Casein kinase 2 inactivation by Mg2+, Mn2+ and Co2+ ions

Jiménez, Juan S.; Benítez, María José; Lechuga, Carmen G.; Collado, Manuel; González-Nicolás, Josefa; Moreno, Francisco J.

doi:10.1007/bf01076457

Cited by 6 publications

(1 citation statement)

References 26 publications

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“…Low cellular Mg 2+ levels stimulate cytokine production in and release from endothelial cells and modulate activity of NF‐κB, a master regulator of cytokine production 19,20 . Intracellular Mg 2+ regulates multiple additional activities linked to SCD, including casein kinase II (CK2), 21 PKC 22–24 and hypoxia‐inducible factor‐1 (HIF‐1) 25 . Thus, regulation of Mg 2+ levels has been proposed as a therapeutic target in SCD 26–28 .…”

Section: Introductionmentioning

confidence: 99%

Magnesium homeostasis in deoxygenated sickle erythrocytes is modulated by endothelin‐1 via Na ⁺ /Mg ²⁺ exchange

et al. 2022

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Painful crises in sickle cell disease (SCD) are associated with increased plasma cytokines levels, including endothelin-1 (ET-1). Reduced red cell magnesium content, mediated in part by increased Na + /Mg 2+ exchanger (NME) activity, contributes to erythrocyte K + loss, dehydration and sickling in SCD. However, the relationship between ET-1 and the NME in SCD has remained unexamined. We observed increased NME activity in sickle red cells incubated in the presence of 500 nM ET-1. Deoxygenation of sickle red cells, in contrast, led to decreased red cell NME activity and cellular dehydration that was reversed by the NME inhibitor, imipramine. Increased NME activity in sickle red cells was significantly blocked by pre-incubation with 100 nM BQ788, a selective blocker of ET-1 type B receptors. These results suggest an important role for ET-1 and for cellular magnesium homeostasis in SCD. Consistent with these results, we observed increased NME activity in sickle red cells of three mouse models of sickle cell disease greater than that in red cells of C57BL/J6 mice. In vivo treatment of BERK sickle transgenic mice with ET-1 receptor antagonists reduced red cell NME activity.Among patients with sickle cell disease (SCD), 5% experience 3-10 potentially lethal vaso-occlusive painful crises annually. 1,2 Vaso-occlusive crises are initiated, in part, by red cell deoxygenation and by elevated plasma levels of cytokines such as endothelin-1 (ET-1), leading to increased adhesive interactions among sickle red cells, between sickle red cells and endothelium and involving plasma factors, through mechanisms that remain incompletely understood. [3][4][5][6] ET-1 plays important roles in the disordered erythrocyte homeostasis, inflammation, vaso-occlusion, tissue injury, and pain common to the pathophysiology of SCD. 7,8 ET-1 levels are increased in SCD, 9,10 and in vivo treatment with ET-1 receptor antagonists improve hematological parameters and reduced oxidant stress in mouse models of SCD. 11 However, the mechanisms by which ET-1 receptor antagonists mediate their beneficial effects in SCD remain unclear.Dysregulated Mg 2+ levels have been reported in SCD and in patients with Type 2 diabetes, 12,13 hypertension, and stroke, all diseases with an important inflammatory component. [14][15][16] Low Mg 2+ levels are accompanied by oxidant stress, impaired vascular function and increased inflammation, all associated with the pathophysiology of SCD. 17,18 Low cellular Mg 2+ levels stimulate cytokine production in and release from endothelial cells and modulate activity of NF-κB, a master regulator of cytokine production. 19,20 Intracellular Mg 2+ regulates multiple additional activities linked to SCD, including casein kinase II (CK2), 21 PKC [22][23][24] and hypoxia-inducible factor-1 (HIF-1). 25 Thus, regulation of Mg 2+ levels has been proposed as a therapeutic target in SCD. [26][27][28] A preliminary study reported that the activity of the Na + /Mg 2+ exchanger (NME) in sickle erythrocytes was significantly reduced after 6 months of...

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Section: Introductionmentioning

confidence: 99%

Magnesium homeostasis in deoxygenated sickle erythrocytes is modulated by endothelin‐1 via Na ⁺ /Mg ²⁺ exchange

et al. 2022

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A novel, calcium‐inhibitable casein kinase in Paramecium cells

et al. 1997

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Separation and Purification of both CK-I and CK-II Casein Kinases in Developing Maize Endosperm — Phosphorylation of Native HMG Proteins

Babatsikos

Yupsanis

2000

Journal of Plant Physiology

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Casein kinase 2 inactivation by Mg2+, Mn2+ and Co2+ ions

Cited by 6 publications

References 26 publications

Magnesium homeostasis in deoxygenated sickle erythrocytes is modulated by endothelin‐1 via Na ⁺ /Mg ²⁺ exchange

Magnesium homeostasis in deoxygenated sickle erythrocytes is modulated by endothelin‐1 via Na ⁺ /Mg ²⁺ exchange

A novel, calcium‐inhibitable casein kinase in Paramecium cells

Separation and Purification of both CK-I and CK-II Casein Kinases in Developing Maize Endosperm — Phosphorylation of Native HMG Proteins

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Casein kinase 2 inactivation by Mg2+, Mn2+ and Co2+ ions

Cited by 6 publications

References 26 publications

Magnesium homeostasis in deoxygenated sickle erythrocytes is modulated by endothelin‐1 via Na + /Mg 2+ exchange

Magnesium homeostasis in deoxygenated sickle erythrocytes is modulated by endothelin‐1 via Na + /Mg 2+ exchange

A novel, calcium‐inhibitable casein kinase in Paramecium cells

Separation and Purification of both CK-I and CK-II Casein Kinases in Developing Maize Endosperm — Phosphorylation of Native HMG Proteins

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Product

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Magnesium homeostasis in deoxygenated sickle erythrocytes is modulated by endothelin‐1 via Na ⁺ /Mg ²⁺ exchange

Magnesium homeostasis in deoxygenated sickle erythrocytes is modulated by endothelin‐1 via Na ⁺ /Mg ²⁺ exchange