Simsek-Duran Fatma, Linden David J, Lonart György
Department of Pathology & Anatomy, Eastern Virginia Medical School, Norfolk, Virginia 23501, USA.
Nat Neurosci. 2004 Dec;7(12):1296-8. doi: 10.1038/nn1348. Epub 2004 Nov 14.
Long-term potentiation (LTP) of granule cell-Purkinje cell synapses in the mouse cerebellum requires phosphorylation by protein kinase A of the active-zone protein RIM1alpha at Ser413. Here, we show that the adapter protein 14-3-3 readily binds phosphorylated Ser413 in RIM1alpha, and that presynaptic transfection with a dominant-negative 14-3-3eta mutant, or a RIM1alpha mutant with enhanced 14-3-3 binding, inhibits LTP. Thus, RIM1alpha phosphorylation triggers presynaptic LTP in part through recruitment of 14-3-3 to phospho-Ser413-RIM1alpha.
小鼠小脑颗粒细胞-浦肯野细胞突触的长期增强（LTP）需要活性区蛋白RIM1α的丝氨酸413位点被蛋白激酶A磷酸化。在此，我们表明衔接蛋白14-3-3能轻易结合RIM1α中磷酸化的丝氨酸413，并且用显性负性14-3-3η突变体或与14-3-3结合增强的RIM1α突变体进行突触前转染会抑制LTP。因此，RIM1α磷酸化部分通过将14-3-3募集到磷酸化丝氨酸413-RIM1α上触发突触前LTP。
