Evidence map›Paper›PMID 33994545›Full record

ReviewSignal transduction and targeted therapy2021

Protein kinase CK2: a potential therapeutic target for diverse human diseases.

Christian Borgo, Claudio D'Amore, Stefania Sarno, Mauro Salvi, Maria Ruzzene

Open access · goldAbstract readReview
In one paragraph

Review in Signal transduction and targeted therapy, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 221 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
221citing papers in PubMed, 2 pooled it
23.4field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

221 citing papers in PubMed, 2 syntheses or guidelines pooled it, 371 citations in OpenAlex.

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  13. CK2α Deficiency Drives Myocardial Fibrosis via Desmin-Induced Mitochondrial Dysfunction.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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161 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Christian BorgoDepartment of Biomedical Sciences, University of Padua, Padua, Italy.
Claudio D'AmoreDepartment of Biomedical Sciences, University of Padua, Padua, Italy.
Stefania SarnoDepartment of Biomedical Sciences, University of Padua, Padua, Italy.
Mauro SalviDepartment of Biomedical Sciences, University of Padua, Padua, Italy.
Maria RuzzeneDepartment of Biomedical Sciences, University of Padua, Padua, Italy. maria.ruzzene@unipd.it.ORCID http://orcid.org/0000-0001-8712-8151
University of Padua · IT

Funding

AFM-Téléthon (French Muscular Dystrophy Association) 22974Associazione Italiana per la Ricerca sul Cancro (Italian Association for Cancer Research) IG 18756Fondazione per la Ricerca sulla Fibrosi Cistica (Fondazione FFC) FFC#11/2019Fondazione per la Ricerca sulla Fibrosi Cistica (Fondazione FFC) FFC#12/2017
6 · The paper itself

Abstract

CK2 is a constitutively active Ser/Thr protein kinase, which phosphorylates hundreds of substrates, controls several signaling pathways, and is implicated in a plethora of human diseases. Its best documented role is in cancer, where it regulates practically all malignant hallmarks. Other well-known functions of CK2 are in human infections; in particular, several viruses exploit host cell CK2 for their life cycle. Very recently, also SARS-CoV-2, the virus responsible for the COVID-19 pandemic, has been found to enhance CK2 activity and to induce the phosphorylation of several CK2 substrates (either viral and host proteins). CK2 is also considered an emerging target for neurological diseases, inflammation and autoimmune disorders, diverse ophthalmic pathologies, diabetes, and obesity. In addition, CK2 activity has been associated with cardiovascular diseases, as cardiac ischemia-reperfusion injury, atherosclerosis, and cardiac hypertrophy. The hypothesis of considering CK2 inhibition for cystic fibrosis therapies has been also entertained for many years. Moreover, psychiatric disorders and syndromes due to CK2 mutations have been recently identified. On these bases, CK2 is emerging as an increasingly attractive target in various fields of human medicine, with the advantage that several very specific and effective inhibitors are already available. Here, we review the literature on CK2 implication in different human pathologies and evaluate its potential as a pharmacological target in the light of the most recent findings.

Indexed as

Cardiovascular DiseasesCasein Kinase IICOVID-19COVID-19 Drug TreatmentCystic FibrosisEye DiseasesMental DisordersSARS-CoV-2HumansMutationPhosphorylationProtein Kinase InhibitorsSignal TransductionCasein Kinase IIProtein Kinase Inhibitors

Identifiers

PMID33994545
PMCPMC8126563
OpenAlexW3162383196

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.