Casein kinase 2 inhibition attenuates cholesterol oxidation product-induced apoptosis by suppressing the activation of the mitochondrial pathway and the caspase-8- and bid-dependent pathways

Jung, Eun Byul; Kim, Yun Jeong; Lee, Chung Soo

doi:10.1016/j.neuint.2013.12.010

Cited by 9 publications

(5 citation statements)

References 51 publications

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“…In this work, we have shown that the apigenin upregulation of functional CD26/DPPIV at the cell surface of intestinal epithelial cells (a) is consistent across multiple well‐differentiated human cell lines, (b) is due to cellular redistribution rather than a change in expression, (c) may be reproduced by multiple inhibitors of CK2 kinase activity, (d) does not involve downregulation of CK2 protein, and (e) is abrogated by siRNA knockdown of available CK2. It is well established that apigenin can inhibit CK2 activity, and indeed, it is used experimentally as a CK2 inhibitor (Ahmad, Wang, & Ahmed, 2006; Jung, Kim, & Lee, 2014; Kim et al., 2018; Kroonen et al., 2012; Suhas et al., 2018). We conclude that the ability of apigenin to upregulate CD26/DPPIV involves inhibition of the kinase activity of CK2 and is dependent upon the presence of functional CK2 enzyme.…”

Section: Resultsmentioning

confidence: 99%

Apigenin upregulation of CD26/DPPIV on colon epithelial cells requires inhibition of casein kinase 2

Lefort

Diaconu

Bentley

et al. 2020

Food Science & Nutrition

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Apigenin (4′,5,7-trihydroxyflavone) is a flavone present in the leafy herb parsley and in the dried flowers of chamomile, among other sources. Apigenin has a broad spectrum of activities that affect a variety of cellular processes, as we have reviewed (Lefort & Blay, 2013). These actions endow apigenin with the capacity to alter the relationship of cells with their surroundings and their interaction with key signaling molecules. We have reported that apigenin has the capacity to upregulate CD26/DPPIV (Lefort & Blay, 2011), a key enabler of such interactions with the external milieu (Cheng, Abdel-Ghany,

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Section: Resultsmentioning

confidence: 99%

Apigenin upregulation of CD26/DPPIV on colon epithelial cells requires inhibition of casein kinase 2

Lefort

Diaconu

Bentley

et al. 2020

Food Science & Nutrition

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“…In a human neuronal blastoma cell lineage overexpressing α-synuclein, promotion of aggregates of α-synuclein due to oxidative stress treatment was linked to an increase CK2 and cathepsin D. Furthermore, CK2 inhibition was shown to lower α-synuclein in stressed cells, linking CK2 to the cellular stress pathway [ 47 ]. Another study showed that CK2 inhibition in rat PC12 adrenal cell line can lower the level of oxidative-stress induced apoptosis by suppressing a number of apoptotic pathways include caspase-8-, bid-, and mitochondrially-mediated apoptosis [ 48 ].…”

Section: Discussionmentioning

confidence: 99%

A kinase inhibitor library screen identifies novel enzymes involved in ototoxic damage to the murine organ of Corti

et al. 2017

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Ototoxicity is a significant side effect of a number of drugs, including the aminoglycoside antibiotics and platinum-based chemotherapeutic agents that are used to treat life-threatening illnesses. Although much progress has been made, the mechanisms that lead to ototoxic loss of inner ear sensory hair cells (HCs) remains incompletely understood. Given the critical role of protein phosphorylation in intracellular processes, including both damage and survival signaling, we screened a library of kinase inhibitors targeting members of all the major families in the kinome. Micro-explants from the organ of Corti of mice in which only the sensory cells express GFP were exposed to 200 μM of the ototoxic aminoglycoside gentamicin with or without three dosages of each kinase inhibitor. The loss of sensory cells was compared to that seen with gentamicin alone, or without treatment. Of the 160 inhibitors, 15 exhibited a statistically significant protective effect, while 3 significantly enhanced HC loss. The results confirm some previous studies of kinase involvement in HC damage and survival, and also highlight several novel potential kinase pathway contributions to ototoxicity.

