Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
10815502 | Cellular Signalling | 2014 | 7 Pages |
Abstract
Prokineticins (PKs) are a pair of signal factors involved in many physiological processes by binding to two closely related G-protein-coupled receptors (GPCRs), PKR1 and PKR2. We recently demonstrated that PKR2 undergoes rapid ligand-induced endocytosis, and PKR2 recycles back to the plasma membrane after the removal of ligand. However, little is known about the molecular mechanisms underlying the PKR2 endocytosis. Here, we studied the involvement of GPCR kinase 2 (GRK2), β-arrestins, clathrin and protein kinase C (PKC) in the PKR2 endocytosis. Our results indicated that PK2-induced PKR2 endocytosis is GRK2- and clathrin-dependent, but β-arrestin-independent. PKC activation also induced PKR2 endocytosis; however, PKC activation is not necessary for the PK2-induced PKR2 endocytosis. PK2 stimulation induced a transient activation of extracellular signal regulated kinase 1/2 (ERK1/2) on PKR2 expressing cells. The internalization and PKC activation are not required for the PK2-induced ERK1/2 activation. Our results indicated that PK2-induced ERK1/2 activation may involve the released βγ subunits of G-protein, phospholipase C β and MEK activation.
Keywords
Concanavalin ApK2AT1ARPKR2Angiotensin type 1A receptorGPCR kinaseConAPhorbol-12-myristate-13-acetateGRKPKCGPCRMDCeGFPPLCβHEKERKpKaERK1/2G-protein-coupled receptorsPMAEndocytosisextracellular signal regulated kinaseMonodansylcadaverineenhanced green fluorescent proteinprotein kinase AProtein kinase CProkineticinProkineticin 2human embryonic kidneySecretin receptor
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Authors
Wenqing Yin, Huadie Liu, Zhen Peng, Danna Chen, Jie Li, Jia-Da Li,