kinase pathway in cancer is extremely common and is an outstanding target for therapy. This meeting will comprehensively address topics of basic research, disease models, and therapeutic intervention for the ultimate purpose of improving patient care. This proposal seeks support for three successive biennial meetings to be held in 2006, 2008 and 2010.

描述（由申请人提供）：PTEN蛋白对各种生理过程中使用的细胞信号负调节。在分子水平上，PTEN是一种磷酸酶，通过从肌醇环中去除磷酸磷酸盐，摧毁了第二层磷脂酰肌醇-3,4,5-三磷酸（PL-3,4,5-P）。当PTEN突变时，细胞中PI-3,4,5-P水平上升。 PI-3激酶蛋白会产生PI-3,4,5-P。 PTEN和PI-3激酶是许多细胞表面受体的关键介质。胰岛素也许是利用PTEN和PI-3激酶的最佳理解信号。他的高度保守途径采用胰岛素受体来刺激PI-3激酶。升高的PI-3,4,5-P水平激活了Akt激酶，这可以磷酸化FOXO家族成员减轻其转录活性。 PTEN还调节细胞中的许多其他蛋白质，并与细胞周期，代谢，细胞生长，凋亡，氧化和迁移的控制有关。异常的PTEN途径信号传导与癌症，糖尿病和帕金森氏病有关。癌症中PTEN/PI-3激酶途径的遗传改变非常普遍，并且是治疗的杰出靶标。这次会议将全面讨论基础研究，疾病模型和治疗干预措施的主题，以改善患者护理。该提案寻求支持将于2006年，2008年和2010年举行的连续三年一次的两年一次会议。