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Phosphorylated Form of Activated IKKbeta and Pancreatic Cancer

磷酸化形式的活化 IKKbeta 与胰腺癌

基本信息

批准号：
8907404
负责人：
Amarnath Natarajan
金额：
$ 3.09万
依托单位：
UNIVERSITY OF NEBRASKA MEDICAL CENTER
依托单位国家：
美国
项目类别：
财政年份：
2014
资助国家：
美国
起止时间：
2014-01-01 至 2015-12-31
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/8907404
关键词：
Address Adverse effects Animal Model Animals Antibodies Apoptosis Autopsy Blood capillaries Cancer Patient Cancer cell line Cessation of life Chronic Clinic Data Development Diagnosis Disease Drug Targeting Ductal Epithelial Cell Embryo Endotoxins Event Genetic Goals Growth Health Human Immune response Immunohistochemistry Infection Inflammatory Isoelectric Focusing Label Lipopolysaccharides Malignant neoplasm of pancreas Mediating Metastatic Neoplasm to the Liver Modeling Mus Mutate Mutation Normal Cell Normal tissue morphology Pancreas Pancreatic Ductal Adenocarcinoma Pathology Patients Pharmaceutical Preparations Pharmacologic Substance Phospho-Specific Antibodies Phosphorylation Phosphotransferases Post-Translational Protein Processing Predisposition Protein Dephosphorylation Proteins Research Project Grants Sampling Specimen Stimulus Survival Rate System TNF gene Technology Testing Therapeutic Therapeutic Intervention Tissues Toxic effect Tumor Cell Line base cancer therapy capillary inhibitor/antagonist innovation kidney cell kinase inhibitor mortality mutant neoplastic cell new technology novel overexpression pancreatic cancer cells pancreatic neoplasm pre-clinical programs small molecule therapeutic target therapy resistant tumor tumor growth tumor microenvironment tumorigenesis

项目摘要

DESCRIPTION (provided by applicant): Kinases are attractive drug targets as evidenced by the number of recent FDA approvals of kinase inhibitors for cancer therapy. The drugs currently in the clinics are against either overexpressed kinases or mutated kinases that are implicated in the disease. However not all druggable kinases are mutated or overexpressed in many cases their activity altered through post-translational modifications. Others and we have identified elevated levels of phosphorylated IKK� in the tumor samples compared to the normal tissues suggesting that the diseased state of IKK� exists phosphorylated state. IKK� like other kinases is regulated by sequential phosphorylation-dephosphorylation events. The lack of phospho-specific antibodies against the various phosphorylated forms of IKK� makes defining the diseased state a challenging endeavor. In this application we will use a novel technology NanoPro 1000 to address this issue in pancreatic tumors and cell lines. This is an exploratory project as we seek to characterize the various post-translational modifications associated with a disease relevant kinase. Our focus on the specific forms of IKK�, rather than IKK� in general, makes this bother novel and innovative.

描述（由申请人提供）：激酶是有吸引力的药物靶点，最近FDA批准用于癌症治疗的激酶抑制剂的数量证明了这一点。目前临床上的药物是针对过度表达的激酶或与疾病有关的突变激酶。然而，并非所有的可药用激酶都是突变的或过表达的，在许多情况下，它们的活性通过翻译后修饰而改变。其他人和我们已经确定，与正常组织相比，肿瘤样本中磷酸化IKK β的水平升高，表明IKK β存在磷酸化状态。IKK与其他激酶一样，由连续的磷酸化-去磷酸化事件调节。缺乏针对IKK各种磷酸化形式的磷酸化特异性抗体使得定义疾病状态成为一项具有挑战性的奋进。在本申请中，我们将使用一种新技术NanoPro 1000来解决胰腺肿瘤和细胞系中的这一问题。这是一个探索性的项目，因为我们试图表征与疾病相关激酶相关的各种翻译后修饰。我们专注于IKK的具体形式，而不是一般的IKK，使这个麻烦新颖和创新。