Evidence map›Paper›PMID 36090057›Full record

ReviewFrontiers in molecular biosciences2022

The protein kinase CK1: Inhibition, activation, and possible allosteric modulation.

Yashoda Krishna Sunkari, Laurent Meijer, Marc Flajolet

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 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

11 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Review
  3. Inhibition of Casein Kinase 1International journal of molecular sciences · 2025
    Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Allosteric regulation and inhibition of protein kinases.Biochemical Society transactions · 2023
    Review
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

3 authors at 2 institutions in 2 countries.

Yashoda Krishna SunkariLaboratory of Molecular and Cellular Neuroscience, The Rockefeller University, New York, NY, United States.
Laurent MeijerPerha Pharmaceuticals, Hôtel de Recherche, Roscoff, France.
Marc FlajoletLaboratory of Molecular and Cellular Neuroscience, The Rockefeller University, New York, NY, United States.
Rockefeller University · USManRos Therapeutics (France) · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Protein kinases play a vital role in biology and deregulation of kinases is implicated in numerous diseases ranging from cancer to neurodegenerative diseases, making them a major target class for the pharmaceutical industry. However, the high degree of conservation that exists between ATP-binding sites among kinases makes it difficult for current inhibitors to be highly specific. In the context of neurodegeneration, several groups including ours, have linked different kinases such as CK1 and Alzheimer's disease for example. Strictly CK1-isoform specific regulators do not exist and known CK1 inhibitors are inhibiting the enzymatic activity, targeting the ATP-binding site. Here we review compounds known to target CK1, as well as other inhibitory types that could benefit CK1. We introduce the DNA-encoded library (DEL) technology that might represent an interesting approach to uncover allosteric modulators instead of ATP competitors. Such a strategy, taking into account known allosteric inhibitors and mechanisms, might help designing modulators that are more specific towards a specific kinase, and in the case of CK1, toward specific isoforms.

Indexed as

allostericAlzheimer’s disease (AD)casein kinase 1 (CK1)DNA-encoded library (DEL)kinase inhibitorNeurodegeneration

Identifiers

PMID36090057
PMCPMC9449355
OpenAlexW4293212095

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.