Evidence map›Paper›PMID 29373579›Full record

ArticlePloS one2018

An AKAP-Lbc-RhoA interaction inhibitor promotes the translocation of aquaporin-2 to the plasma membrane of renal collecting duct principal cells.

Katharina Schrade, Jessica Tröger, Adeeb Eldahshan, Kerstin Zühlke, Kamal R Abdul Azeez, Jonathan M Elkins, Martin Neuenschwander, Andreas Oder, Mohamed Elkewedi, Sarah Jaksch and 17 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

18 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. A multiscale model of the regulation of aquaporin 2 recycling.NPJ systems biology and applications · 2022
    Article
  5. Article
  6. Disruptors of AKAP-Dependent Protein-Protein Interactions.Methods in molecular biology (Clifton, N.J.) · 2022
    Article
  7. Review
  8. Review
  9. Review
  10. Review
  11. Review
  12. Review
  13. Article
  14. An Antifungal for Antidiuresis?Journal of the American Society of Nephrology : JASN · 2019
    Article
  15. Review
  16. Article
  17. Form follows function: polymorphisms in mAKAP alter cardiac cAMP/PKA signaling.American journal of physiology. Heart and circulatory physiology · 2018
    Article
  18. 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

27 authors at 7 institutions in 3 countries.

Katharina SchradeMax Delbrück Center for Molecular Medicine Berlin (MDC), Berlin, Germany.
Jessica TrögerMax Delbrück Center for Molecular Medicine Berlin (MDC), Berlin, Germany.
Adeeb EldahshanMax Delbrück Center for Molecular Medicine Berlin (MDC), Berlin, Germany.
Kerstin ZühlkeMax Delbrück Center for Molecular Medicine Berlin (MDC), Berlin, Germany.
Kamal R Abdul AzeezStructural Genomics Consortium, University of Oxford, Oxford, United Kingdom.
Jonathan M ElkinsStructural Genomics Consortium, University of Oxford, Oxford, United Kingdom.
Martin NeuenschwanderLeibniz-Forschungsinstitut für Molekulare Pharmakologie (FMP), Berlin, Germany.
Andreas OderLeibniz-Forschungsinstitut für Molekulare Pharmakologie (FMP), Berlin, Germany.
Mohamed ElkewediMax Delbrück Center for Molecular Medicine Berlin (MDC), Berlin, Germany.
Sarah JakschMax Delbrück Center for Molecular Medicine Berlin (MDC), Berlin, Germany.
Karsten AndraeZuse Institute Berlin (ZIB), Germany.
Jinliang LiUniversity of Miami Miller School of Medicine, Miami, United States of America.
Joao FernandesMax Delbrück Center for Molecular Medicine Berlin (MDC), Berlin, Germany.
Paul Markus MüllerMax Delbrück Center for Molecular Medicine Berlin (MDC), Berlin, Germany.
Stephan GrunwaldMax Delbrück Center for Molecular Medicine Berlin (MDC), Berlin, Germany.
Stephen F MarinoMax Delbrück Center for Molecular Medicine Berlin (MDC), Berlin, Germany.
Tanja VukićevićMax Delbrück Center for Molecular Medicine Berlin (MDC), Berlin, Germany.
Jenny EichhorstLeibniz-Forschungsinstitut für Molekulare Pharmakologie (FMP), Berlin, Germany.
Burkhard WiesnerLeibniz-Forschungsinstitut für Molekulare Pharmakologie (FMP), Berlin, Germany.
Marcus WeberZuse Institute Berlin (ZIB), Germany.
Michael KapiloffUniversity of Miami Miller School of Medicine, Miami, United States of America.
Oliver RocksMax Delbrück Center for Molecular Medicine Berlin (MDC), Berlin, Germany.
Oliver DaumkeMax Delbrück Center for Molecular Medicine Berlin (MDC), Berlin, Germany.
Thomas WielandInstitute of Experimental Pharmacology and Toxicology, Medical Faculty Mannheim, Heidelberg University, Heidelberg, Germany.
Stefan KnappStructural Genomics Consortium, University of Oxford, Oxford, United Kingdom.
Jens Peter von KriesLeibniz-Forschungsinstitut für Molekulare Pharmakologie (FMP), Berlin, Germany.
Enno KlussmannMax Delbrück Center for Molecular Medicine Berlin (MDC), Berlin, Germany.ORCID 0000-0003-4004-5003
Max Delbrück Center · DELeibniz-Forschungsinstitut für Molekulare Pharmakologie · DEUniversity of Miami · USUniversity of Oxford · GBZuse Institute Berlin · DEGoethe University Frankfurt · DEHeidelberg University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Stimulation of renal collecting duct principal cells with antidiuretic hormone (arginine-vasopressin, AVP) results in inhibition of the small GTPase RhoA and the enrichment of the water channel aquaporin-2 (AQP2) in the plasma membrane. The membrane insertion facilitates water reabsorption from primary urine and fine-tuning of body water homeostasis. Rho guanine nucleotide exchange factors (GEFs) interact with RhoA, catalyze the exchange of GDP for GTP and thereby activate the GTPase. However, GEFs involved in the control of AQP2 in renal principal cells are unknown. The A-kinase anchoring protein, AKAP-Lbc, possesses GEF activity, specifically activates RhoA, and is expressed in primary renal inner medullary collecting duct principal (IMCD) cells. Through screening of 18,431 small molecules and synthesis of a focused library around one of the hits, we identified an inhibitor of the interaction of AKAP-Lbc and RhoA. This molecule, Scaff10-8, bound to RhoA, inhibited the AKAP-Lbc-mediated RhoA activation but did not interfere with RhoA activation through other GEFs or activities of other members of the Rho family of small GTPases, Rac1 and Cdc42. Scaff10-8 promoted the redistribution of AQP2 from intracellular vesicles to the periphery of IMCD cells. Thus, our data demonstrate an involvement of AKAP-Lbc-mediated RhoA activation in the control of AQP2 trafficking.

Indexed as

A Kinase Anchor ProteinsAquaporin 2Cell MembraneHEK293 CellsHumansKidney Tubules, CollectingMinor Histocompatibility AntigensProtein BindingProtein TransportProto-Oncogene ProteinsrhoA GTP-Binding ProteinSmall Molecule LibrariesStructure-Activity RelationshipAKAP13 protein, humanA Kinase Anchor ProteinsAquaporin 2Minor Histocompatibility AntigensProto-Oncogene ProteinsrhoA GTP-Binding ProteinSmall Molecule Libraries

Identifiers

PMID29373579
PMCPMC5786306
OpenAlexW2785330210

What OpenQuestion holds

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Registered trials

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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.