2022-12-27 11:00 ~ 2022-12-27 12:00
地點: 生化所209研討室
主講人: Jen Liou博士
主講人背景: 美國UT Southwestern Medical Center生理學研究所副教授
演講主持人: 陳瑞華特聘研究員
演講摘要:
Phosphatidylinositol 4,5-bisphosphate (PIP2) in the plasma membrane is a critical lipid molecule that regulates nearly all functional processes occurring at the cell surface. Additionally, PIP2 is hydrolyzed following receptor-induced activation of phospholipase C to generate second messengers for signal transduction. It is crucial to quickly replenish PIP2 in the plasma membrane following receptor-induced hydrolysis to sustain signaling outputs and to maintain PIP2-dependent cellular functions. Replenishment of plasma membrane PIP2 in receptor-stimulated cells involves transport of phosphatidylinositol (PI) from the endoplasmic reticulum (ER) to the plasma membrane for PIP2 re-synthesis. ER-plasma membrane contact sites are subcellular loci characterized by the close apposition of the ER to the plasma membrane. Recent findings revealed that the PI transfer proteins, Nir2 and Nir3, dynamically localize at ER-plasma membrane contacts to mediate replenishment of PIP2 hydrolyzed following receptor stimulation. Deficiency in Nir2 and Nir3 suppressed replenishment of PIP2 in the plasma membrane and Ca2+ signaling in receptor-stimulated cells. A third mammalian Nir protein, Nir1, has been linked to several human diseases including retinal dystrophy. Unlike Nir2 and Nir3, Nir1 lacks a PI transfer protein domain and readily localizes at ER-plasma membrane contacts in resting cells. The presence of Nir1 promotes Nir2 localization at ER-plasma membrane contacts to mediate PIP2 replenishment following receptor stimulation. Together, Nir proteins maintain plasma membrane PIP2 homeostasis at ER-plasma membrane contacts to support cell signaling and plasma membrane functions in receptor-stimulated cells.
洽詢人員: 劉小姐
洽詢電話: 27855696#2061
洽詢信箱: liukchun@gate.sinica.edu.tw
中央研究院 生物化學研究所
