Evidence map›Paper›PMID 36275622›Full record

ReviewFrontiers in molecular biosciences2022

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

Andrea Baier, Ryszard Szyszka

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in molecular biosciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

12 citing papers in PubMed, 14 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. CK and LRRK2 Involvement in Neurodegenerative Diseases.International journal of molecular sciences · 2024
    Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Yeast Protein Asf1 Possesses Modulating Activity towards Protein Kinase CK2.International journal of molecular sciences · 2022
    Article
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

2 authors at 1 institution in 1 country.

Andrea BaierInstitute of Biological Sciences, The John Paul II Catholic University of Lublin, Lublin, Poland.
Ryszard SzyszkaInstitute of Biological Sciences, The John Paul II Catholic University of Lublin, Lublin, Poland.
John Paul II Catholic University of Lublin · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

CK1CK2inhibitorsneurodegenerative diseasesphosphorylationTTBK

Identifiers

PMID36275622
PMCPMC9582958
OpenAlexW4303184310

What OpenQuestion 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 OpenQuestion graph.