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Signaling Mechanisms of TMEM16a Regulation

TMEM16a 调节的信号机制

基本信息

批准号：
10463761
负责人：
Anne E Carlson
金额：
$ 30.64万
依托单位：
UNIVERSITY OF PITTSBURGH AT PITTSBURGH
依托单位国家：
美国
项目类别：
财政年份：
2018
资助国家：
美国
起止时间：
2018-09-25 至 2024-08-31
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/10463761
关键词：
African Binding Binding Sites Blood Vessels Blood flow Cardiac Cardiovascular Diseases Cardiovascular system Catalysis Cell membrane Cells Charge Chemosensitization Data Development Disease Dominant-Negative Mutation Electrolyte Balance Electrophysiology (science)Embryo Endoplasmic Reticulum Eukaryota Fertilization Fluorometry Genes Goals Health Human Hypertension Individual Inositol Knockout Mice Label Lipids Malignant Neoplasms Measures Mediating Modeling Muscle Contraction Mutation Neurons Oocytes Outcome Partner in relationship Pathology Pathway interactions Patients Phosphatidylinositol 4,5-Diphosphate Phosphatidylinositols Phospholipase C Phospholipids Physiological Physiological Processes Play Proteins Public Health Publishing RNA Interference Refractory Regulation Regulatory Pathway Research Role Sensory Series Signal Pathway Signal Transduction Site-Directed Mutagenesis Smooth Muscle Specificity Structure Surface System Testing Therapeutic Transmembrane Domain United States Variant Vascular Smooth Muscle Vascular resistance Whole-Cell Recordings Work Xenopus Xenopus laevis base cardiovascular risk factor craniofacial design egg experimental study hypertension treatment hypertensive interest neuronal excitability novel novel therapeutics overexpression patch clamp prevent synaptotagmin unnatural amino acids uterine contractility

项目摘要

The TMEM16a gene encodes for a Ca2+-activated Cl- channel that is broadly expressed in eukaryotes and plays an important role in human health and disease. TMEM16a channels are required for numerous physiologic processes, including regulation of neuronal and cardiac excitability, uterine contractility, regulation of electrolyte balance, and sensory transduction. Their importance is evidenced by the embryonic lethality of TMEM16a knockout mice, and by the association of mutations in this channel with craniofacial cancers. Aside from their Ca2+-dependent activation, it is not understood how these channels are regulated. Our lab is interested in uncovering the signaling mechanisms that modulate the activity of TMEM16a channels. Our goal is to understand the primary TMEM16a regulatory pathways, and to facilitate the development of novel therapeutic options for treating disorders caused by TMEM16a deficiencies.

TMEM 16 a基因编码Ca 2+激活的Cl-通道，该通道在真核生物中广泛表达，在人类健康和疾病中起着重要作用。需要TMEM 16 a通道，生理过程，包括调节神经元和心脏兴奋性，子宫收缩性，调节电解质平衡和感觉传导。它们的重要性可以从胚胎 TMEM 16 a基因敲除小鼠的致死率，以及该通道中的突变与颅面癌的除了它们的Ca 2+依赖性激活外，尚不清楚这些通道是如何调节的。我们的实验室有兴趣揭示调节TMEM 16 a活性的信号传导机制渠道我们的目标是了解TMEM 16 a的主要调控途径，并促进TMEM 16 a的表达。开发用于治疗由TMEM 16 a缺陷引起的病症的新的治疗选择。