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“…An enzyme activity assay was performed to determine whether Tat and morphine exposure alters CK2 enzyme kinetics. CK2 activity was determined in cytoplasmic extracts using the CycLex CK2 activity kit (# CY-1170, MBL Life Science, CycLex Co. Ltd, Nagano, Japan) per the manufacturer's instructions and previous publications (Jung et al, 2014; Lee et al, 2014; Oinuma et al, 2010). Briefly, 5 µ g samples obtained from lysates of cells co-treated with Tat and morphine, or vehicle-treated control striatal neurons (receiving no experimental treatments) were incubated in wells pre-coated with a synthetic CK2-specific peptide with a serine 46 moiety that can be phosphorylated by CK2.…”

Section: Methodsmentioning

confidence: 99%

Casein Kinase 2 Mediates HIV- and Opioid-Induced Pathologic Phosphorylation of TAR DNA Binding Protein 43 in the Basal Ganglia

et al. 2023

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Aberrant phosphorylation and subsequent aggregation of the trans-activation response (TAR) element DNA binding protein 43 (TDP-43) is a common feature of multiple neurodegenerative disorders and contributes to disease severity. Here, we investigated whether pathologic phosphorylation of TDP-43 (pTDP-43) is a hallmark of human immunodeficiency virus (HIV)- infected brains. We evaluated pTDP-43 immunoreactivity and TDP-43 kinases in HIV-infected (HIV + ) and seronegative post-mortem brain samples. We then used an inducible transgenic mouse model of the HIV-1 protein Tat and primary neuronal cultures, to decipher the underlying mechanism of the proteinopathy. Since opioid use disorder (OUD) can exaggerate HIV neuropathology, we explored interactions between HIV-1 Tat and morphine, a prototypical opioid, for all outcome measures. Cytoplasmic pTDP-43 and TDP-43 immunoreactivities were increased in neurons of the basal ganglia of post-mortem, HIV+ human tissues compared to seronegative controls. An evaluation of TDP-43 kinases revealed an increase in the levels of cytoplasmic casein kinase 2 (CK2) in HIV-positive human tissues but not CK1δ. There was a significant positive correlation between pTDP-43 and CK2 levels. Eight weeks of Tat induction and 2-week subcutaneous morphine exposure (10–40 mg/kg, increasing by 10 mg/kg/b.i.d.) independently produced similar outcomes for cytoplasmic pTDP-43 and CK2 levels in the mouse striatum. In primary, mouse striatal neuronal cultures, co-exposure to Tat and morphine for 24 h increased pTDP-43 levels and CK2 activity. Co-treatment with the CK2 antagonist CX-4945 prevented the Tat- and morphine-induced increases in pTDP-43 levels. Our results demonstrate that CK2 may be a viable therapeutic target for treating pTDP-43 proteinopathy in neuroHIV and OUD. Summary Statement HIV/HIV-1 Tat and morphine independently increase pathologic phosphorylation of TAR DNA binding protein 43 in the striatum. HIV- and opioid-induced pathologic phosphorylation of TAR DNA binding protein 43 may involve enhanced CK2 activity and protein levels.

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Casein kinase 2 inhibition attenuates cholesterol oxidation product-induced apoptosis by suppressing the activation of the mitochondrial pathway and the caspase-8- and bid-dependent pathways

Cited by 9 publications

References 51 publications

Apigenin upregulation of CD26/DPPIV on colon epithelial cells requires inhibition of casein kinase 2

Apigenin upregulation of CD26/DPPIV on colon epithelial cells requires inhibition of casein kinase 2

A kinase inhibitor library screen identifies novel enzymes involved in ototoxic damage to the murine organ of Corti

Casein Kinase 2 Mediates HIV- and Opioid-Induced Pathologic Phosphorylation of TAR DNA Binding Protein 43 in the Basal Ganglia

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