Evidence map›Paper›PMID 36434320›Full record

ArticleJournal of cell communication and signaling2023

Renal FGF23 signaling depends on redox protein Memo1 and promotes orthovanadate-sensitive protein phosphotyrosyl phosphatase activity.

Katalin Bartos, Suresh Krishna Ramakrishnan, Sophie Braga-Lagache, Barbara Hänzi, Fanny Durussel, Arjun Prakash Sridharan, Yao Zhu, David Sheehan, Nancy E Hynes, Olivier Bonny and 1 more

Open access · hybridAbstract read
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In one paragraph

Article in Journal of cell communication and signaling, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.9field-weighted citation impact, top 28% 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

2 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. 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

11 authors at 6 institutions in 4 countries.

Katalin Bartos *Department of Nephrology and Hypertension, Bern University Hospital and Department of Biomedical Research, University of Bern, Freiburgstrasse 15, 3010, Bern, Switzerland.
Suresh Krishna Ramakrishnan *National Center of Competence in Research (NCCR) Kidney Control of Homeostasis (Kidney.CH), University of Zurich, Zurich, Switzerland.
Sophie Braga-LagacheProteomics and Mass Spectrometry Core Facility, Department for Biomedical Research (DBMR), University of Berne, Berne, Switzerland.
Barbara HänziDepartment of Biomedical Sciences, University of Lausanne, Lausanne, Switzerland.
Fanny DurusselDepartment of Biomedical Sciences, University of Lausanne, Lausanne, Switzerland.
Arjun Prakash SridharanProteomic Research Group, School of Biochemistry and Cell Biology, University College Cork, Cork, Ireland.
Yao ZhuProteomic Research Group, School of Biochemistry and Cell Biology, University College Cork, Cork, Ireland.
David SheehanProteomic Research Group, School of Biochemistry and Cell Biology, University College Cork, Cork, Ireland.
Nancy E HynesFriedrich Miescher Institute for Biomedical Research and University of Basel, Basel, Switzerland.
Olivier BonnyNational Center of Competence in Research (NCCR) Kidney Control of Homeostasis (Kidney.CH), University of Zurich, Zurich, Switzerland.
Matthias B MoorDepartment of Nephrology and Hypertension, Bern University Hospital and Department of Biomedical Research, University of Bern, Freiburgstrasse 15, 3010, Bern, Switzerland. matthias.moor@dbmr.unibe.ch.ORCID http://orcid.org/0000-0002-7717-651X
University of Bern · CHUniversity College Cork · IEUniversity of Lausanne · CHUniversity of Zurich · CHKhalifa University of Science and Technology · AEUniversity of Basel · CH

Funding

Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung 310030-182312Swiss National Centre of Competence in Research Kidney Control of Homeostasis 183774
6 · The paper itself

Abstract

Memo1 deletion in mice causes premature aging and an unbalanced metabolism partially resembling Fgf23 and Klotho loss-of-function animals. We report a role for Memo's redox function in renal FGF23-Klotho signaling using mice with postnatally induced Memo deficiency in the whole body (cKO). Memo cKO mice showed impaired FGF23-driven renal ERK phosphorylation and transcriptional responses. FGF23 actions involved activation of oxidation-sensitive protein phosphotyrosyl phosphatases in the kidney. Redox proteomics revealed excessive thiols of Rho-GDP dissociation inhibitor 1 (Rho-GDI1) in Memo cKO, and we detected a functional interaction between Memo's redox function and oxidation at Rho-GDI1 Cys79. In isolated cellular systems, Rho-GDI1 did not directly affect FGF23-driven cell signaling, but we detected disturbed Rho-GDI1 dependent small Rho-GTPase protein abundance and activity in the kidney of Memo cKO mice. Collectively, this study reveals previously unknown layers in the regulation of renal FGF23 signaling and connects Memo with the network of small Rho-GTPases.

Indexed as

FGFRPhosphatasesRedox proteomicsRhoARhoGDI1Signal transduction

Identifiers

PMID36434320
PMCPMC10409928
OpenAlexW4310081331

What Socratic holds

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LicenceCC BY
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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.