Evidence map›Paper›PMID 36102907›Full record

ArticleThe Journal of cell biology2022

Engineered kinases as a tool for phosphorylation of selected targets in vivo.

Katarzyna Lepeta, Chantal Roubinet, Milena Bauer, M Alessandra Vigano, Gustavo Aguilar, Oguz Kanca, Amanda Ochoa-Espinosa, Dimitri Bieli, Clemens Cabernard, Emmanuel Caussinus and 1 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of cell biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.7field-weighted citation impact, top 36% 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

3 citing papers in PubMed, 6 citations in OpenAlex.

  1. Altering cell size asymmetry inbioRxiv : the preprint server for biology · 2025
    Article
  2. Article
  3. Engineering signalling pathways in mammalian cells.Nature biomedical engineering · 2024
    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

11 authors at 4 institutions in 3 countries.

Katarzyna LepetaBiozentrum, University of Basel, Basel, Switzerland.ORCID 0000-0002-6870-0009
Chantal RoubinetMRC Laboratory for Molecular Cell Biology, University College London, London, UK.ORCID 0000-0002-9335-4523
Milena BauerBiozentrum, University of Basel, Basel, Switzerland.
M Alessandra ViganoBiozentrum, University of Basel, Basel, Switzerland.ORCID 0000-0003-2009-0384
Gustavo AguilarBiozentrum, University of Basel, Basel, Switzerland.ORCID 0000-0002-0524-9388
Oguz KancaDepartment of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX.
Amanda Ochoa-EspinosaDepartment of Biomedicine, University of Basel, Basel, Switzerland.ORCID 0000-0003-1943-790X
Dimitri BieliMabylon AG, Schlieren, Switzerland.
Clemens CabernardDepartment of Biology, University of Washington, Seattle, WA.ORCID 0000-0003-3706-6401
Emmanuel Caussinus1 Avenue Georges Ferrenbach, Kaysersberg-Vignoble, France.
Markus AffolterBiozentrum, University of Basel, Basel, Switzerland.ORCID 0000-0002-5171-0016
University of Basel · CHBaylor College of Medicine · USMRC Laboratory for Molecular Cell Biology · GBUniversity of Washington · US

Funding

Cellular and molecular mechanisms underlying the formation of sibling cell size asymmetryR01GM126029 · NIGMS · UNIVERSITY OF WASHINGTON · PI CLEMENS C. CABERNARD, CLEMENS C · 2018 to 2022
$1.6M
NIGMS NIH HHS R01 GM126029NIH HHS 1R01GM126029Swiss National Science Foundation 310030_192659/1
6 · The paper itself

Abstract

Reversible protein phosphorylation by kinases controls a plethora of processes essential for the proper development and homeostasis of multicellular organisms. One main obstacle in studying the role of a defined kinase-substrate interaction is that kinases form complex signaling networks and most often phosphorylate multiple substrates involved in various cellular processes. In recent years, several new approaches have been developed to control the activity of a given kinase. However, most of them fail to regulate a single protein target, likely hiding the effect of a unique kinase-substrate interaction by pleiotropic effects. To overcome this limitation, we have created protein binder-based engineered kinases that permit a direct, robust, and tissue-specific phosphorylation of fluorescent fusion proteins in vivo. We show the detailed characterization of two engineered kinases based on Rho-associated protein kinase (ROCK) and Src. Expression of synthetic kinases in the developing fly embryo resulted in phosphorylation of their respective GFP-fusion targets, providing for the first time a means to direct the phosphorylation to a chosen and tagged target in vivo. We presume that after careful optimization, the novel approach we describe here can be adapted to other kinases and targets in various eukaryotic genetic systems to regulate specific downstream effectors.

Indexed as

Proteinsrho-Associated Kinasessrc-Family KinasesAnimalsDrosophilaPhosphorylationProtein EngineeringSignal TransductionSubstrate SpecificityProteinsrho-Associated Kinasessrc-Family Kinases

Identifiers

PMID36102907
PMCPMC9477969
OpenAlexW4295678660

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.