Evidence map›Paper›PMID 26582204›Full record

ArticleThe Journal of biological chemistry2016

The A-kinase Anchoring Protein GSKIP Regulates GSK3β Activity and Controls Palatal Shelf Fusion in Mice.

Veronika Anita Deák, Philipp Skroblin, Carsten Dittmayer, Klaus-Peter Knobeloch, Sebastian Bachmann, Enno Klussmann

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.6field-weighted citation impact, top 30% 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

10 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. Phosphodiesterases: Evolving Concepts and Implications for Human Therapeutics.Annual review of pharmacology and toxicology · 2025
    Review
  3. Article
  4. Loss ofMolecular and cellular biology · 2022
    Article
  5. Article
  6. Disruptors of AKAP-Dependent Protein-Protein Interactions.Methods in molecular biology (Clifton, N.J.) · 2022
    Article
  7. Article
  8. Article
  9. Review
  10. 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

6 authors at 4 institutions in 1 country.

Veronika Anita DeákFrom the Max Delbrück Center for Molecular Medicine in the Helmholtz Association (MDC), Robert-Rössle-Strasse 10, 13125 Berlin.
Philipp SkroblinFrom the Max Delbrück Center for Molecular Medicine in the Helmholtz Association (MDC), Robert-Rössle-Strasse 10, 13125 Berlin.
Carsten Dittmayerthe Institute of Anatomy, Charité University Medicine, Philippstrasse 12, 10115 Berlin, Germany.
Klaus-Peter Knobelochthe Institute for Neuropathology, University of Freiburg, Breisacher Strasse 64, 79106 Freiburg, and.
Sebastian Bachmannthe Institute of Anatomy, Charité University Medicine, Philippstrasse 12, 10115 Berlin, Germany.
Enno KlussmannFrom the Max Delbrück Center for Molecular Medicine in the Helmholtz Association (MDC), Robert-Rössle-Strasse 10, 13125 Berlin, the DZHK (German Centre for Cardiovascular Research), partner site Berlin, Oudenarder Strasse 16, 13347 Berlin, Germany enno.klussmann@mdc-berlin.de.ORCID http://orcid.org/0000-0003-4004-5003
Charité - Universitätsmedizin Berlin · DEMax Delbrück Center · DEGerman Centre for Cardiovascular Research · DEUniversity of Freiburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A-kinase anchoring proteins (AKAPs) represent a family of structurally diverse proteins, all of which bind PKA. A member of this family is glycogen synthase kinase 3β (GSK3β) interaction protein (GSKIP). GSKIP interacts with PKA and also directly interacts with GSK3β. The physiological function of the GSKIP protein in vivo is unknown. We developed and characterized a conditional knock-out mouse model and found that GSKIP deficiency caused lethality at birth. Embryos obtained through Caesarean section at embryonic day 18.5 were cyanotic, suffered from respiratory distress, and failed to initiate breathing properly. Additionally, all GSKIP-deficient embryos showed an incomplete closure of the palatal shelves accompanied by a delay in ossification along the fusion area of secondary palatal bones. On the molecular level, GSKIP deficiency resulted in decreased phosphorylation of GSK3β at Ser-9 starting early in development (embryonic day 10.5), leading to enhanced GSK3β activity. At embryonic day 18.5, GSK3β activity decreased to levels close to that of wild type. Our findings reveal a novel, crucial role for GSKIP in the coordination of GSK3β signaling in palatal shelf fusion.

Indexed as

AllelesAnimalsCleft PalateEmbryo LossEmbryo, MammalianFemaleGene Expression Regulation, DevelopmentalGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHemizygoteMaleMice, Inbred C57BLMice, KnockoutPalatePhenotypePhosphorylationGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaGsk3b protein, mouseGSKIP protein, mousePhosphoserineRepressor ProteinsRNA, MessengerA-kinase anchoring protein (AKAP)animal modelcell signalingcleft palatecyclic AMP (cAMP)developmentglycogen synthase kinase 3 (GSK-3)GSK3β interaction proteinprotein kinase A (PKA)

Identifiers

PMID26582204
PMCPMC4705389
OpenAlexW2225176933

What OpenQuestion holds

Textmetadata
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.