2017
DOI: 10.1016/j.jchemneu.2016.12.003
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Ca 2+ dependent surface trafficking of norepinephrine transporters depends on threonine 30 and Ca 2+ calmodulin kinases

Abstract: The antidepressant-sensitive norepinephrine (NE) transporter (NET) inactivates NE released during central and peripheral neuronal activity by transport into presynaptic cells. Altered NE clearance due to dysfunction of NET has been associated with the development of mental illness and cardiovascular diseases. NET activity in vivo is influenced by stress, neuronal activity, hormones and drugs. We investigated the mechanisms of Ca2+ regulation of NET and found that Ca2+ influenced both Vmax and Km for NE transpo… Show more

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Cited by 4 publications
(5 citation statements)
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“…Nonetheless, the pathophysiological processes in which CaMKII and the main subtypes, including CaMKIIα and CaMKIIβ, may be involved in and play a major role are not still clearly known. In this study, we revealed that CUMS caused a widespread upregulation in the phosphorylation levels of total CaMKII, CaMKII α and CaMKII β expression in the rat hippocampus (Figure 15, P<0.01), in agreement with previous results (37,46,48,74); however, the increased phosphorylation of CaMKII, CaMKII α and CaMKII β protein induced by CUMS was strikingly abrogated by treatment with GXDSF in a dose-dependent manner (Figure 15, P<0.01), indicating that the neuroprotective effects of GXDSF upon the amelioration of the depression-like behaviours induced by CUMS may be closely associated with protein CaMKII-mediated phosphorylation. Furthermore, the autophosphorylation of the primary antibodies used in our results, including p-CaMKII, p-CaMKIIα, and p-CaMKIIβ, is on threonine 286 which allows the kinase to switch from a calmodulin-dependent to a calmodulin-independent state and is required for various cellular functions, including hippocampal long-term potentiation, special learning, and hippocampus-dependent memory.…”
Section: Effects Of Gxdsf On the Expression Levels Of Camkⅱ And Creb/...supporting
confidence: 92%
See 3 more Smart Citations
“…Nonetheless, the pathophysiological processes in which CaMKII and the main subtypes, including CaMKIIα and CaMKIIβ, may be involved in and play a major role are not still clearly known. In this study, we revealed that CUMS caused a widespread upregulation in the phosphorylation levels of total CaMKII, CaMKII α and CaMKII β expression in the rat hippocampus (Figure 15, P<0.01), in agreement with previous results (37,46,48,74); however, the increased phosphorylation of CaMKII, CaMKII α and CaMKII β protein induced by CUMS was strikingly abrogated by treatment with GXDSF in a dose-dependent manner (Figure 15, P<0.01), indicating that the neuroprotective effects of GXDSF upon the amelioration of the depression-like behaviours induced by CUMS may be closely associated with protein CaMKII-mediated phosphorylation. Furthermore, the autophosphorylation of the primary antibodies used in our results, including p-CaMKII, p-CaMKIIα, and p-CaMKIIβ, is on threonine 286 which allows the kinase to switch from a calmodulin-dependent to a calmodulin-independent state and is required for various cellular functions, including hippocampal long-term potentiation, special learning, and hippocampus-dependent memory.…”
Section: Effects Of Gxdsf On the Expression Levels Of Camkⅱ And Creb/...supporting
confidence: 92%
“…Furthermore, the autophosphorylation of the primary antibodies used in our results, including p-CaMKII, p-CaMKIIα, and p-CaMKIIβ, is on threonine 286 which allows the kinase to switch from a calmodulin-dependent to a calmodulin-independent state and is required for various cellular functions, including hippocampal long-term potentiation, special learning, and hippocampus-dependent memory. In addition, CaMKII modified CREB binds to DNA efficiently as a monomer, which had been proved in the previous reports (45,47,48,(72)(73)(74). As summarized above, it was speculated that CREB was phosphorylated at serine 133 via regulation of CaMKII-mediated phosphorylation in the GXDSFtreated CUMS model rats, resulting in improved BDNF, NGF and synitaxine-1 expression, upregulated monoamine neurotransmitters, and ameliorated synaptic plasticity and neuronal circuit formation, which indicates that the CaMKII-CREB-BDNF signalling pathway plays a role in the antidepressant-like effect of GXDSF.…”
Section: Effects Of Gxdsf On the Expression Levels Of Camkⅱ And Creb/...mentioning
confidence: 52%
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“…SLC6A2-mediated norepinephrine uptake requires cell membrane localization of the transporter, which is induced by membrane depolarization ( 19 , 20 ). Fibroblasts isolated from the CC maintained SLC6A2 expression in primary cultures (Fig.…”
Section: Fibroblasts Mediate Vasodilation By Reduction Of Norepinephr...mentioning
confidence: 99%