【摘 要】
：
G protein-coupled receptors (GPCRs) are the largest family of membrane receptors that participate in cellular signal transduction to elicit a myriad of cellular responses, including changes in the cel
【机 构】
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Cellular Biophysics Science and Technology Division, Coming Incorporated USA
【出 处】
：
BITs 3rd Annual World Cancer Congress-2012(2012第五届世界癌症大会)
论文部分内容阅读
G protein-coupled receptors (GPCRs) are the largest family of membrane receptors that participate in cellular signal transduction to elicit a myriad of cellular responses, including changes in the cellular nucleus that modulate the activities of various transcription factors.Many GPCRs are oncogenic and promote cellular transformation and mitogenesis in various disease and experimental states.Further, cellular metabolism is essential for cell proliferation, with abnormal metabolism a principal hallmark of human cancer.However, nothing is known about the role of GPCR signaling in modulating de novo purine biosynthesis.Here, we present the first evidence using fluorescent live-cell imaging and label-free dynamic mass redistribution assays that the de novo purine biosynthesis is under control of GPCR signaling.By screening a library of GPCR ligands in conjunction with live-cell imaging of a metabolic multienzyme complex for de novo purine biosynthesis, the purinosome, we demonstrated that the activation of endogenous G i-coupled receptors correlates with purinosome assembly/disassembly in native HeLa cells.Given the implications of GPCRs in mitogenic signaling as well as the purinosome in controlling metabolic flux via de novo purine biosynthesis, we hypothesize that regulation of purinosome assembly/disassembly may represent one of downstream events of mitogenic GPCR signaling in human cancer cells1.
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