Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2022 Oct 6:9:916063.
doi: 10.3389/fmolb.2022.916063. eCollection 2022.

CK2 and protein kinases of the CK1 superfamily as targets for neurodegenerative disorders

Andrea Baier  1 , Ryszard Szyszka  1
Affiliations
Review

CK2 and protein kinases of the CK1 superfamily as targets for neurodegenerative disorders

Andrea Baier et al. Front Mol Biosci. .

Abstract

Casein kinases are involved in a variety of signaling pathways, and also in inflammation, cancer, and neurological diseases. Therefore, they are regarded as potential therapeutic targets for drug design. Recent studies have highlighted the importance of the casein kinase 1 superfamily as well as protein kinase CK2 in the development of several neurodegenerative pathologies, such as Alzheimer's disease, Parkinson's disease, Huntington's disease, and amyotrophic lateral sclerosis. CK1 kinases and their closely related tau tubulin kinases as well as CK2 are found to be overexpressed in the mammalian brain. Numerous substrates have been detected which play crucial roles in neuronal and synaptic network functions and activities. The development of new substances for the treatment of these pathologies is in high demand. The impact of these kinases in the progress of neurodegenerative disorders, their bona fide substrates, and numerous natural and synthetic compounds which are able to inhibit CK1, TTBK, and CK2 are discussed in this review.

Keywords: CK1; CK2; TTBK; inhibitors; neurodegenerative diseases; phosphorylation.

PubMed Disclaimer

Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

References

    1. Ackermann K., Neidhart T., Gerber J., Waxmann A., Pyerin W. (2005). The catalytic subunit α′ gene of human protein kinase CK2 (CSNK2A2): Genomic organization, promoter identification and determination of Ets1 as a key regulator. Mol. Cell. Biochem. 274, 91–101. 10.1007/s11010-005-3076-2 - DOI - PubMed
    1. Adler P., Mayne J., Walker K., Ning Z., Figeys D. (2019). Therapeutic targeting of casein kinase 1δ/ε in an Alzheimer’s disease mouse model. J. Proteome Res. 18, 3383–3393. 10.1021/acs.jproteome.9b00312 - DOI - PubMed
    1. Ahmed T., Javed S., Javed S., Tariq A., Šamec D., Tejada S., et al. (2017). Resveratrol and Alzheimer’s disease: Mechanistic insights. Mol. Neurobiol. 54, 2622–2635. 10.1007/s12035-016-9839-9 - DOI - PubMed
    1. Akter R., Rahman H., Behl T., Chowdhury M. A. R., Manirujjaman M., Bulbul I. J., et al. (2021). Prospective role of polyphenolic compounds in the treatment of neurodegenerative diseases. CNS Neurol. Disord. Drug Targets 20, 430–450. 10.2174/1871527320666210218084444 - DOI - PubMed
    1. Alquezar C., Salado I. G., de la Encarnación A., Pérez D. I., Moreno F., Gil C., et al. (2016). Targeting TDP-43 phosphorylation by casein kinase-1δ inhibitors: A novel strategy for the treatment of frontotemporal dementia. Mol. Neurodegener. 11, 36. 10.1186/s13024-016-0102-7 - DOI - PMC - PubMed